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Entity

Name
Neoplasms
Namespace
MESHD
Namespace Version
20170725
Namespace URL
https://arty.scai.fraunhofer.de/artifactory/bel/namespace/mesh-diseases/mesh-diseases-20170725.belns

Appears in Networks 69

Anhedonia_Model_Deliverable_1.3 v0.1.3

Anhedonia Model with 110 new articles (including 5 full texts) from Klaus until 9th March

BEL Framework Large Corpus Document v20170611

Approximately 61,000 statements. This is a modified version of the original to use namespace files hosted on Artifactory

BEL Framework Small Corpus Document v20150611

Approximately 2000 hand curated statements drawn from 57 PubMeds.

BEL Framework Example 3 Document v2015611

Example of modeling a full abstract taken from the BEL V1.0 Language Overview.

Neurotransmitter and Insulin NeuroMMSig enrichments v0.0.1

Enrichment of NeuroMMSig mechanisms: neurotransmitters and insuline signalling

Alzheimer's Disease Knowledge Assembly v5.0.4

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.2

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.3

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.4

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.5

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.6

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.7

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.8

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.9

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v3.4.10

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model Versions 1 and 2 - Re-Reviewed v1.0.0

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.1

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.8

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.9

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.10

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.11

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.12

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.15

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.16

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.17

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Anhedonia_Model_Deliverable_1.3 v0.2.4

Anhedonia Model Complete coding until 14th of May.

Anhedonia_Model_Deliverable_1.3 v0.2.5

Anhedonia Model Complete coding until 14th of May.

Anhedonia_Model_Deliverable_1.3 v0.2.6

Anhedonia Model Complete coding until 14th of May.

Anhedonia_Model_Deliverable_1.3 v0.2.0

Anhedonia Model Complete coding until 14th of May.

PTSD and TBI BEL Model v1.0.20

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Colorectal Cancer Knowledge Assembly - Drugs Pathways and General Biology v1.1.0

Colorectal Cancer Knowledge Assembly with drug associations and Pathways + general CRC biology

Anhedonia_Model_Final v1.0.1

Anhedonia Model Complete coding until 14th of May.

PTSD and TBI BEL Model v1.0.22

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.23

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD and TBI BEL Model v1.0.24

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Anhedonia_Model_Final v1.0.2

Anhedonia Model Complete coding generated from an equivalent of 421 articles (321 abstracts+10 full text (*10 abstracts)). It also contains part of projection models, since all the statements with non projection information discarded from projection model.

PTSD and TBI BEL Model v1.0.25

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 348 pubmed articles and 2 articles from other sources like Book. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

PTSD BEL Model v1.0.26

PTSD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD). This version contains knowledge extracted from 323 pubmed articles and 2 articles from other sources like Book. Out of these,523 articles belongs 323 PTSD articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

TBI BEL Model v1.0.27

TBI BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Traumatic Brain Injury. This version contains knowledge extracted from 523 pubmed articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

TBRD - PTSD and TBI BEL Model v1.0.30

TBRD BEL model is a disease model based on Biological Expression Language (BEL) containing the core mechanisms of Post Traumatic Stress Disorder (PTSD) and Traumatic Brain Injury (TBI). This version contains knowledge extracted from 847 pubmed articles and 2 articles from other sources like Book. Out of these,523 articles belongs 323 PTSD articles. This work is from the collaboration between CohenVeterans Bioscience and Fraunhofer SCAI

Alzheimer's Disease Knowledge Assembly v5.0.6

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

Alzheimer's Disease Knowledge Assembly v5.0.9

This knowledge assembly is specific to Alzheimer's Disease for the AETIONOMY project. It encodes the pathological mechanisms in neurons in the human brain as well as additional evidence from mice and rats. This model includes different pathways such as apoptosis signaling, calcium signaling, cholesterol homeostasis, endocytosis, GSK activation, inflammatory responses, oxidative stress of mitochondria and endoplasmic reticulum, etc. In this version, we have added additional mechanisms/pathways to describe the functional consequences of SNPs linked with genes implicated in Alzheimer's Disease through GWAS.

Colorectal Cancer Knowledge Assembly - Drugs Pathways v1.0.0

Colorectal Cancer Knowledge Assembly with drug associations and Pathways.

colorectal cancer Knowledge Assembly - Drugs v1.0.1

colorectal cancer Knowledge Assembly with drug associations.

Colorectal Cancer Model v1.0.0

Colorectal Cancer Model built for i:DSem-BMBF project.

colorectal cancer Drugs resistance v1.0.1.0

colorectal cancer Knowledge Assembly with drug associations.

CRC_combined v1.1

BEL Document

Colorectal Cancer Model v2.0.0

Colorectal Cancer Model

Colorectal Cancer Model v0.0.0

Colorectal Cancer Model

Colorectal Cancer Model v2.0.3

Colorectal Cancer Model

Colorectal Cancer Model v2.0.4

Colorectal Cancer Model, uploaded by reagon

Colorectal Cancer Model v2.0.5

Colorectal Cancer Model, uploaded by reagon

Colorectal Cancer Model v2.0.6

Colorectal Cancer Model, uploaded by reagon

AB_Test1 v1.1.1

test BEl doc.

Test1 v1.1.1

test BEl doc.

AB_Test2 v1.1.1

test BEl doc.

DR_1 v1.1.1

test BEl doc.

Test3 v1.1.1

test BEl doc.

AB_Test4 v1.1.1

test BEl doc.

Test4 v1.1.2

test BEl doc.

In-Edges 413

act(p(MGI:Met), ma(kin)) increases path(MESHD:Neoplasms)

Targeting the activated, human MET oncogene to adult liver caused slowly progressing hepatocarcinogenesis. PubMed:15772665

Annotations
Experimental Factor Ontology (EFO)
LNCAP cell
NCBI Taxonomy Ids
10090
Uberon
liver
Cell Ontology (CL)
macrophage
MeSH
Cell Nucleus
Disease Ontology (DO)
breast cancer
MeSH
Sputum
MeSH
Head and Neck Neoplasms

act(p(HGNC:STAT3), ma(tscript)) increases path(MESHD:Neoplasms)

Signal transduction and activator of transcription 3 (STAT3) signaling is constitutively activated in various tumors, and is involved in cell survival and proliferation during oncogenesis. PubMed:15077160

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
prostate gland
Cell Ontology (CL)
fat cell
MeSH
Cell Nucleus
Disease Ontology (DO)
multiple myeloma

p(MGI:Ccnd1) increases path(MESHD:Neoplasms)

Mammary hyperplasia and carcinoma in MMTV-cyclin D1 transgenic mice.We report here that overexpression of cyclin D1 resulted in abnormal mammary cell proliferation including the development of mammary adenocarcinomas. We conclude that overexpression of cyclin D1 deregulates cell proliferation and can induce tumorigenic changes in mammary tissues, suggesting that cyclin D1 indeed plays an important oncogenic role in breast cancer. PubMed:8208295

Annotations
Experimental Factor Ontology (EFO)
Hep G2 cell
NCBI Taxonomy Ids
10090
Uberon
mammary gland
Cell Ontology (CL)
macrophage
MeSH
Cell Nucleus
Disease Ontology (DO)
breast cancer
MeSH
Sputum
MeSH
Head and Neck Neoplasms

p(HGNC:HELLS) decreases path(MESHD:Neoplasms)

loss of function of HELLS/SMARCA6 by allelic loss and aberrant proteins by tumor-specific exon creation may result in epigenetic deregulation, leading lung cells to malignancy or its progression. PubMed:15305370

Annotations
Experimental Factor Ontology (EFO)
PC-3 cell
NCBI Taxonomy Ids
9606
Uberon
lung
Cell Ontology (CL)
macrophage
MeSH
Cytoplasm
Disease Ontology (DO)
gastric adenocarcinoma

act(p(MGI:Kras), ma(gtp)) increases path(MESHD:Neoplasms)

Inactivation of Icmt inhibited cell growth and K-Ras-induced oncogenic transformation, both in soft agar assays and in a nude mice model. PubMed:14966563

Annotations
Experimental Factor Ontology (EFO)
COS-1 cell
NCBI Taxonomy Ids
10090
Uberon
skeletal muscle tissue
Cell Ontology (CL)
macrophage
MeSH
Cell Membrane
Disease Ontology (DO)
atherosclerosis

p(HGNC:CTNNB1) increases path(MESHD:Neoplasms)

Deregulation of the pathway results in the aberrant accumulation of beta-catenin in the nucleus, often leading to cancer. PubMed:12000790

Annotations
Experimental Factor Ontology (EFO)
MEF cell line
NCBI Taxonomy Ids
9606
Uberon
neural crest
Cell Ontology (CL)
preadipocyte
MeSH
Cell Nucleus
Disease Ontology (DO)
colon cancer

act(p(MGI:Braf), ma(kin)) increases path(MESHD:Neoplasms)

The effect of inactivating Icmt was not limited to the inhibition of K-Ras-induced transformation: inactivation of Icmt blocked transformation by an oncogenic form of B-Raf PubMed:14966563

Annotations
Experimental Factor Ontology (EFO)
COS-1 cell
NCBI Taxonomy Ids
10090
Uberon
skeletal muscle tissue
Cell Ontology (CL)
macrophage
MeSH
Cell Membrane
Disease Ontology (DO)
atherosclerosis

p(MGI:Ctnnb1) increases path(MESHD:Neoplasms)

An increase in b-catenin levels increases the pool of nuclear beta-catenin-TCF/LEF complexes, which, in turn, activate a gene expression program to establish the oncogenic phenotype. PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
293 cell
NCBI Taxonomy Ids
10090
Uberon
skeletal muscle tissue
Cell Ontology (CL)
dendritic cell
MeSH
Cell Nucleus
Disease Ontology (DO)
estrogen-receptor negative breast cancer

p(HGNC:ERBB2) increases path(MESHD:Neoplasms)

Overexpression of HER-2/neu leads to elevated tumorigenicity, enhanced metastatic potential, increased resistance to TNF-alpha-induced apoptosis and resistance to treatments such as paclitaxel and tamoxifen. PubMed:12845342

Annotations
Experimental Factor Ontology (EFO)
THP-1 cell
NCBI Taxonomy Ids
9606
Uberon
mammary gland
Cell Ontology (CL)
hepatocyte
MeSH
Cell Nucleus
Disease Ontology (DO)
colon cancer

act(p(MGI:Ppara), ma(tscript)) increases path(MESHD:Neoplasms)

