MEK inhibitors block growth of Ataxia Telangiectasia Mutated (ATM) mutant lung tumors

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14740%2F17%3A00100425" target="_blank" >RIV/00216224:14740/17:00100425 - isvavai.cz</a>

Výsledek na webu

<a href="http://mct.aacrjournals.org/content/16/10_Supplement/PR14" target="_blank" >http://mct.aacrjournals.org/content/16/10_Supplement/PR14</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1158/1538-8514.SYNTHLETH-PR14" target="_blank" >10.1158/1538-8514.SYNTHLETH-PR14</a>

Jazyk výsledku

angličtina

Název v původním jazyce

MEK inhibitors block growth of Ataxia Telangiectasia Mutated (ATM) mutant lung tumors

Popis výsledku v původním jazyce

Introduction: Lung cancer is the leading cause of cancer death worldwide. In the past decade, deep sequencing projects have shed light on the molecular drivers commonly found altered in NSCLC. As a result, the first molecularly targeted agents have been approved for the treatment of tumors presenting activating oncogenic events in EGFR or EML4/ALK. However, the translation into therapies for tumors presenting loss-of-function mutations has proven challenging and constitutes an unexplored and promising field. In order to narrow the gap between cancer genomics and effective treatments for tumors harboring mutations in well-defined tumor suppressor genes (such as PTEN, BRG1 or ATM), we have developed a genetically tractable lung cancer cell model. Focusing on lung adenocarcinoma, we have engineered a panel of isogenic cell lines capturing the molecular heterogeneity found in patients. This panel has been screened against a collection of drugs, comprising classical chemotherapeutics and kinase inhibitors, providing a comprehensive evaluation for hundreds of gene-drug interactions.

Název v anglickém jazyce

MEK inhibitors block growth of Ataxia Telangiectasia Mutated (ATM) mutant lung tumors

Popis výsledku anglicky

Introduction: Lung cancer is the leading cause of cancer death worldwide. In the past decade, deep sequencing projects have shed light on the molecular drivers commonly found altered in NSCLC. As a result, the first molecularly targeted agents have been approved for the treatment of tumors presenting activating oncogenic events in EGFR or EML4/ALK. However, the translation into therapies for tumors presenting loss-of-function mutations has proven challenging and constitutes an unexplored and promising field. In order to narrow the gap between cancer genomics and effective treatments for tumors harboring mutations in well-defined tumor suppressor genes (such as PTEN, BRG1 or ATM), we have developed a genetically tractable lung cancer cell model. Focusing on lung adenocarcinoma, we have engineered a panel of isogenic cell lines capturing the molecular heterogeneity found in patients. This panel has been screened against a collection of drugs, comprising classical chemotherapeutics and kinase inhibitors, providing a comprehensive evaluation for hundreds of gene-drug interactions.

Druh

O - Ostatní výsledky

CEP obor

—

OECD FORD obor

30204 - Oncology

Projekt

<a href="/cs/project/LQ1601" target="_blank" >LQ1601: CEITEC 2020</a><br>

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů