Oncogene ablation-resistant pancreatic cancer cells depend on mitochondrial function
Andrea Viale (),
Piergiorgio Pettazzoni,
Costas A. Lyssiotis,
Haoqiang Ying,
Nora Sánchez,
Matteo Marchesini,
Alessandro Carugo,
Tessa Green,
Sahil Seth,
Virginia Giuliani,
Maria Kost-Alimova,
Florian Muller,
Simona Colla,
Luigi Nezi,
Giannicola Genovese,
Angela K. Deem,
Avnish Kapoor,
Wantong Yao,
Emanuela Brunetto,
Ya’an Kang,
Min Yuan,
John M. Asara,
Y. Alan Wang,
Timothy P. Heffernan,
Alec C. Kimmelman,
Huamin Wang,
Jason B. Fleming,
Lewis C. Cantley,
Ronald A. DePinho and
Giulio F. Draetta ()
Additional contact information
Andrea Viale: The University of Texas MD Anderson Cancer Center
Piergiorgio Pettazzoni: The University of Texas MD Anderson Cancer Center
Costas A. Lyssiotis: Weill Cornell Medical College
Haoqiang Ying: The University of Texas MD Anderson Cancer Center
Nora Sánchez: The University of Texas MD Anderson Cancer Center
Matteo Marchesini: The University of Texas MD Anderson Cancer Center
Alessandro Carugo: The University of Texas MD Anderson Cancer Center
Tessa Green: The University of Texas MD Anderson Cancer Center
Sahil Seth: Institute for Applied Cancer Science, The University of Texas MD Anderson Cancer Center
Virginia Giuliani: Institute for Applied Cancer Science, The University of Texas MD Anderson Cancer Center
Maria Kost-Alimova: Institute for Applied Cancer Science, The University of Texas MD Anderson Cancer Center
Florian Muller: The University of Texas MD Anderson Cancer Center
Simona Colla: The University of Texas MD Anderson Cancer Center
Luigi Nezi: The University of Texas MD Anderson Cancer Center
Giannicola Genovese: The University of Texas MD Anderson Cancer Center
Angela K. Deem: The University of Texas MD Anderson Cancer Center
Avnish Kapoor: The University of Texas MD Anderson Cancer Center
Wantong Yao: The University of Texas MD Anderson Cancer Center
Emanuela Brunetto: Pathology Unit, San Raffaele Scientific Institute, Milan 20132, Italy
Ya’an Kang: The University of Texas MD Anderson Cancer Center
Min Yuan: Beth Israel Deaconess Medical Center
John M. Asara: Beth Israel Deaconess Medical Center
Y. Alan Wang: The University of Texas MD Anderson Cancer Center
Timothy P. Heffernan: Institute for Applied Cancer Science, The University of Texas MD Anderson Cancer Center
Alec C. Kimmelman: Dana-Farber Cancer Institute
Huamin Wang: The University of Texas MD Anderson Cancer Center
Jason B. Fleming: The University of Texas MD Anderson Cancer Center
Lewis C. Cantley: Weill Cornell Medical College
Ronald A. DePinho: The University of Texas MD Anderson Cancer Center
Giulio F. Draetta: The University of Texas MD Anderson Cancer Center
Nature, 2014, vol. 514, issue 7524, 628-632
Abstract:
KRAS mutations are a driver event of pancreatic ductal adenocarcinoma; here, a subpopulation of dormant tumour cells, relying on oxidative phosphorylation for survival, is shown to be responsible for tumour relapse after treatment targeting the KRAS pathway.
Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:514:y:2014:i:7524:d:10.1038_nature13611
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DOI: 10.1038/nature13611
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