Sustained activation of PPARalpha by these agents leads to the development of liver tumors in rats and mice. PubMed:11764000

Annotations
Experimental Factor Ontology (EFO)
HUVEC cell line
NCBI Taxonomy Ids
10090
Uberon
liver
Cell Ontology (CL)
endothelial cell of umbilical vein
MeSH
Extracellular Space
Disease Ontology (DO)
multiple myeloma

p(HGNC:ETV6) decreases path(MESHD:Neoplasms)

One of sixty cytogenetically aberrant myeloid malignancies, an AML with a complex karyotype including del(5q) and del(20q), showed a hemizygous interstitial deletion of the ETV6 and CDKN1B loci. PubMed:9171997

Annotations
Experimental Factor Ontology (EFO)
NIH-3T3 cell
NCBI Taxonomy Ids
9606
Uberon
bone tissue
Cell Ontology (CL)
platelet
MeSH
Cytoplasm
Disease Ontology (DO)
multiple myeloma
MeSH
Sputum
MeSH
Head and Neck Neoplasms

p(MGI:Ptges) increases path(MESHD:Neoplasms)

cotransfection of COX-2 and mPGES-1 into HEK293 cells resulted in cellular transformation manifested by colony formation in soft agar culture and tumor formation when implanted subcutaneously into nude mice. PubMed:12626523

Annotations
Experimental Factor Ontology (EFO)
U-937 cell
NCBI Taxonomy Ids
10090
Uberon
colon
Cell Ontology (CL)
respiratory epithelial cell
MeSH
Cytoplasm
Disease Ontology (DO)
B-cell lymphoma

act(p(MGI:Klf4), ma(tscript)) decreases path(MESHD:Neoplasms)

Here we show that KLF4 protein expression was decreased or lost in primary tumors and, in particular, lymph node metastases when compared with that in normal gastric mucosa. PubMed:15805274

Annotations
Experimental Factor Ontology (EFO)
C subscript(2) C subscript(12) cell
NCBI Taxonomy Ids
10090
Uberon
prostate gland
Cell Ontology (CL)
osteoblast
MeSH
Cell Membrane
Disease Ontology (DO)
non-small cell lung carcinoma
MeSH
Sputum
MeSH
Head and Neck Neoplasms

a(CHEBI:progesterone) increases path(MESHD:Neoplasms)

In 1993, we were able to induce mammary carcinomas in BALB/c female mice using progesterone PubMed:12473170

Annotations
Experimental Factor Ontology (EFO)
MCF7 cell
NCBI Taxonomy Ids
9606
Uberon
breast
Cell Ontology (CL)
epithelial cell
MeSH
Cell Membrane
Disease Ontology (DO)
neuroblastoma

act(p(RGD:Ppara), ma(tscript)) increases path(MESHD:Neoplasms)

Sustained activation of PPARalpha by these agents leads to the development of liver tumors in rats and mice. PubMed:11764000

Annotations
Experimental Factor Ontology (EFO)
HUVEC cell line
NCBI Taxonomy Ids
10116
Uberon
liver
Cell Ontology (CL)
endothelial cell of umbilical vein
MeSH
Extracellular Space
Disease Ontology (DO)
multiple myeloma

act(p(HGNC:PAX2), ma(tscript)) increases path(MESHD:Neoplasms)

we identify a paired-box gene, PAX2, that is crucially involved in cell proliferation and carcinogenesis in the endometrium PubMed:16355216

Annotations
Experimental Factor Ontology (EFO)
NIH-3T3 cell
NCBI Taxonomy Ids
9606
Uberon
endometrium
Cell Ontology (CL)
smooth muscle cell
MeSH
Cytoplasm
Disease Ontology (DO)
endometrial cancer
MeSH
Sputum
MeSH
Head and Neck Neoplasms

p(HGNC:AXIN2) negativeCorrelation path(MESHD:Neoplasms)

axin1 and axin2 loss-of-function mutations have also been detected in rare cases of colorectal cancer124,125. PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
colon
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Hematopoietic Stem Cells

act(p(HGNC:HRAS), ma(gtp)) increases path(MESHD:Neoplasms)

Ras-driven epidermal neoplasias generated on the surface of immunodeficient SCID mice were treated topically with DMSO vehicle or SP600125 daily for 5 weeks. DMSO and untreated control tissues displayed typical findings of neoplasia, including invasion and disruption of the BMZ, as visualized by type VII collagen staining (Fig. 2A). In contrast, tissues treated with SP600125 lacked invasive neoplasia and retained sharp delineation of the BMZ, with a humanspecific desmoglein-3 antibody confirming the human origin of these tissues (Fig. 2A). PubMed:17440097

Annotations
Experimental Factor Ontology (EFO)
293 cell
NCBI Taxonomy Ids
9606
Uberon
carotid artery segment
Cell Ontology (CL)
endothelial cell
MeSH
Cytoplasm
Disease Ontology (DO)
atherosclerosis
MeSH
Blood Vessels

p(MGI:Kras, var(p.Gly12Asp)) increases path(MESHD:Neoplasms)

Based on these observations, a mouse model of lung adenocarcinoma has been generated in which nasal instillation of Ad-Cre to the lungs of K-Ras+/LSL-G12D conditional mutant mice (Figure 1a) results in the expression of oncogenic K-RasG12D and the development of lesions that resemble human tumors (Jackson et al., 2001). PubMed:19151761

Annotations
Experimental Factor Ontology (EFO)
293 cell
NCBI Taxonomy Ids
10090
Uberon
lung
Cell Ontology (CL)
keratinocyte
MeSH
Cytoplasm
Disease Ontology (DO)
atherosclerosis
MeSH
Blood Vessels

p(HGNC:AXIN1) negativeCorrelation path(MESHD:Neoplasms)

axin1 and axin2 loss-of-function mutations have also been detected in rare cases of colorectal cancer124,125. PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
colon
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Hematopoietic Stem Cells

bp(GOBP:"Wnt signaling pathway") positiveCorrelation path(MESHD:Neoplasms)

A constitutive Wnt signaling pathway has been linked to breast, colon, and other cancers (for reviews, see Bienz and Clevers, 2000; Polakis, 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
breast
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

bp(GOBP:"Wnt signaling pathway") positiveCorrelation path(MESHD:Neoplasms)

A constitutive Wnt signaling pathway has been linked to breast, colon, and other cancers (for reviews, see Bienz and Clevers, 2000; Polakis, 2000). PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
colon
Cell Ontology (CL)
fat cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Muscles

p(HGNC:IHH) negativeCorrelation path(MESHD:Neoplasms)

loss of Indian hedgehog, also contribute to the progression of colorectal cancer157 PubMed:18432252

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
9606
Uberon
colon
Cell Ontology (CL)
stem cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Hematopoietic Stem Cells

g(HGNC:CCND1) positiveCorrelation path(MESHD:Neoplasms)

Cyclin D1 overexpression/amplification is associated with numerous cancers. PubMed:15225871

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
NCBI Taxonomy Ids
10090
Uberon
lung
Cell Ontology (CL)
epithelial cell
MeSH
Cell Membrane
Disease Ontology (DO)
cancer
MeSH
Blood

p(HGNC:TNFRSF1A) increases path(MESHD:Neoplasms)

In support of this, TNFR1 has recently been implicated in murine epidermal tumorigenesis. Genetic deletion of Tnfr1 diminished occurrence of neoplasia in mice induced by both NF-κB blockade and chemical carcinogenesis (33,34). PubMed:17440097

Annotations
Experimental Factor Ontology (EFO)
293 cell
NCBI Taxonomy Ids
9606
Uberon
carotid artery segment
Cell Ontology (CL)
keratinocyte
MeSH
Cytoplasm
Disease Ontology (DO)
atherosclerosis
MeSH
Blood Vessels

act(p(HGNC:TNFRSF1A)) increases path(MESHD:Neoplasms)

In contrast, tissues treated with TNFR1 antibody, although hyperplastic, retained BMZ structure and proper desmoglein-3 expression, indicating intact tissue polarity (Fig. 5A and B). Blockade of TNFR1 signaling was accompanied by the absence of detectable pJNK in the tissues treated by the TNFR1 antibody (Supplementary Fig. S7). In addition, TNFR1 blockade reduced the mitotic index and limited mitotic cells to the basal layer, whereas proliferating cells were widespread and abundant in the control tumor tissue (Fig. 5C and D). These findings indicate that antagonizing TNFR1 function prevents Ras-driven tumorigenesis. PubMed:17440097

Annotations
Experimental Factor Ontology (EFO)
293 cell
NCBI Taxonomy Ids
9606
Uberon
carotid artery segment
Cell Ontology (CL)
keratinocyte
MeSH
Cytoplasm
Disease Ontology (DO)
atherosclerosis
MeSH
Blood Vessels

p(HGNC:KRAS, var(p.Gly12Val)) increases path(MESHD:Neoplasms)

We found that the K12V oncogene induces a more aggressive tumorigenic phenotype than the K12D oncogene, whereas K12C does not induce tumors in this model. PubMed:16679305

Annotations
Experimental Factor Ontology (EFO)
NIH-3T3 cell
NCBI Taxonomy Ids
10090

p(HGNC:KRAS, var(p.Gly12Cys)) causesNoChange path(MESHD:Neoplasms)

We found that the K12V oncogene induces a more aggressive tumorigenic phenotype than the K12D oncogene, whereas K12C does not induce tumors in this model. PubMed:16679305

Annotations
Experimental Factor Ontology (EFO)
NIH-3T3 cell
NCBI Taxonomy Ids
10090

p(HGNC:KRAS, var(p.Gly12Asp)) increases path(MESHD:Neoplasms)

We found that the K12V oncogene induces a more aggressive tumorigenic phenotype than the K12D oncogene, whereas K12C does not induce tumors in this model. PubMed:16679305

Annotations
Experimental Factor Ontology (EFO)
NIH-3T3 cell
NCBI Taxonomy Ids
10090

p(INTERPRO:"Serine/threonine-protein kinase MARK/par1") negativeCorrelation path(MESHD:Neoplasms)

