Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

EMT is the dominant program in human colon cancer (Affymetrix)

ABSTRACT: mRNA profiling data for 67 colorectal cancer at baseline Supporting data for PMID: 21251323 mRNA profiles at baseline for 67 colorectal cancer cell lines

ORGANISM(S): Homo sapiens

SUBMITTER: Michael Nebozhyn

PROVIDER: E-GEOD-28567 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

EMT is the dominant program in human colon cancer.

Loboda Andre A Nebozhyn Michael V MV Watters James W JW Buser Carolyne A CA Shaw Peter Martin PM Huang Pearl S PS Van't Veer Laura L Tollenaar Rob A E M RA Jackson David B DB Agrawal Deepak D Dai Hongyue H Yeatman Timothy J TJ

BMC medical genomics 20110120

<h4>Background</h4>Colon cancer has been classically described by clinicopathologic features that permit the prediction of outcome only after surgical resection and staging.<h4>Methods</h4>We performed an unsupervised analysis of microarray data from 326 colon cancers to identify the first principal component (PC1) of the most variable set of genes. PC1 deciphered two primary, intrinsic molecular subtypes of colon cancer that predicted disease progression and recurrence.<h4>Results</h4>Here we r ...[more]

PMID: 21251323

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Project description:Pancreatic ductal adenocarcinoma (PDAC) is a nearly uniformly lethal malignancy, with most patients facing an adverse clinical outcome. Given the pivotal role of aberrant Notch signaling in the initiation and progression of PDAC, we investigated the effect of MRK-003, a potent and selective γ-secretase inhibitor, in preclinical PDAC models. We used a panel of human PDAC cell lines, as well as patient-derived PDAC xenografts, to determine whether pharmacological targeting of the Notch pathway could inhibit pancreatic tumor growth and potentiate gemcitabine sensitivity. In vitro, MRK-003 treatment downregulated the canonical Notch target gene Hes-1, significantly inhibited anchorage independent growth, and reduced the subset of CD44+CD24+ and aldehyde dehydrogenase (ALDH)+ cells that have been attributed with tumor initiating capacity. Ex vivo pretreatment of PDAC cells with MRK-003 in culture significantly inhibited the subsequent engraftment in immunocompromised mice. In vivo, MRK-003 monotherapy significantly blocked tumor growth in 5 of 9 (56%) patient-derived PDAC xenografts. Moreover, a combination of MRK-003 and gemcitabine showed enhanced antitumor effects compared to gemcitabine alone in 4 of 9 (44%) PDAC xenografts. Baseline gene expression analysis of the treated xenografts indicated that upregulation of nuclear factor kappa B (NFκB) pathway components was associated with the sensitivity to single MRK-003, while upregulation in B-cell receptor (BCR) signaling and nuclear factor erythroid-derived 2-like 2 (NRF2) pathway correlated with response to the combination of MRK-003 with gemcitabine. The preclinical findings presented here provide further rationale for small molecule inhibition of Notch signaling as a therapeutic strategy in PDAC. Pancreatic ductal adenocarcinoma xenografts were grown in Athymic Nude-Foxn1nu mice. RNA was extracted and profiled in Affymetrix platform to identify genes correlating with sensitivity to MRK-003

Dataset Information

EMT is the dominant program in human colon cancer (Affymetrix)

Publications

EMT is the dominant program in human colon cancer.

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