Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Bioenergetic Alterations in Colorectal Polyp and Cancer

ABSTRACT: Background: The change of cellular energy metabolism in colorectal carcinogenesis is poorly understood. It is widely accepted tht most, if not all, colorectal cancers (CRCs) arise from adenomatous polyps (APs). Our aim was to characterize the mitochondrial and bioenergetic alternations in the adenoma-carcinoma sequence. Results: Two glycolysis-related genes, aldolase B (ALDOB) and solute carrier family 16 member 4 (SLC16A4), were upregulated in polyps. This result was further confirmed by the real-time PCR analysis showing that the both ALDOB and SLC16A4 mRNA expressions were higher in the polyps with villous component compared with their adjacent normal mucosa.

ORGANISM(S): Homo sapiens

PROVIDER: GSE81804 | GEO | 2017/05/23

SECONDARY ACCESSION(S): PRJNA322588

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling of colorectal tissues in the early adenoma-carcinoma sequence

Project description:Colorectal cancer (CRC) is the third most common cancer worldwide. Colorectal polyps are recognised pre-cursors of CRC, however hyperplastic polyps lack malignant potential. The purpose of this study was to identify differences in gene expression between normal colonic mucosa, hyperplastic and adenomatous polyps from disease-free individuals. By comparing polyps believed to have malignant potential (adenomatous polyps) with hyperplastic polyps it is hoped that new insights into colorectal carcinogenesis can be achieved. 24 colonic samples comprising 8 normal colonic mucosa, 8 hyperplastic polyps and 8 adenomatous polyps.

2012-08-25 | E-GEOD-40362 | biostudies-arrayexpress

Gene expression profiling of colorectal tissues in the early adenoma-carcinoma sequence

2012-08-25 | GSE40362 | GEO

BAC CGH array profiling using Phi29-amplified colon mucosa of microdissected samples from APC and MYH mutation carriers.

Project description:Details of the series are available in the publication Cardoso J. et al., âChromosomal instability in MYH- and APC-mutant adenomatous polypsâ, Cancer Research, accepted for publication. Abstract of the publication: âThe vast majority of colorectal cancers display genetic instability, either in the chromosomal (CIN) or microsatellite (MIN) forms. While CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near-diploid. Recently, bi-allelic germline mutations in the MYH gene, were found to be responsible for MAP (MYH associated polyposis), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant FAP (familial adenomatous polyposis) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser-capture microdissection, isothermal genomic DNA amplification, and array-CGH (comparative genomic hybridization). Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% of the MAP polyps showed aneuploid changes, which is significantly higher than the 60% found among FAP polyps. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19 and 22, and gains affecting chromosome 7 and 13. The observation that aneuploidy is already detectable at early stages of MYH-driven tumorigenesis raises the possibility that CIN may contribute significantly to accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.â Details of the series are available in the publication Cardoso J. et al., âChromosomal instability in MYH- and APC-mutant adenomatous polypsâ, Cancer Research, accepted for publication.

2010-06-30 | E-GEOD-3898 | biostudies-arrayexpress

Methylation profiling by array of a solitary Peutz-Jeghers colon polyp in a healthy individual

Project description:Colon polyps represent precursor lesions of colon cancers and their malignant potential varies according to histological subtype. A rare subtype of colon polyps is the Peutz-Jeghers (PJ) polyp. PJ polyps mostly occur in the context of Peutz-Jeghers Syndrome which is characterized by the development of multiple polyps in the intestinal tract and hyperpigmentation of oral mucosa and lips. Peutz-Jeghers Syndrome is an autosomal dominant disorder caused by germline mutations of the Serine Threonin Kinase STK11 (LKB1). PJ polyps very rarely occur outside of Peutz-Jeghers Syndrome and are then referred to as solitary PJ polyps. Contrary to Peutz-Jeghers Syndrome, the genetic basis and the malignant potential of solitary PJ polyps is currently unknown. To date, only one study described a sporadic PJ polyp finding no mutations of STK11, indicating that the molecular profile of solitary PJ polyps differs from Peutz-Jeghers syndrome. Methylome analysis revealed global hypomethylation and CpG island hypermethylation, two features that have been described as hallmarks of the colorectal cancer epigenome. These results provide a paradigm for a premalignant lesion that is defined by epigenetic changes.

2017-01-23 | E-MTAB-5255 | biostudies-arrayexpress

Small RNA sequencing of sessile serrated polyps identifies miRNA profile associated with colon cancer

Project description:RNA sequencing analysis of small RNA expression in sessile serrated adenoma/polyps, hyperplastic polyps, adenomatous polyps, uninvolved colon and control colon

2018-10-18 | GSE118504 | GEO

BAC CGH array profiling using Phi29-amplified colon mucosa of microdissected samples from APC and MYH mutation carriers.