The Par1 kinases, also known as microtubule affinity-regulating kinases (MARKs), are important for the establishment of cell polarity from worms to mammals. Dysregulation of these kinases has been implicated in autism, Alzheimer’s disease and cancer. Here we show that MARK/Par1 is activated downstream of NMDA receptors in primary hippocampal neurons. Further, we show that this activation is dependent on protein kinase A (PKA), through the phosphorylation of Ser431 of Par4/LKB1, the major upstream kinase of MARK/Par1. PubMed:25932647

p(HGNC:PIN1) association path(MESHD:Neoplasms)

However, little is known about the role of Pin1 in cancer or in modulating transcription factor activity. PubMed:11432833

p(HGNC:PIN1) positiveCorrelation path(MESHD:Neoplasms)

Thus, Pin1 is up-regulated in human tumors and cooperates with Ras signaling in increasing c-Jun transcriptional activity towards cyclin D1. PubMed:11432833

Annotations
NCBI Taxonomy Ids
9606
NeuroMMSigDB
MAPK-ERK subgraph

p(HGNC:GDE1) increases path(MESHD:Neoplasms)

Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. PubMed:20962322

path(MESHD:"Multiple Myeloma") association path(MESHD:Neoplasms)

Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. PubMed:20962322

p(SFAM:"MMP Family") association path(MESHD:Neoplasms)

Overexpression of MMPs is associated with a wide range of pathophysiological processes, including vascular disease, multiple sclerosis, Alzheimer's disease, and cancer. PubMed:19882751

p(HGNC:MMP3) association path(MESHD:Neoplasms)

Also matrix metalloproteinase-3 (MMP-3) or stromelysin-1 contributes to several pathologies, such as cancer, asthma and rheumatoid arthritis, and has also been associated with neurodegenerative diseases like Alzheimer's disease, Parkinson's disease and multiple sclerosis. PubMed:22862420

g(HGNC:CDH1) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

act(p(HGNC:PTPN13), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

p(HGNC:TRIM3) decreases path(MESHD:Neoplasms)

Tripartite motif (TRIM3) is recently identified as a tumour suppressor in glioblastoma but this tumour-suppressive function has not been investigated in CRC. PubMed:26691157

p(HGNC:STAT3, pmod(Ph)) increases path(MESHD:Neoplasms)

Geitinib (Gef) is an orally active inhibitor targeting the adenosine tri phosphate-binding domain of EGFR, and cucurbitacin B (CuB) is a selective inhibitor of JAK/STAT signaling with potent antitumor activity via suppression of STAT3 phosphorylation, but the underlying mechanism is not clear. PubMed:26183715

path(DO:"Muir-Torre syndrome") association path(MESHD:Neoplasms)

Muir-Torre syndrome, a Lynch syndrome variant, is characterized by sebaceous neoplasia plus one or more malignancies, typically colon cancer. PubMed:26826402

g(MGI:Dnmt1) association path(MESHD:Neoplasms)

Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the Apc(Min/+) mouse model of intestinal cancer. PubMed:26883721

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

g(HGNC:APC) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

g(HGNC:CTNNB1) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

g(HGNC:CTNNB1) positiveCorrelation path(MESHD:Neoplasms)

The loss of β-catenin inhibitory components is a well-established mechanism of carcinogenesis but β-catenin hyperactivity can also be enhanced through its coactivators. PubMed:26455321

act(p(HGNC:PTPRG), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

path(MESHD:"Carcinoma, Medullary") negativeCorrelation path(MESHD:Neoplasms)

Lymph node metastasis of MC was significantly lower than that of poorly differentiated adenocarcinoma/undifferentiated adenocarcinoma (PDA/UDA). In addition, MC had a higher MMRd rate (0.892, 95% CI 0.758-0.956), higher BRAF(V600E) mutation rate (0.652, 95% CI 0.143-0.954) and lower KRAS mutation rate (0.171, 95% CI 0.065-0.378) than PDA/UDA and conventional adenocarcinoma. PubMed:27001432

g(HGNC:DCC) decreases path(MESHD:Neoplasms)

DCC (Deleted in Colorectal Carcinoma) has been demonstrated to constrain tumor progression by inducing apoptosis unless engaged by its ligand netrin-1.This has been shown in breast and colorectal cancers PubMed:26882243

g(HGNC:DCC) decreases path(MESHD:Neoplasms)

Deleted in colorectal carcinoma (DCC) is a well known tumor suppressor gene. PubMed:23353777

act(p(HGNC:PTPRF), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

act(p(HGNC:PTPRT), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

g(dbSNP:rs714) increases path(MESHD:Neoplasms)

Overall, the pooled analysis showed that the DCC rs714 conferred increased risk of cancer only in Asians PubMed:26891331

g(HGNC:PIK3CA) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

bp(GOBP:"interleukin-23-mediated signaling pathway") increases path(MESHD:Neoplasms)

Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier. We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. PubMed:23034650

g(HGNC:L1TD1P1) association path(MESHD:Neoplasms)

Although human LINE-1 (L1) elements are actively mobilized in many cancers, a role for somatic L1 retrotransposition in tumor initiation has not been conclusively demonstrated. PubMed:27197217

p(HGNC:CTNNB1) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

p(HGNC:BRAF, var(p.Val600Glu)) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

g(MGI:Kras) negativeCorrelation path(MESHD:Neoplasms)

Colorectal adenomas significantly increased from 0.52 ± 0.15 in K-ras(+/+) mice to 0.87 ± 0.14 in K-ras(+/-) mice (mean ± SEM per mouse, P < 0.01); total tumour volume increased 2.13-fold (P < 0.05). Comparing K-ras(+/+) with K-ras(+/-) murine adenomas, Ki-67-positive proliferating tumour cells significantly increased from 7.77 ± 0.64% to 9.15 ± 0.92% and cleaved caspase-3-positive apoptotic tumour cells decreased from 1.40 ± 0.37% to 0.80 ± 0.22% (mean ± SEM, P < 0.05 for both). PubMed:24354449

g(HGNC:NTN4) association path(MESHD:Neoplasms)

Netrin-4 displays pathologic roles in tumorigenesis and neovascularization. PubMed:26732856

p(HGNC:PSMD4) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

act(p(HGNC:PTPN3), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

p(HGNC:PTGS2) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

act(p(HGNC:PTPN14), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

g(HGNC:KRAS) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

p(MGI:Ptges) increases path(MESHD:Neoplasms)

cotransfection of COX-2 and mPGES-1 into HEK293 cells resulted in cellular transformation manifested by colony formation in soft agar culture and tumor formation when implanted subcutaneously into nude mice. PubMed:12626523

p(HGNC:PCNA) biomarkerFor path(MESHD:Neoplasms)

Long-term use of cyclooxygenase-2 (COX-2) inhibitors can reduce the incidence of digestive cancers, such as colorectal cancers. Proliferating cell nuclear antigen (PCNA) is an important marker of cellular abnormal proliferation. This study was to evaluate the roles and correlation of COX-2 and PCNA in the onset and development of familial adenomatous polyposis (FAP) diseases. PubMed:19895739

p(HGNC:PCNA) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

p(HGNC:PIN1) association path(MESHD:Neoplasms)

However, little is known about the role of Pin1 in cancer or in modulating transcription factor activity. PubMed:11432833

p(HGNC:PIN1) positiveCorrelation path(MESHD:Neoplasms)

Thus, Pin1 is up-regulated in human tumors and cooperates with Ras signaling in increasing c-Jun transcriptional activity towards cyclin D1. PubMed:11432833

Annotations
NCBI Taxonomy Ids
9606
NeuroMMSigDB
MAPK-ERK subgraph

p(HGNC:GRN) association path(MESHD:Neoplasms)

Granulin (GRN, or progranulin) is a protein involved in wound repair, inflammation, and neoplasia. GRN has also been directly implicated in frontotemporal dementia and may contribute to Alzheimer's disease pathogenesis. However, GRN regulation expression is poorly understood. A high-throughput experimental microRNA assay showed that GRN is the strongest target for miR-107 in human H4 neuroglioma cells. miR-107 has been implicated in Alzheimer's disease pathogenesis, and sequence elements in the open reading frame-rather than the 3' untranslated region-of GRN mRNA are recognized by miR-107 and are highly conserved among vertebrate species. To better understand the mechanism of this interaction, FLAG-tagged Argonaute constructs were used following miR-107 transfection. GRN mRNA interacts preferentially with Argonaute 2. In vitro and in vivo studies indicate that regulation of GRN by miR-107 may be functionally important. Glucose supplementation in cultured cells that leads to increased miR-107 levels also results in decreased GRN expression, including changes in cell compartmentation and decreased secretion of GRN protein. This effect was eliminated following miR-107 transfection. We also tested a mouse model where miR-107 has been shown to be down-regulated. In brain tissue subjacent to 1.0 mm depth controlled cortical impact, surviving hippocampal neurons show decreased miR-107 with augmentation of neuronal GRN expression. These findings indicate that miR-107 contributes to GRN expression regulation with implications for brain disorders. PubMed:20489155

p(HGNC:MMP3) association path(MESHD:Neoplasms)

Also matrix metalloproteinase-3 (MMP-3) or stromelysin-1 contributes to several pathologies, such as cancer, asthma and rheumatoid arthritis, and has also been associated with neurodegenerative diseases like Alzheimer's disease, Parkinson's disease and multiple sclerosis. PubMed:22862420

p(HGNC:PIN1) association path(MESHD:Neoplasms)

However, little is known about the role of Pin1 in cancer or in modulating transcription factor activity. PubMed:11432833

p(HGNC:PIN1) positiveCorrelation path(MESHD:Neoplasms)

Thus, Pin1 is up-regulated in human tumors and cooperates with Ras signaling in increasing c-Jun transcriptional activity towards cyclin D1. PubMed:11432833

Annotations
NCBI Taxonomy Ids
9606
MeSH
Neoplasms
NeuroMMSigDB
MAPK-ERK subgraph

p(SFAM:"MMP Family") association path(MESHD:Neoplasms)

Overexpression of MMPs is associated with a wide range of pathophysiological processes, including vascular disease, multiple sclerosis, Alzheimer's disease, and cancer. PubMed:19882751

p(HGNC:GDE1) increases path(MESHD:Neoplasms)

Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. PubMed:20962322

path(MESHD:"Multiple Myeloma") association path(MESHD:Neoplasms)

