KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy

Understanding the early evolution of cancer heterogeneity during the initial steps of tumorigenesis can uncover vulnerabilities of cancer cells that may be masked at later stages. We describe a comprehensive approach employing gene expression analysis in early lesions to identify novel therapeutic t...

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Detalles Bibliográficos
Autores principales: Ambrogio, Chiara, Nadal, Ernest, Villanueva, Alberto, Gómez-López, Gonzalo, Cash, Timothy P, Barbacid, Mariano, Santamaría, David
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BMJ Publishing Group 2016
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5070278/
https://www.ncbi.nlm.nih.gov/pubmed/27843638
http://dx.doi.org/10.1136/esmoopen-2016-000076
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author Ambrogio, Chiara
Nadal, Ernest
Villanueva, Alberto
Gómez-López, Gonzalo
Cash, Timothy P
Barbacid, Mariano
Santamaría, David
author_facet Ambrogio, Chiara
Nadal, Ernest
Villanueva, Alberto
Gómez-López, Gonzalo
Cash, Timothy P
Barbacid, Mariano
Santamaría, David
author_sort Ambrogio, Chiara
collection PubMed
description Understanding the early evolution of cancer heterogeneity during the initial steps of tumorigenesis can uncover vulnerabilities of cancer cells that may be masked at later stages. We describe a comprehensive approach employing gene expression analysis in early lesions to identify novel therapeutic targets and the use of mouse models to test synthetic lethal drug combinations to treat human Kirsten rat sarcoma viral oncogene homologue (KRAS)-driven lung adenocarcinoma.
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spelling pubmed-50702782016-11-14 KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy Ambrogio, Chiara Nadal, Ernest Villanueva, Alberto Gómez-López, Gonzalo Cash, Timothy P Barbacid, Mariano Santamaría, David ESMO Open Review Understanding the early evolution of cancer heterogeneity during the initial steps of tumorigenesis can uncover vulnerabilities of cancer cells that may be masked at later stages. We describe a comprehensive approach employing gene expression analysis in early lesions to identify novel therapeutic targets and the use of mouse models to test synthetic lethal drug combinations to treat human Kirsten rat sarcoma viral oncogene homologue (KRAS)-driven lung adenocarcinoma. BMJ Publishing Group 2016-09-06 /pmc/articles/PMC5070278/ /pubmed/27843638 http://dx.doi.org/10.1136/esmoopen-2016-000076 Text en Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/ This is an Open Access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
spellingShingle Review
Ambrogio, Chiara
Nadal, Ernest
Villanueva, Alberto
Gómez-López, Gonzalo
Cash, Timothy P
Barbacid, Mariano
Santamaría, David
KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
title KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
title_full KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
title_fullStr KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
title_full_unstemmed KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
title_short KRAS-driven lung adenocarcinoma: combined DDR1/Notch inhibition as an effective therapy
title_sort kras-driven lung adenocarcinoma: combined ddr1/notch inhibition as an effective therapy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5070278/
https://www.ncbi.nlm.nih.gov/pubmed/27843638
http://dx.doi.org/10.1136/esmoopen-2016-000076
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