Abstract 2154: ERK/MAPK pathway inhibits tumorigenesis and cellular reprogramming of pancreatic cancer cells
Autor: | Frédéric Lessard, Véronique Bourdeau, Julien Fitamant, Filippos Kottakis, Karine Moineau-Vallée, Benjamin Le Calvé, Nabeel Bardeesy, Xavier Deschenes-Ximard, Gerardo Ferbeyre, Emmanuelle Saint-Germain, Rushika M. Perera |
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Rok vydání: | 2015 |
Předmět: | |
Zdroj: | Cancer Research. 75:2154-2154 |
ISSN: | 1538-7445 0008-5472 |
DOI: | 10.1158/1538-7445.am2015-2154 |
Popis: | Reprogrammation of cancer cells into stem-like state is one the most important mechanisms implicated in tumor initiation, metastasis and resistance to chemotherapies. Acquisition of stem-like cell property is directly correlated with the level of activation of the ERK/MAPK pathway. Our study focuses on the implication of the downregulation of this pathway during the transition of pancreatic benign neoplasms to pancreatic ductal adenocarcinoma. This transformation is directly correlated with the acquisition of stem-like cells properties. Conversely, hyperactivation of the ERK pathway using phosphatase inhibitors abrogates the stem-like cell phenotype. We analyzed the variation of genes expression by microarrays analysis between cells obtained from pancreatic intraepithelial neoplasias and pancreatic cancer. These analyses implicate the expression of DUSPs and genes related to stem cell biology in tumor progression during pancreatic cancer. Citation Format: Benjamin le Calvé, Xavier Deschenes-Ximard, Filippos Kottakis, Véronique Bourdeau, Frédéric Lessard, Karine Moineau-Vallée, Emmanuelle Saint-Germain, Julien Fitamant, Rushika Miriam Perera, Nabeel Bardeesy, Gerardo Ferbeyre. ERK/MAPK pathway inhibits tumorigenesis and cellular reprogramming of pancreatic cancer cells. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2154. doi:10.1158/1538-7445.AM2015-2154 |
Databáze: | OpenAIRE |
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