Importantly, miR-16 inhibition decreased animal survival in a xenograft model of MM by increasing tumor load and host angiogenesis. PubMed:20962322

p(HGNC:EPCAM) association path(MESHD:Neoplasms)

As observed from in vivo live animal imaging, EpCAM aptamers displayed a maximum tumor uptake at around 10 min followed by a rapid clearance after 80 min, while the signal of peak uptake and disappearance of antibody appeared at 3 h and 6 h after intravenous injection, respectively. PubMed:26199647

Annotations
MeSH
Peroxisomes
Experimental Factor Ontology (EFO)
MDAMB435
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Heterografts
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10117

p(HGNC:HMGB1) association path(MESHD:Neoplasms)

Tumor angiogenesis is enforced by autocrine regulation of high-mobility group box 1. PubMed:22391561

Annotations
MeSH
Peroxisomes
Experimental Factor Ontology (EFO)
COLO205
MeSH
Neoplasms
Evidence and Conclusion Ontology
combinatorial
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:HMGB1) association path(MESHD:Neoplasms)

Collectively, these data identify HMGB1 as an important modulator of tumor angiogenesis and suggest the feasibility of targeting HMGB1 for multi-level cancer treatment. PubMed:22391561

Annotations
MeSH
Peroxisomes
Experimental Factor Ontology (EFO)
COLO205
MeSH
Neoplasms
Evidence and Conclusion Ontology
combinatorial
MeSH
Blood Platelets
MeSH
Endothelium, Vascular
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

bp(MESHPP:"Alu Elements") association path(MESHD:Neoplasms)

Our study underscores the complexity of colorectal cancer aggravated by mobility of Alu elements and stresses the importance of personalized strategies, using a systematic and dynamic view, for effective cancer therapy. PubMed:25997618

Annotations
MeSH
Peroxisomes
Experimental Factor Ontology (EFO)
COLO205
MeSH
Neoplasms
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
point mutation
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:CD24) positiveCorrelation path(MESHD:Neoplasms)

This finding of CSC markers represented by one positive and one negative is in line with CSCs in other tumors, such as CD34+CD38- for acute myeloid leukemia; CD44+CD24- for breast and pancreatic tumors. PubMed:22895640

Annotations
Experimental Factor Ontology (EFO)
SW620 cell
MeSH
Colonic Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

a(CHEBI:sertraline) decreases path(MESHD:Neoplasms)

Sertraline, though not paroxetine, significantly inhibited tumor growth. PubMed:18636148

Annotations
Experimental Factor Ontology (EFO)
SW620 cell
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

p(HGNC:KRAS) association path(MESHD:Neoplasms)

It was observed that even the minimal initial concentration of KRAS mutation before the treatment has the ability to make the tumor refractory to the treatment. PubMed:26551156

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HeLa cell
Experimental Factor Ontology (EFO)
HepG2
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

complex(a(CHEBI:oxaliplatin), a(CHEMBLID:CHEMBL185), a(SCHEM:Leucovorin)) decreases path(MESHD:Neoplasms)

Oxaliplatin (trans-l-diaminocyclohexane oxalatoplatinum; l-OHP), a third-generation platinum antitumor drug, is currently approved in combination with 5-flurouracil (5-FU)/leucovorin (FOLFOX) for standard first- and second-line treatment of metastatic or advanced-stage colorectal cancer. PubMed:24492717

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Tissues
NCBI Taxonomy Names
Mus musculus

a(SCHEM:antioxidant) decreases path(MESHD:Neoplasms)

Pterostilbene (PT) possesses antioxidant and anticancer effects that are mediated by ER-β. PubMed:26472352

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(SFAM:"RAF Family") association path(MESHD:Neoplasms)

The Ras/Raf/MEK/ERK signaling pathway plays a key role in physiological processes and is often dysregulated in cancer as well as developmental disorders such as the neuro-cardio-facio-cutaneous syndromes. PubMed:22471666

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
LEOPARD Syndrome
MeSH
Neoplasms
Evidence and Conclusion Ontology
MTT assay
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

a(SCHEM:Trastuzumab) decreases path(MESHD:Neoplasms)

Monoclonal antibodies such as Trastuzumab and Cetuximab showed promising effects on several solid tumors. PubMed:21255939

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW1116 cell
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

path(MESHD:"Neoplastic Cells, Circulating") biomarkerFor path(MESHD:Neoplasms)

As technologies emerge to characterize CTCs at the molecular level, biological information can be obtained in real time, with the promise of serving as a 'surrogate tumour biopsy'. PubMed:21789147

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Serum
MeSH
Plasma
NCBI Taxonomy Names
Homo sapiens

complex(a(CHEBI:nanoparticle), a(SCHEM:Doxorubicin)) decreases path(MESHD:Neoplasms)

In vitro chemosensitivity assay revealed that apatite-DOX nanoparticles executed high cytotoxicity in several human cancer cell lines compared to free drugs and consequently apatite-DOX-facilitated enhanced tumor inhibitory effect was observed in colorectal tumor model within BALB/cA nude mice, thereby shedding light on their potential applications in cancer therapy. PubMed:23613726

Annotations
MeSH
Peroxisomes
Experimental Factor Ontology (EFO)
SW620 cell
Experimental Factor Ontology (EFO)
WiDr cell
Experimental Factor Ontology (EFO)
HCT116
Experimental Factor Ontology (EFO)
HCT15
MeSH
Neoplasms
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Colon
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10117

p(HGNC:MAPK3) association path(MESHD:Neoplasms)

CSE1L is secreted from tumor and its phosphorylation is regulated by ERK1/2. PubMed:26070816

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Mucous Membrane
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:TRAP1) association path(MESHD:Neoplasms)

TRAP1 is a HSP90 molecular chaperone deregulated in human tumors and responsible for specific features of cancer cells, i.e., protection from apoptosis, drug resistance, metabolic regulation, and protein quality control/ubiquitination. PubMed:25239454

Annotations
Experimental Factor Ontology (EFO)
cell line
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens

p(HGNC:HRAS) association path(MESHD:Neoplasms)

The Ras/Raf/MEK/ERK signaling pathway plays a key role in physiological processes and is often dysregulated in cancer as well as developmental disorders such as the neuro-cardio-facio-cutaneous syndromes. PubMed:22471666

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
LEOPARD Syndrome
MeSH
Neoplasms
Evidence and Conclusion Ontology
MTT assay
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:HRAS) association path(MESHD:Neoplasms)

Here, the similarities but also the differential effects of RAS and BRAF oncogenic signalling are examined and further implications in personalized cancer diagnosis and therapy are discussed. PubMed:25361007

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
SW620 cell
Experimental Factor Ontology (EFO)
WiDr cell
Experimental Factor Ontology (EFO)
HCT116
Experimental Factor Ontology (EFO)
HCT15
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:HRAS) association path(MESHD:Neoplasms)

Constitutive activation of the EGFR/RAS/PI3K cell-signaling pathway that may occur through molecular aberrations in core pathway components occurs in many solid tumours, including colorectal cancer(CRC), non-small-cell lung cancer(NSCLC) and breast cancer. PubMed:20718710

p(HGNC:CD38) negativeCorrelation path(MESHD:Neoplasms)

This finding of CSC markers represented by one positive and one negative is in line with CSCs in other tumors, such as CD34+CD38- for acute myeloid leukemia; CD44+CD24- for breast and pancreatic tumors. PubMed:22895640

Annotations
Experimental Factor Ontology (EFO)
SW620 cell
MeSH
Colonic Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

tloc(p(HGNC:CSE1L), fromLoc(GOCC:intracellular), toLoc(GOCC:"extracellular space")) association path(MESHD:Neoplasms)

CSE1L is secreted from tumor and its phosphorylation is regulated by ERK1/2. PubMed:26070816

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Mucous Membrane
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:TP53) negativeCorrelation path(MESHD:Neoplasms)

Patients with low expression of P53 had a 63.9%(23/36) response rate, significantly higher than that of patients with high P53 expression(28.8%,17/59)(P<0.01). PubMed:21866459

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Rectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
Evidence and Conclusion Ontology
protein expression
MeSH
Organoids
NCBI Taxonomy Names
Homo sapiens

p(HGNC:YAP1) association path(MESHD:Neoplasms)

Hippo negatively regulates its major effectors, YAP1 and TAZ kinases, which act as transcriptional co-activators inducing expression of genes involved not only in tissue repair and proliferation but are also oncoproteins involved in tumour development and progression. PubMed:26160682

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Neoplasms
Evidence and Conclusion Ontology
flow cytometry
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens

a(SCHEM:Irinotecan) decreases path(MESHD:Neoplasms)

We have previously shown that 5-methylselenocysteine (MSC) enhances therapeutic efficacy of irinotecan in various human tumor xenografts. PubMed:19632930

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
MDAMB231
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
Evidence and Conclusion Ontology
protein expression
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens

p(HGNC:IL6) association path(MESHD:Neoplasms)

There exists abundant evidence demonstrating that deregulated overexpression of IL-6 was associated with tumor progression through inhibition of cancer cell apoptosis, stimulation of angiogenesis, and drug resistance. PubMed:22651903

Annotations
Experimental Factor Ontology (EFO)
cell line
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

p(HGNC:IL6) association path(MESHD:Neoplasms)

Clinical studies have revealed that increased serum IL-6 concentrations in patients are associated with advanced tumor stages of various cancers (e.g., multiple myeloma, non-small cell lung carcinoma, colorectal cancer, renal cell carcinoma, prostate cancer, breast cancer and ovarian cancer) and short survival in patients. PubMed:22651903

p(HGNC:IL6) biomarkerFor path(MESHD:Neoplasms)

Therefore, blocking IL-6 signaling is a potential therapeutic strategy for cancer (i.e., anti-IL-6 therapy) characterized by pathological IL-6 overproduction. PubMed:22651903

Annotations
Experimental Factor Ontology (EFO)
cell line
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

p(HGNC:PEBP1) association path(MESHD:Neoplasms)

Our data illuminate, for the first time, the NRF2-KEAP 1 pathway as a possible target for personalized therapeutic intervention in RKIP depleted cancers. PubMed:22279539

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Serum
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:BRAF) association path(MESHD:Neoplasms)

Here, the similarities but also the differential effects of RAS and BRAF oncogenic signalling are examined and further implications in personalized cancer diagnosis and therapy are discussed. PubMed:25361007