Project description:Details of the series are available in the publication Cardoso J. et al., “Chromosomal instability in MYH- and APC-mutant adenomatous polyps”, Cancer Research, accepted for publication. Abstract of the publication: “The vast majority of colorectal cancers display genetic instability, either in the chromosomal (CIN) or microsatellite (MIN) forms. While CIN tumors are per definition aneuploid, MIN colorectal cancers, caused by loss of mismatch repair function, are usually near-diploid. Recently, bi-allelic germline mutations in the MYH gene, were found to be responsible for MAP (MYH associated polyposis), an autosomal recessive predisposition to multiple colorectal polyps, often indistinguishable from the dominant FAP (familial adenomatous polyposis) syndrome caused by inherited APC mutations. Here, we analyzed MYH- and APC-mutant polyps by combining laser-capture microdissection, isothermal genomic DNA amplification, and array-CGH (comparative genomic hybridization). Smoothed quantile regression methods were applied to the MAP and FAP genomic profiles to discriminate chromosomes predominantly affected by gains and losses. Up to 80% of the MAP polyps showed aneuploid changes, which is significantly higher than the 60% found among FAP polyps. Both MAP and FAP adenomas were characterized by frequent losses at chromosome 1p, 17, 19 and 22, and gains affecting chromosome 7 and 13. The observation that aneuploidy is already detectable at early stages of MYH-driven tumorigenesis raises the possibility that CIN may contribute significantly to accelerated tumor progression, increased cancer risk, and poor prognosis in MAP.” Keywords: repeat, BAC, CGH

2005-12-25 | GSE3898 | GEO

Modulation of Serpin family levels detected by proteomics to monitor colorectal adenoma to carcinoma progression

Project description:Colorectal cancer (CRC) remains a major cause of cancer related-death in developed countries. The risk of death is correlated with the stage of CRC determined at the primary diagnosis and early diagnosis is associated with enhanced survival rate. Consequently, there is an interest in using proteomics technologies to identify specific markers of adenomatous polyps as well as advanced stages of CRC.This study supports the concept that serum proteins can discriminate adenoma and CRC patients from unaffected patients and highlights the value of the SERPIN family as potential biomarkers of CRC.

2016-08-26 | PXD001794 | Pride

Transcription profiling by array of Apc+/Delta716 mouse intestinal polyps vs normal intestinal mucosa

Project description:The APC (Adenomatous Polyposis Coli) gene encodes a large multidomain protein that plays an integral role in the Wnt/beta-catenin signaling pathway. The loss-of-function mutation in APC is considered the earliest genetic alteration in the course of adenoma-carcinoma sequence of colorectal cancer progression, and the resulting constitutive activation of Wnt/beta-catenin signaling is required for the maintenance of advanced colorectal cancer. In order to identify genes affected by loss of Apc function, we performed transcription profiling of mouse small intestinal tissues comparing polyps with normal mucosa of Apc+/Delta716 mice. We isolated total RNA from intestinal polyps and normal intestinal mucosa from 3 individual Apc+/Delta716 mice. Total RNA samples were then employed to perform microarray analysis (Agilent Whole Mouse Genome Microarray Ver. 2.0, 4x44K).

2020-11-01 | E-MTAB-9187 | biostudies-arrayexpress

Colorectal Adenomas and Consensus Molecular Subtyping

Project description:Consensus molecular subtyping in adenomatous and serrated polyps

2018-12-19 | GSE108317 | GEO

Dynamic tumor growth patterns in a novel murine model of colorectal cancer

Project description:Colorectal cancer often arises from adenomatous polyps. Polyps can grow and progress to cancer, but may also remain static in size, regress, or resolve. Prediciting which progress to cancer and which remain benign is difficult. We developed a long-lived murine model of colorectal cancer with tumors that can be followed by colonoscopy. Our aim was to assess whether these tumors have similar growth patterns and histologic fates to human colorectal polyps to identify features to aid in risk stratification of colonic tumors. Long-lived Apc^Min/+ mice were treated with 4% dextran sodium sulfate to promote colonic tumorigenesis. Tumor growth patterns were characterized by serial colonoscopy, and pathology was determined. Serial biopsies of tumors were obtained for immunohistochemistry and gene expression profiling by microarray analysis with Affymetrix Whole Genome array. Tumors (n=424) grew, remained static, regressed, or resolved over time with different relative frequencies. Newly developed tumors demonstrated dynamic growth patterns with higher rates of growth and resolution, while more established tumors tended to remain static in size. Colonic tumors were hyperplastic lesions (3%), adenomas (73%), intramucosal carcinomas (20%), or adenocarcinomas (3%). Differentially expressed genes between adenomas and intramucosal carcinomas were identified. We did not identify differentially expressed genes between early and late biopsies from the same tumor. This novel murine model of intestinal tumorigenesis develops colonic tumors that can be monitored by serial colonoscopy, mirror growth patterns seen in human colorectal polyps, and progress to colorectal cancer. Further characterization of cellular and molecular features are needed to determine which features can be used to risk-stratify polyps for progress to colorectal cancer and potentially guide prevention strategies.

2014-05-03 | GSE46626 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data