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Study Comparing Pathological Responses Observed on Colorectal Cancer Metastases Resected After Preoperative Treatment Combining Cetuximab With FOLFOX or FOLFIRI in RAS and B-RAF WT Tumors

ABSTRACT: To analyze the pathological tumor response on resected colorectal cancer metastases after preoperative treatment with cetuximab combined with FOLFOX or FOLFIRI regimen in a prospective cohort (RAS and B-RAF WT tumors) and to correlate this response with patient’s outcome.

DISEASE(S): Metastatic Colorectal Cancer,Potentialy Or Borderline Resecable Metastatic Colorectal Cancer(ras And B-raf W-t) At Diagnosis And For Whom A Multidisciplinary Meeting Recommended Chemotherapy First In A Curative Intent.,Colorectal Neoplasms

PROVIDER: 2145197 | ecrin-mdr-crc |

REPOSITORIES: ECRIN MDR

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Study Comparing Pathological Responses Observed on Colorectal Cancer Metastases Resected After Preoperative Bevacizumab With FOLFOX or FOLFIRI.

Project description:The study is designed to analyze the pathological tumor response on resected colorectal cancer metastases after preoperative treatment with bevacizumab combined with FOLFOX or FOLFIRI regimen in a prospective cohort and to correlate this response with patient’s outcome.

| 2145196 | ecrin-mdr-crc

Expression profiling of BRAFV600E melanoma cell lines upon RAF inhibition

Project description:Microarray expression analysis to identify global changes in transcription in response to RAF inhibition. Genes under RAF control were identified in a panel of BRAFV600E tumor cells, following the short-term inhibition of RAF using a pan-RAF kinase inhibitor, PLX4032 (Plexxikon). For comparison with changes in gene expression in response to MEK inhibition using PD0325901 (Pfizer), the following array data was referenced: (http://www.ncbi.nlm.nih.gov/geo/ (accession no. GSE10086)).

2010-07-18 | GSE20051 | GEO

Expression profiling of BRAFV600E melanoma cell lines upon RAF inhibition

2010-07-18 | E-GEOD-20051 | biostudies-arrayexpress

RAF conformational autoinhibition and 14-3-3 proteins promote paradoxical activation

Project description:RAF kinase inhibitors can, in some conditions, increase RAF kinase signaling. This process, which is commonly referred to as “paradoxical activation” (PA), is incompletely understood. RAF kinases are regulated by autoinhibitory conformational changes, and the role of these conformational changes in PA is unclear. Our mathematical investigations reveal that a dynamic equilibrium between autoinhibited and non-autoinhibited forms of RAF, along with the RAF inhibitor stabilization of the non-autoinhibited form, can be sufficient to create PA. Using both computational and experimental methods we demonstrate that 14-3-3 proteins, which stabilize both RAF autoinhibition and RAF dimerization, potentiate PA. Our model led us to hypothesize that increased 14-3-3 expression would amplify PA for the third generation RAF inhibitors that normally display minimal to no PA. Our subsequent experiments find that 14-3-3 overexpression increases PA, increases RAF dimerization, and promotes resistance to these inhibitors, effectively “breaking” these “paradox breaker” and pan-RAF inhibitors. Overall, this work reveals a robust mechanism for PA based solely on equilibrium dynamics of canonical interactions in RAF signaling.

2025-05-08 | GSE179932 | GEO

Genome-wide analysis of RAF inhibition in HCT116 cells in culture

Project description:gene expression profile of HCT116 p53+/+ cells in response to RAF inhibition Total RNA obtained from HCT116 cells treated with or without 10nM SB590885

2016-05-28 | GSE81973 | GEO

Gene Expression data for melanocyte stem cells and melanoblasts isolated from the skin of wild-type mice and B-raf and C-raf double knock-out mice

Project description:Melanocyte are melanin-producing cells located in the bottom layer of the skin's epidermis and in the hair follicle. Melanin is the pigment primarily responsible notably for skin and hair color. Our team had previously shown a role for B-raf and C-raf genes in the maintenance of melanocyte stem cells located in mice hair follicle (Valluet et al, 2012). The aim of the present project was to understand the role of B-RAF and C-RAF kinases in melanocyte stem cell self-renewal. To reach this goal, we have generated a new mouse model in which cells of the melanocyte lineage can be followed by GFP expression. We performed gene array on melanocyte stem cell B-raf+/+; C-raf+/+ and B-raf-/-; C-raf-/-in order to identify the RAF kinases target genes which are involved in melanocyte stem cell self-renewal. Moreover, to better characterize the melanocyte stem cell population, we compared its gene expression profile to the melanoblast one (melanocyte stem cell's progenitors).

2019-09-02 | GSE86385 | GEO

Wildtype C-Raf gene dosage and dimerization drive prostate cancer metastasis

Project description:To investigate the function of C-Raf overexpression in driving metastasis, we established C-Raf overexpression lines and C-Raf metastasis derived lines from mice in RWPE-1 and BPH-1 cells.

2024-01-02 | GSE235178 | GEO

Genome-wide analysis of RAF inhibition in HCT116 cells in culture

Project description:gene expression profile of HCT116 p53+/+ cells in response to RAF inhibition Total RNA obtained from HCT116 cells treated with or without 10nM SB590885 Gaurisankar, Sa

2016-05-28 | E-GEOD-81973 | biostudies-arrayexpress

Changes in gene expression profile in mammalian cells upon Raf activation

Project description:Comparison of the changes in the gene expression profile of cells in which there is an activation of the Raf oncogene in the absence of any other extracellular signals Keywords: Response to oncogenic activation of the MAPK pathway

2007-09-18 | GSE9062 | GEO

Raf/MEK signatures in zebrafish liver cells

Project description:An inducible oncogenic cell line ZFL-ΔRaf1-ER was established, in which oncogenic human Raf-1(ΔRaf1) can be activated in zebrafish liver cells by administration of 4-hydroxytamoxifen (4HT). Transcriptional profilling of the ZFL-ΔRaf1-ER cells with and without administration of 4HT and/or the MEK inhibitor U0126 defined the gene signatures transcriptionally regulated by hyperactive Raf/MEK/MAPK signaling in zebrafish liver cells.

2011-07-07 | GSE29308 | GEO

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