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
SW620 cell
Experimental Factor Ontology (EFO)
WiDr cell
Experimental Factor Ontology (EFO)
HCT116
Experimental Factor Ontology (EFO)
HCT15
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:EGFR) association path(MESHD:Neoplasms)

We have found that Ca-channel blockers and EGFR tyrosine kinase inhibitors are effective in preclinical human melanoma models in breaking the apoptosis resistance of this tumor. PubMed:15902326

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Melanoma
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Breast
NCBI Taxonomy Names
Homo sapiens

p(HGNC:EGFR) association path(MESHD:Neoplasms)

Constitutive activation of the EGFR/RAS/PI3K cell-signaling pathway that may occur through molecular aberrations in core pathway components occurs in many solid tumours, including colorectal cancer(CRC), non-small-cell lung cancer(NSCLC) and breast cancer. PubMed:20718710

a(SCHEM:Cetuximab) decreases path(MESHD:Neoplasms)

Monoclonal antibodies such as Trastuzumab and Cetuximab showed promising effects on several solid tumors. PubMed:21255939

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW1116 cell
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

bp(GOBP:"apoptotic process") association path(MESHD:Neoplasms)

The apoptosis and antiapoptotic signaling pathways are important for regulating carcinogenesis and cancer progression, and for determining prognosis. PubMed:21264751

Annotations
Experimental Factor Ontology (EFO)
cell line
MeSH
Carcinogenesis
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Heterografts
NCBI Taxonomy Names
Rattus norvegicus

p(HGNC:AGXT) increases path(MESHD:Neoplasms)

In this study we have measured several potential drug resistance mechanisms consisting of the multidrug resistance gene product P-glycoprotein, glutathione, glutathione-transferase and -peroxidase, and the DNA repair enzyme O6-alkylguanine-DNA-alkyltransferase in samples of colon carcinoma and normal adjacent mucosa from 23 untreated patients.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient. PubMed:1672623

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Mucous Membrane
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:ABCB1) association path(MESHD:Neoplasms)

Not only was the targeted region of this monoclonal Fab antibody identified as a 16-peptide epitope (ALKDKKELEGSGKIAT) comprising residues 883-898 within the transmembrane (TM) domain of human P-gp, but also the binding ability with it was verified. PubMed:24348182

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Neoplasms
Evidence and Conclusion Ontology
enzyme_linked immunoabsorbent assay
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens

complex(a(CHEMBLID:CHEMBL105), a(CHEMBLID:CHEMBL917)) decreases path(MESHD:Neoplasms)

Bolus MMC with short duration FUdR as well as long-term FUdR alone provided better hepatic tumor response and survival than short-term FUdR alone. PubMed:8007682

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Liver Neoplasms
Evidence and Conclusion Ontology
MTT assay
MeSH
Tissues
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10117

p(HGNC:AKR1B1) positiveCorrelation path(MESHD:Neoplasms)

Overexpression of aldose reductase in human cancer tissues. PubMed:17136009

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:AKR1B1) positiveCorrelation path(MESHD:Neoplasms)

Some recent studies have shown overexpression of AR and AR-like proteins in human liver cancers and some cancer cell lines such as HepG2 and HeLa cells. PubMed:17136009

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HeLa cell
Experimental Factor Ontology (EFO)
HepG2
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:CSE1L, pmod(Ph)) biomarkerFor path(MESHD:Neoplasms)

Serum phospho-CSE1L may be a marker for monitoring the efficacy of targeted therapy. PubMed:26070816

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Serum
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

bp(GOBP:"cell adhesion") association path(MESHD:Neoplasms)

All five classes of cell adhesion molecules (CAM) - integrins, cadherins, immunoglobulin-like CAMs, selectins and CD44s - are characteristically dysregulated in human cancer. PubMed:18393855

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Breast
NCBI Taxonomy Names
Homo sapiens

path(MESHD:"Neoplasm Metastasis") association path(MESHD:Neoplasms)

An approach to the therapy of metastases from cancer of the upper rectum: a working hypothesis. PubMed:4052924

Annotations
MeSH
Peroxisomes
Experimental Factor Ontology (EFO)
SW620 cell
Experimental Factor Ontology (EFO)
WiDr cell
Experimental Factor Ontology (EFO)
HCT116
Experimental Factor Ontology (EFO)
HCT15
MeSH
Neoplasms
MeSH
Neoplasm Metastasis
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Rectum
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10117

p(HGNC:USP22) association path(MESHD:Neoplasms)

PURPOSE: Increasing experimental evidences suggest that ubiquitin-specific protease 22 (USP22), a cancer stem cell marker, plays a crucial role in pathological processes of epithelial malignancies and other solid tumors, which makes it a potential target for cancer therapy. PubMed:21773699

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Tissues
NCBI Taxonomy Names
Rattus norvegicus

p(HGNC:USP22) negativeCorrelation path(MESHD:Neoplasms)

Immunohistochemical analyses of tumor sections revealed that USP22 expression in animals decreased when USP22 expression was inhibited by miRNA. PubMed:21773699

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens

p(HGNC:CD44) association path(MESHD:Neoplasms)

In this study, we established a CD44(+) colorectal cancer stem cell line with particular emphasis on its self-renewal capacity, enhanced tumor initiation and drug resistance. PubMed:23736004

Annotations
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Neoplasms
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

p(HGNC:CD44) increases path(MESHD:Neoplasms)

P6C cells stably expressed CD44 and possessed a high capacity to form tumor spheres. PubMed:23736004

Annotations
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

p(HGNC:PDK1) association path(MESHD:Neoplasms)

Pyruvate dehydrogenase kinase-1 (PDK1) and PDK3 participate in the metabolic switch of cancer cells; however, the medical significance of PDK1 and PDK3 in cancer progression is not known. PubMed:21763680

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Colonic Neoplasms
Evidence and Conclusion Ontology
cell viability assay
MeSH
Bone Marrow Cells
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10117

p(MGI:Braf) association path(MESHD:Neoplasms)

Aberrant B-Raf signaling in human cancer -- 10 years from bench to bedside. PubMed:22471666

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Neoplasms
Evidence and Conclusion Ontology
MTT assay
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(MGI:Braf) association path(MESHD:Neoplasms)

As B-Raf displays aberrant activity in tumor entities for which no or only limited effective therapies are available, e.g., melanoma, ovarian, and colorectal carcinoma, a lot of hope and effort has been placed on strategies inhibiting its activity. PubMed:22471666

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Melanoma
MeSH
Neoplasms
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
MTT assay
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:ACLY) association path(MESHD:Neoplasms)

Furthermore, ACLy was significantly increased in cancer cells that had acquired resistance to SN38. PubMed:24132143

Annotations
Experimental Factor Ontology (EFO)
SW620 cell
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens

p(SFAM:"GST Family") increases path(MESHD:Neoplasms)

In this study we have measured several potential drug resistance mechanisms consisting of the multidrug resistance gene product P-glycoprotein, glutathione, glutathione-transferase and -peroxidase, and the DNA repair enzyme O6-alkylguanine-DNA-alkyltransferase in samples of colon carcinoma and normal adjacent mucosa from 23 untreated patients.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient. PubMed:1672623

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Mucous Membrane
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

p(HGNC:PDK3) association path(MESHD:Neoplasms)

Further analysis using immunohistochemical staining revealed that PDK3 levels were positively associated with severity of cancer and negatively associated with disease-free survival. PubMed:21763680

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Bone Marrow Cells
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10117

p(SFAM:"GPX Family") increases path(MESHD:Neoplasms)

In this study we have measured several potential drug resistance mechanisms consisting of the multidrug resistance gene product P-glycoprotein, glutathione, glutathione-transferase and -peroxidase, and the DNA repair enzyme O6-alkylguanine-DNA-alkyltransferase in samples of colon carcinoma and normal adjacent mucosa from 23 untreated patients.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient. PubMed:1672623

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Mucous Membrane
NCBI Taxonomy Names
Homo sapiens
NCBI Taxonomy Ids
10117

a(SCHEM:"Proteasome inhibitor") decreases path(MESHD:Neoplasms)

These results show that hypoxic tumor cells, which are generally more resistant to genotoxic agents, are hypersensitive to proteasome inhibitors and suggest that combining bortezomib with therapies that target the normoxic fraction of human tumors can lead to more effective tumor control. PubMed:19010906

p(HGNC:ABCC4) negativeCorrelation path(MESHD:Neoplasms)

Patients with low expression of MRP4 had a 66.7%(24/36) response rate, significantly higher than that of patients with high MRP4 expression (29.1%,16/59)(P<0.05). PubMed:21866459

Annotations
MeSH
Chromatin
Experimental Factor Ontology (EFO)
HCT116
MeSH
Rectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
Evidence and Conclusion Ontology
protein expression
MeSH
Organoids
NCBI Taxonomy Names
Homo sapiens

p(HGNC:CEP55) association path(MESHD:Neoplasms)

Identification of tumor-associated antigens may facilitate vaccination strategies to treat patients with malignant diseases. We have found that the centrosomal protein, Cep55/c10orf3 acts as a novel breast carcinoma-associated tumor-associated antigen. PubMed:19609239

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
breast cancer
Disease Ontology (DO)
colorectal cancer
Disease Ontology (DO)
lung cancer
MeSH
Neoplasms

act(p(HGNC:CEP55), ma(tscript)) association path(MESHD:Neoplasms)

Identification of tumor-associated antigens may facilitate vaccination strategies to treat patients with malignant diseases. We have found that the centrosomal protein, Cep55/c10orf3 acts as a novel breast carcinoma-associated tumor-associated antigen. PubMed:19609239

Annotations
NCBI Taxonomy Ids
9606
Experimental Factor Ontology (EFO)
SW480
Disease Ontology (DO)
breast cancer
Disease Ontology (DO)
colorectal cancer
Disease Ontology (DO)
lung cancer
MeSH
Neoplasms

p(HGNC:CEP55) association path(MESHD:Neoplasms)

Identification of tumor-associated antigens may facilitate vaccination strategies to treat patients with malignant diseases. We have found that the centrosomal protein, Cep55/c10orf3 acts as a novel breast carcinoma-associated tumor-associated antigen. PubMed:19609239

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW480
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
lung cancer
Disease Ontology (DO)
breast cancer
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

act(p(HGNC:CEP55), ma(tscript)) association path(MESHD:Neoplasms)

Identification of tumor-associated antigens may facilitate vaccination strategies to treat patients with malignant diseases. We have found that the centrosomal protein, Cep55/c10orf3 acts as a novel breast carcinoma-associated tumor-associated antigen. PubMed:19609239

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
SW480
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
lung cancer
Disease Ontology (DO)
breast cancer
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
9606

a(CHEBI:lenalidomide) decreases path(MESHD:Neoplasms)

lenalidomide and bevacizumab have antitumor activity in various tumor types. PubMed:27085994

Annotations
MeSH
Microtubules
Experimental Factor Ontology (EFO)
HT-29
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Allografts
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
NCBI Taxonomy Ids
10117

bp(GOBP:"interleukin-23-mediated signaling pathway") increases path(MESHD:Neoplasms)

Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier. We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. PubMed:23034650

Annotations
NCBI Taxonomy Ids
10090

g(dbSNP:rs2976392) causesNoChange path(MESHD:Neoplasms)

In contrast, the PSCA rs2976392 SNP did not modulate the cancer risk. PubMed:26891331

p(HGNC:PTGS2) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

p(HGNC:PSMD4) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

g(dbSNP:rs714) increases path(MESHD:Neoplasms)

Overall, the pooled analysis showed that the DCC rs714 conferred increased risk of cancer only in Asians PubMed:26891331

path(MESHD:"Carcinoma, Medullary") negativeCorrelation path(MESHD:Neoplasms)

Lymph node metastasis of MC was significantly lower than that of poorly differentiated adenocarcinoma/undifferentiated adenocarcinoma (PDA/UDA). In addition, MC had a higher MMRd rate (0.892, 95% CI 0.758-0.956), higher BRAF(V600E) mutation rate (0.652, 95% CI 0.143-0.954) and lower KRAS mutation rate (0.171, 95% CI 0.065-0.378) than PDA/UDA and conventional adenocarcinoma. PubMed:27001432

Annotations
Uberon
lymph node

g(dbSNP:rs2294008) increases path(MESHD:Neoplasms)

PSCA rs2294008 was associated with increased overall cancer risk PubMed:26891331

g(HGNC:PIK3CA) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Annotations
NCBI Taxonomy Ids
9606
Uberon
colon

p(HGNC:TRIM3) decreases path(MESHD:Neoplasms)

Tripartite motif (TRIM3) is recently identified as a tumour suppressor in glioblastoma but this tumour-suppressive function has not been investigated in CRC. PubMed:26691157

p(HGNC:STAT3, pmod(Ph)) increases path(MESHD:Neoplasms)

Geitinib (Gef) is an orally active inhibitor targeting the adenosine tri phosphate-binding domain of EGFR, and cucurbitacin B (CuB) is a selective inhibitor of JAK/STAT signaling with potent antitumor activity via suppression of STAT3 phosphorylation, but the underlying mechanism is not clear. PubMed:26183715

g(HGNC:L1TD1P1) association path(MESHD:Neoplasms)

Although human LINE-1 (L1) elements are actively mobilized in many cancers, a role for somatic L1 retrotransposition in tumor initiation has not been conclusively demonstrated. PubMed:27197217

g(HGNC:CDH1) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

p(HGNC:CTNNB1) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

g(HGNC:KRAS) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Annotations
NCBI Taxonomy Ids
9606
Uberon
colon

p(MGI:Ptges) increases path(MESHD:Neoplasms)

cotransfection of COX-2 and mPGES-1 into HEK293 cells resulted in cellular transformation manifested by colony formation in soft agar culture and tumor formation when implanted subcutaneously into nude mice. PubMed:12626523

Annotations
NCBI Taxonomy Ids
10090

p(HGNC:BRAF, var(p.Val600Glu)) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Annotations
NCBI Taxonomy Ids
9606
Uberon
colon

g(HGNC:DCC) decreases path(MESHD:Neoplasms)

DCC (Deleted in Colorectal Carcinoma) has been demonstrated to constrain tumor progression by inducing apoptosis unless engaged by its ligand netrin-1.This has been shown in breast and colorectal cancers PubMed:26882243

path(DO:"Muir-Torre syndrome") association path(MESHD:Neoplasms)

Muir-Torre syndrome, a Lynch syndrome variant, is characterized by sebaceous neoplasia plus one or more malignancies, typically colon cancer. PubMed:26826402

p(HGNC:PCNA) biomarkerFor path(MESHD:Neoplasms)

Long-term use of cyclooxygenase-2 (COX-2) inhibitors can reduce the incidence of digestive cancers, such as colorectal cancers. Proliferating cell nuclear antigen (PCNA) is an important marker of cellular abnormal proliferation. This study was to evaluate the roles and correlation of COX-2 and PCNA in the onset and development of familial adenomatous polyposis (FAP) diseases. PubMed:19895739

p(HGNC:PCNA) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

g(MGI:Kras) negativeCorrelation path(MESHD:Neoplasms)

Colorectal adenomas significantly increased from 0.52 ± 0.15 in K-ras(+/+) mice to 0.87 ± 0.14 in K-ras(+/-) mice (mean ± SEM per mouse, P < 0.01); total tumour volume increased 2.13-fold (P < 0.05). Comparing K-ras(+/+) with K-ras(+/-) murine adenomas, Ki-67-positive proliferating tumour cells significantly increased from 7.77 ± 0.64% to 9.15 ± 0.92% and cleaved caspase-3-positive apoptotic tumour cells decreased from 1.40 ± 0.37% to 0.80 ± 0.22% (mean ± SEM, P < 0.05 for both). PubMed:24354449

g(HGNC:CTNNB1) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

g(HGNC:CTNNB1) positiveCorrelation path(MESHD:Neoplasms)

The loss of β-catenin inhibitory components is a well-established mechanism of carcinogenesis but β-catenin hyperactivity can also be enhanced through its coactivators. PubMed:26455321

g(MGI:Dnmt1) association path(MESHD:Neoplasms)

Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the Apc(Min/+) mouse model of intestinal cancer. PubMed:26883721

Annotations
NCBI Taxonomy Ids
10090

g(HGNC:APC) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

p(HGNC:CEP55) association path(MESHD:Neoplasms)

Identification of tumor-associated antigens may facilitate vaccination strategies to treat patients with malignant diseases. We have found that the centrosomal protein, Cep55/c10orf3 acts as a novel breast carcinoma-associated tumor-associated antigen. PubMed:19609239

act(p(HGNC:CEP55), ma(tscript)) association path(MESHD:Neoplasms)

Identification of tumor-associated antigens may facilitate vaccination strategies to treat patients with malignant diseases. We have found that the centrosomal protein, Cep55/c10orf3 acts as a novel breast carcinoma-associated tumor-associated antigen. PubMed:19609239

act(p(HGNC:PTPRT), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
9606

g(HGNC:DCC) decreases path(MESHD:Neoplasms)

DCC (Deleted in Colorectal Carcinoma) has been demonstrated to constrain tumor progression by inducing apoptosis unless engaged by its ligand netrin-1.This has been shown in breast and colorectal cancers PubMed:26882243

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

g(HGNC:DCC) decreases path(MESHD:Neoplasms)

Deleted in colorectal carcinoma (DCC) is a well known tumor suppressor gene. PubMed:23353777

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

act(p(HGNC:PTPN13), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
9606

p(HGNC:PTGS2) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

p(HGNC:PSMD4) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

path(DO:"Muir-Torre syndrome") association path(MESHD:Neoplasms)

Muir-Torre syndrome, a Lynch syndrome variant, is characterized by sebaceous neoplasia plus one or more malignancies, typically colon cancer. PubMed:26826402

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

act(p(HGNC:PTPRF), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
9606

path(MESHD:"Carcinoma, Medullary") negativeCorrelation path(MESHD:Neoplasms)

Lymph node metastasis of MC was significantly lower than that of poorly differentiated adenocarcinoma/undifferentiated adenocarcinoma (PDA/UDA). In addition, MC had a higher MMRd rate (0.892, 95% CI 0.758-0.956), higher BRAF(V600E) mutation rate (0.652, 95% CI 0.143-0.954) and lower KRAS mutation rate (0.171, 95% CI 0.065-0.378) than PDA/UDA and conventional adenocarcinoma. PubMed:27001432

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus
Uberon
lymph node

g(HGNC:PIK3CA) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon
NCBI Taxonomy Ids
9606

act(p(HGNC:PTPRG), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
9606

p(HGNC:TRIM3) decreases path(MESHD:Neoplasms)

Tripartite motif (TRIM3) is recently identified as a tumour suppressor in glioblastoma but this tumour-suppressive function has not been investigated in CRC. PubMed:26691157

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

p(HGNC:STAT3, pmod(Ph)) increases path(MESHD:Neoplasms)

Geitinib (Gef) is an orally active inhibitor targeting the adenosine tri phosphate-binding domain of EGFR, and cucurbitacin B (CuB) is a selective inhibitor of JAK/STAT signaling with potent antitumor activity via suppression of STAT3 phosphorylation, but the underlying mechanism is not clear. PubMed:26183715

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

g(HGNC:CDH1) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon

bp(GOBP:"Wnt signaling pathway") association path(MESHD:Neoplasms)

Activation of WNT signaling promotes the invasive activities of several types of cancer cells, but it is not clear if it regulates the same processes in colorectal cancer (CRC) cells, or what mechanisms are involved. PubMed:26619963

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

p(HGNC:CTNNB1) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

g(HGNC:L1TD1P1) association path(MESHD:Neoplasms)

Although human LINE-1 (L1) elements are actively mobilized in many cancers, a role for somatic L1 retrotransposition in tumor initiation has not been conclusively demonstrated. PubMed:27197217

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

g(HGNC:CTNNB1) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon

g(HGNC:CTNNB1) positiveCorrelation path(MESHD:Neoplasms)

The loss of β-catenin inhibitory components is a well-established mechanism of carcinogenesis but β-catenin hyperactivity can also be enhanced through its coactivators. PubMed:26455321

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

act(p(HGNC:PTPN14), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
9606

g(HGNC:NTN4) association path(MESHD:Neoplasms)

Netrin-4 displays pathologic roles in tumorigenesis and neovascularization. PubMed:26732856

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus

bp(GOBP:"interleukin-23-mediated signaling pathway") increases path(MESHD:Neoplasms)

Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier. We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. PubMed:23034650

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon
NCBI Taxonomy Ids
10090

act(p(HGNC:PTPN3), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
9606

p(HGNC:PCNA) biomarkerFor path(MESHD:Neoplasms)

Long-term use of cyclooxygenase-2 (COX-2) inhibitors can reduce the incidence of digestive cancers, such as colorectal cancers. Proliferating cell nuclear antigen (PCNA) is an important marker of cellular abnormal proliferation. This study was to evaluate the roles and correlation of COX-2 and PCNA in the onset and development of familial adenomatous polyposis (FAP) diseases. PubMed:19895739

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

p(HGNC:PCNA) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus

g(HGNC:KRAS) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon
NCBI Taxonomy Ids
9606

g(MGI:Kras) negativeCorrelation path(MESHD:Neoplasms)

Colorectal adenomas significantly increased from 0.52 ± 0.15 in K-ras(+/+) mice to 0.87 ± 0.14 in K-ras(+/-) mice (mean ± SEM per mouse, P < 0.01); total tumour volume increased 2.13-fold (P < 0.05). Comparing K-ras(+/+) with K-ras(+/-) murine adenomas, Ki-67-positive proliferating tumour cells significantly increased from 7.77 ± 0.64% to 9.15 ± 0.92% and cleaved caspase-3-positive apoptotic tumour cells decreased from 1.40 ± 0.37% to 0.80 ± 0.22% (mean ± SEM, P < 0.05 for both). PubMed:24354449

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon
NCBI Taxonomy Ids
10090

p(HGNC:BRAF, var(p.Val600Glu)) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon
NCBI Taxonomy Ids
9606

g(MGI:Dnmt1) association path(MESHD:Neoplasms)

Previous studies employed mice with a hypomorphic mutation in DNA methyltransferase 1 (Dnmt1), which exhibited constitutive global DNA hypomethylation and decreased tumorigenesis in the Apc(Min/+) mouse model of intestinal cancer. PubMed:26883721

Appears in Networks:
Annotations
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
NCBI Taxonomy Names
Mus musculus
NCBI Taxonomy Ids
10090

g(HGNC:APC) biomarkerFor path(MESHD:Neoplasms)

These results support (i) that calcium and vitamin D modify APC, β-catenin, and E-cadherin expression in humans in directions hypothesized to reduce risk for colorectal neoplasms, (ii) calcium and vitamin D as potential chemopreventive agents against colorectal neoplasms, and (iii) the potential of APC, β-catenin, and E-cadherin expression as modifiable, preneoplastic risk biomarkers for colorectal neoplasms. PubMed:22964475

Appears in Networks:
Annotations
MeSH
Cytoplasm
MeSH
Condylomata Acuminata
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Plasma
NCBI Taxonomy Names
Mus musculus
Uberon
colon

p(HGNC:ABCB1) association path(MESHD:Neoplasms)

Not only was the targeted region of this monoclonal Fab antibody identified as a 16-peptide epitope (ALKDKKELEGSGKIAT) comprising residues 883-898 within the transmembrane (TM) domain of human P-gp, but also the binding ability with it was verified. PubMed:24348182

Annotations
Experimental Factor Ontology (EFO)
HT-29
MeSH
Microtubules
MeSH
Neoplasms
Evidence and Conclusion Ontology
enzyme_linked immunoabsorbent assay
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

act(p(HGNC:PTPRF), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
keratinocyte
NCBI Taxonomy Ids
9606

p(HGNC:YAP1) association path(MESHD:Neoplasms)

Hippo negatively regulates its major effectors, YAP1 and TAZ kinases, which act as transcriptional co-activators inducing expression of genes involved not only in tissue repair and proliferation but are also oncoproteins involved in tumour development and progression. PubMed:26160682

Annotations
Experimental Factor Ontology (EFO)
HT-29
MeSH
Chromatin
MeSH
Neoplasms
Evidence and Conclusion Ontology
dominant_negative mutant
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

g(dbSNP:rs2976392) causesNoChange path(MESHD:Neoplasms)

In contrast, the PSCA rs2976392 SNP did not modulate the cancer risk. PubMed:26891331

p(SFAM:"GPX Family") increases path(MESHD:Neoplasms)

In this study we have measured several potential drug resistance mechanisms consisting of the multidrug resistance gene product P-glycoprotein, glutathione, glutathione-transferase and -peroxidase, and the DNA repair enzyme O6-alkylguanine-DNA-alkyltransferase in samples of colon carcinoma and normal adjacent mucosa from 23 untreated patients.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient.All of these, with the exception of P-glycoprotein, showed significant increases in tumor tissue levels when compared with normal tissue from the same patient. PubMed:1672623

Annotations
Experimental Factor Ontology (EFO)
HCT15
MeSH
Intracellular Space
MeSH
Colorectal Neoplasms
MeSH
Mucous Membrane
NCBI Taxonomy Names
Mus musculus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:PCNA) biomarkerFor path(MESHD:Neoplasms)

Long-term use of cyclooxygenase-2 (COX-2) inhibitors can reduce the incidence of digestive cancers, such as colorectal cancers. Proliferating cell nuclear antigen (PCNA) is an important marker of cellular abnormal proliferation. This study was to evaluate the roles and correlation of COX-2 and PCNA in the onset and development of familial adenomatous polyposis (FAP) diseases. PubMed:19895739

p(HGNC:PCNA) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

p(HGNC:ABCC4) negativeCorrelation path(MESHD:Neoplasms)

Patients with low expression of MRP4 had a 66.7%(24/36) response rate, significantly higher than that of patients with high MRP4 expression (29.1%,16/59)(P<0.05). PubMed:21866459

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Peroxisomes
MeSH
Rectal Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
Evidence and Conclusion Ontology
protein expression
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

bp(MESHPP:"Alu Elements") association path(MESHD:Neoplasms)

Our study underscores the complexity of colorectal cancer aggravated by mobility of Alu elements and stresses the importance of personalized strategies, using a systematic and dynamic view, for effective cancer therapy. PubMed:25997618

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Chromatin
MeSH
Neoplasms
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Serum
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

composite(p(HGNC:HIF1A), p(HGNC:LOX)) increases path(MESHD:Neoplasms)

Taken together, these findings provide compelling evidence that LOX and HIF-1 act in synergy to foster tumor formation, and they suggest that HIF-1/LOX mutual regulation is a pivotal mechanism in the adaptation of tumor cells to hypoxia. PubMed:21239473

Annotations
Experimental Factor Ontology (EFO)
SW480
MeSH
Intracellular Space
MeSH
Neoplasms
MeSH
Mucus
NCBI Taxonomy Names
Crataegus azarolus
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

p(HGNC:PTGS2) positiveCorrelation path(MESHD:Neoplasms)

The positive expression rates of COX-2 in normal colonic mucosa, FAP adenoma, and carcinoma tissues were 0 (0/34), 80.6% (29/36), and 93.8% (30/32), respectively. Proliferation index (PI) in normal mucosa, FAP adenoma, and carcinoma tissues were 17.79+/-7.49, 34.47+/-10.57, and 71.75+/-9.22, respectively. Expressions of COX-2 and PCNA were significantly higher in the FAP adenoma and the carcinoma tissues than in the normal colonic mucosa(P<0.01). The expression of PCNA was significantly higher in the FAP carcinoma tissues than in the FAP adenoma (P<0.01). The expression of PCNA was higher in the FAP adenoma tissues with positive COX-2 than in the FAP adenomas tissues with negative COX-2 (P<0.01). PubMed:19895739

p(SFAM:"RAF Family") association path(MESHD:Neoplasms)

The Ras/Raf/MEK/ERK signaling pathway plays a key role in physiological processes and is often dysregulated in cancer as well as developmental disorders such as the neuro-cardio-facio-cutaneous syndromes. PubMed:22471666

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Peroxisomes
MeSH
LEOPARD Syndrome
MeSH
Neoplasms
Evidence and Conclusion Ontology
gain_of_function mutant phenotype
MeSH
Blood Platelets
MeSH
Endothelium, Vascular
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

path(DO:"Muir-Torre syndrome") association path(MESHD:Neoplasms)

Muir-Torre syndrome, a Lynch syndrome variant, is characterized by sebaceous neoplasia plus one or more malignancies, typically colon cancer. PubMed:26826402

p(HGNC:IL6) association path(MESHD:Neoplasms)

There exists abundant evidence demonstrating that deregulated overexpression of IL-6 was associated with tumor progression through inhibition of cancer cell apoptosis, stimulation of angiogenesis, and drug resistance. PubMed:22651903

Annotations
Experimental Factor Ontology (EFO)
MDAMB231
MeSH
Peroxisomes
MeSH
Neoplasms
Evidence and Conclusion Ontology
gain_of_function mutant phenotype
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:IL6) association path(MESHD:Neoplasms)

Clinical studies have revealed that increased serum IL-6 concentrations in patients are associated with advanced tumor stages of various cancers (e.g., multiple myeloma, non-small cell lung carcinoma, colorectal cancer, renal cell carcinoma, prostate cancer, breast cancer and ovarian cancer) and short survival in patients. PubMed:22651903

p(HGNC:IL6) biomarkerFor path(MESHD:Neoplasms)

Therefore, blocking IL-6 signaling is a potential therapeutic strategy for cancer (i.e., anti-IL-6 therapy) characterized by pathological IL-6 overproduction. PubMed:22651903

Annotations
Experimental Factor Ontology (EFO)
MDAMB231
MeSH
Peroxisomes
MeSH
Neoplasms
Evidence and Conclusion Ontology
gain_of_function mutant phenotype
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:STAT3, pmod(Ph)) increases path(MESHD:Neoplasms)

Geitinib (Gef) is an orally active inhibitor targeting the adenosine tri phosphate-binding domain of EGFR, and cucurbitacin B (CuB) is a selective inhibitor of JAK/STAT signaling with potent antitumor activity via suppression of STAT3 phosphorylation, but the underlying mechanism is not clear. PubMed:26183715

g(dbSNP:rs11942466) decreases path(MESHD:Neoplasms)

The rs11942466 polymorphism in the amphiregulin (AREG) gene region was associated with a pathological complete response (ypCR) (odds ratio: 0.26; 95% confidence interval: 0.06-0.79; P=0.014). PubMed:25026457

Annotations
Experimental Factor Ontology (EFO)
HT-29
Experimental Factor Ontology (EFO)
HCT 116 cell
MeSH
Intracellular Space
MeSH
Colorectal Neoplasms
MeSH
Lung
NCBI Taxonomy Names
Crataegus azarolus
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

p(HGNC:PEBP1) association path(MESHD:Neoplasms)

Our data illuminate, for the first time, the NRF2-KEAP 1 pathway as a possible target for personalized therapeutic intervention in RKIP depleted cancers. PubMed:22279539

Annotations
Experimental Factor Ontology (EFO)
HT-29
MeSH
Peroxisomes
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
Macrophages
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

complex(a(CHEBI:oxaliplatin), a(CHEMBLID:CHEMBL185), a(SCHEM:Leucovorin)) decreases path(MESHD:Neoplasms)

Oxaliplatin (trans-l-diaminocyclohexane oxalatoplatinum; l-OHP), a third-generation platinum antitumor drug, is currently approved in combination with 5-flurouracil (5-FU)/leucovorin (FOLFOX) for standard first- and second-line treatment of metastatic or advanced-stage colorectal cancer. PubMed:24492717

Annotations
Experimental Factor Ontology (EFO)
HT-29
MeSH
Chromatin
MeSH
Colorectal Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Tissues
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:CD24) positiveCorrelation path(MESHD:Neoplasms)

This finding of CSC markers represented by one positive and one negative is in line with CSCs in other tumors, such as CD34+CD38- for acute myeloid leukemia; CD44+CD24- for breast and pancreatic tumors. PubMed:22895640

Annotations
Experimental Factor Ontology (EFO)
SW620 cell
MeSH
Microtubules
MeSH
Neoplasms
Evidence and Conclusion Ontology
cell viability assay
MeSH
Endothelium
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:CTNNB1) association path(MESHD:Neoplasms)

We therefore suggest that PSMD4 or beta-catenin might be potential targets for suppressing tumor aggressiveness, and consequently, improving outcomes in patients whose tumors express cNrf2. PubMed:27033953

p(HGNC:EGFR) association path(MESHD:Neoplasms)

We have found that Ca-channel blockers and EGFR tyrosine kinase inhibitors are effective in preclinical human melanoma models in breaking the apoptosis resistance of this tumor. PubMed:15902326

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Intracellular Space
MeSH
Melanoma
MeSH
Neoplasms
MeSH
Breast
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:EGFR) association path(MESHD:Neoplasms)

Constitutive activation of the EGFR/RAS/PI3K cell-signaling pathway that may occur through molecular aberrations in core pathway components occurs in many solid tumours, including colorectal cancer(CRC), non-small-cell lung cancer(NSCLC) and breast cancer. PubMed:20718710

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
MeSH
Peroxisomes
MeSH
Carcinoma, Non-Small-Cell Lung
MeSH
Colorectal Neoplasms
MeSH
Breast Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

act(p(HGNC:PTPN14), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
keratinocyte
NCBI Taxonomy Ids
9606

act(p(HGNC:PTPN3), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
keratinocyte
NCBI Taxonomy Ids
9606

bp(GOBP:"interleukin-23-mediated signaling pathway") increases path(MESHD:Neoplasms)

Many epithelial cancers develop proximally to microbial communities, which are physically separated from immune cells by an epithelial barrier. We investigated mechanisms responsible for tumour-elicited inflammation in a mouse model of colorectal tumorigenesis, which, like human colorectal cancer, exhibits upregulation of IL-23 and IL-17. Here we show that IL-23 signalling promotes tumour growth and progression, and development of a tumoural IL-17 response. PubMed:23034650

Annotations
Experimental Factor Ontology (EFO)
DLD-1 cell
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon
Uberon
colon
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:TRAP1) association path(MESHD:Neoplasms)

TRAP1 is a HSP90 molecular chaperone deregulated in human tumors and responsible for specific features of cancer cells, i.e., protection from apoptosis, drug resistance, metabolic regulation, and protein quality control/ubiquitination. PubMed:25239454

Annotations
Experimental Factor Ontology (EFO)
COLO205
MeSH
Chromatin
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

act(p(HGNC:PTPRT), ma(phos)) decreases path(MESHD:Neoplasms)

A mutational analysis of the tyrosine phosphatase gene superfamily in human cancers identified 83 somatic mutations in six PTPs (PTPRF, PTPRG, PTPRT, PTPN3, PTPN13, PTPN14), affecting 26% of colorectal cancers and a smaller fraction of lung, breast, and gastric cancers. PubMed:15155950

Annotations
Experimental Factor Ontology (EFO)
293 cell
MeSH
Cytoplasm
MeSH
Neoplasms
MeSH
Colon
Cell Ontology (CL)
keratinocyte
NCBI Taxonomy Ids
9606

g(HGNC:KRAS) association path(MESHD:Neoplasms)

KRAS mutation was noted more frequently in LST (13/36, 36.1%) than polypoid neoplasms (5/34, 14.7%, p‚Äâ=‚Äâ0.041). When comparing with LST-NG, LST-G had a significantly higher frequency of KRAS mutation. (9/16, 56.3% vs. 4/20, 20.0%, p‚Äâ=‚Äâ0.024). BRAF mutation (V600E) was found in 2 of 36 (5.6%)LSTs and 1 of 34 (2.9%) polypoid lesions. The two LST lesions with BRAF mutation were pathologically proven to be serrated adenoma. PIK3CA mutation (exon 9 E545K) was identified only in LST (5/36, 13.9%). Mutations in KRAS, BRAF or PIK3CA occurred in a mutually exclusive manner. All mutations were absent in the specimens obtained from depressed type neoplasms. PubMed:25551625

Annotations
Experimental Factor Ontology (EFO)
DLD-1 cell
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon
Uberon
colon
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
9606

g(MGI:Kras) negativeCorrelation path(MESHD:Neoplasms)

Colorectal adenomas significantly increased from 0.52 ± 0.15 in K-ras(+/+) mice to 0.87 ± 0.14 in K-ras(+/-) mice (mean ± SEM per mouse, P < 0.01); total tumour volume increased 2.13-fold (P < 0.05). Comparing K-ras(+/+) with K-ras(+/-) murine adenomas, Ki-67-positive proliferating tumour cells significantly increased from 7.77 ± 0.64% to 9.15 ± 0.92% and cleaved caspase-3-positive apoptotic tumour cells decreased from 1.40 ± 0.37% to 0.80 ± 0.22% (mean ± SEM, P < 0.05 for both). PubMed:24354449

Annotations
Experimental Factor Ontology (EFO)
DLD-1 cell
MeSH
Cytoplasm
MeSH
Colorectal Neoplasms
MeSH
Colon
Uberon
colon
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

a(CHEBI:irinotecan) decreases path(MESHD:Neoplasms)

We have previously shown that 5-methylselenocysteine (MSC) enhances therapeutic efficacy of irinotecan in various human tumor xenografts. PubMed:19632930

Annotations
Experimental Factor Ontology (EFO)
MDAMB435
MeSH
Intracellular Space
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Heterografts
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

path(MESHD:"Carcinoma, Medullary") negativeCorrelation path(MESHD:Neoplasms)

Lymph node metastasis of MC was significantly lower than that of poorly differentiated adenocarcinoma/undifferentiated adenocarcinoma (PDA/UDA). In addition, MC had a higher MMRd rate (0.892, 95% CI 0.758-0.956), higher BRAF(V600E) mutation rate (0.652, 95% CI 0.143-0.954) and lower KRAS mutation rate (0.171, 95% CI 0.065-0.378) than PDA/UDA and conventional adenocarcinoma. PubMed:27001432

a(CHEBI:maltodextrin) decreases path(MESHD:Neoplasms)

Here we show that Fibersol-2, a digest-resistant maltodextrin, not only inhibits proliferation of colorectal SW480 cancer cell lines by increasing reactive oxygen species (ROS), but decreases the numbers of the adenoma count in Multiple Intestinal Neoplasia (MIN) mice carrying a mutation in the Adenomatous Polyposis Coli gene by 84 d of age. These observations provide direct evidence that Fibersol-2 intrinsically contains anti-cancer activity, independent of the intestinal metabolism and any potential interactions with the microbiota. PubMed:27143108

p(HGNC:CSE1L, pmod(Ph)) biomarkerFor path(MESHD:Neoplasms)

Serum phospho-CSE1L may be a marker for monitoring the efficacy of targeted therapy. PubMed:26070816

Annotations
Experimental Factor Ontology (EFO)
HCT116
MeSH
Chromatin
MeSH
Neoplasms
Evidence and Conclusion Ontology
RNAi
MeSH
Serum
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

complex(a(CHEMBLID:CHEMBL105), a(CHEMBLID:CHEMBL917)) decreases path(MESHD:Neoplasms)

Bolus MMC with short duration FUdR as well as long-term FUdR alone provided better hepatic tumor response and survival than short-term FUdR alone. PubMed:8007682

Annotations
Experimental Factor Ontology (EFO)
cancer cell line
MeSH
Chromatin
MeSH
Liver Neoplasms
Evidence and Conclusion Ontology
MTT assay
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10117

a(SCHEM:"Proteasome inhibitor") decreases path(MESHD:Neoplasms)

These results show that hypoxic tumor cells, which are generally more resistant to genotoxic agents, are hypersensitive to proteasome inhibitors and suggest that combining bortezomib with therapies that target the normoxic fraction of human tumors can lead to more effective tumor control. PubMed:19010906

Annotations
Experimental Factor Ontology (EFO)
HeLa
MeSH
Intracellular Space
MeSH
Neoplasms
Evidence and Conclusion Ontology
western blot
MeSH
Colon
NCBI Taxonomy Names
Homo sapiens
Disease Ontology (DO)
colorectal cancer
Uberon
intestinal epithelium
Cell Ontology (CL)
stem cell
NCBI Taxonomy Ids
10090

p(HGNC:PDK3) association path(MESHD:Neoplasms)

Further analysis using immunohistochemical staining revealed that PDK3 levels were positively associated with severity of cancer and negatively associated with disease-free survival. PubMed:21763680

Annotations
Experimental Factor Ontology (EFO)
HeLa cell
MeSH
Peroxisomes
MeSH
Neoplasms
Evidence and Conclusion Ontology
immunohistochemistry
MeSH
<