V
Victor Olivas
Researcher at University of California, San Francisco
Publications - 42
Citations - 3569
Victor Olivas is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Lung cancer & KRAS. The author has an hindex of 20, co-authored 39 publications receiving 2800 citations. Previous affiliations of Victor Olivas include University of California, Berkeley.
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Journal ArticleDOI
Activation of the AXL kinase causes resistance to EGFR-targeted therapy in lung cancer
Zhenfeng Zhang,Zhenfeng Zhang,Jae Cheol Lee,Luping Lin,Victor Olivas,Valerie Au,Thomas LaFramboise,Mohamed Abdel-Rahman,Xiaoqi Wang,Alan D. Levine,Jin Kyung Rho,Yun Jung Choi,Chang-Min Choi,Sang We Kim,Se Jin Jang,Young Soo Park,Woo Sung Kim,Dae Ho Lee,Jung Shin Lee,Vincent A. Miller,Maria E. Arcila,Marc Ladanyi,Philicia Moonsamy,Charles L. Sawyers,Titus J. Boggon,Patrick C. Ma,Carlota Costa,Miquel Taron,Rafael Rosell,Balazs Halmos,Trever G. Bivona,Trever G. Bivona +31 more
TL;DR: Increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation are reported.
Journal ArticleDOI
The Hippo effector YAP promotes resistance to RAF- and MEK-targeted cancer therapies
Luping Lin,Amit J. Sabnis,Elton Chan,Victor Olivas,Lindsay Cade,Evangelos Pazarentzos,Saurabh Asthana,Dana S. Neel,Jenny Jiacheng Yan,Xinyuan Lu,Luu Pham,Mingxue M Wang,Niki Karachaliou,Maria Gonzalez Cao,Jose Luis Manzano,Jose Luis Ramirez,Jose M. Torres,Fiamma Buttitta,Charles M. Rudin,Eric A. Collisson,Alain Algazi,Eric Robinson,Iman Osman,Eva Muñoz-Couselo,Javier Cortes,Dennie T. Frederick,Zachary A. Cooper,Martin McMahon,Antonio Marchetti,Rafael Rosell,Keith T. Flaherty,Jennifer A. Wargo,Trever G. Bivona +32 more
TL;DR: Through a genetic screen in BRAF-mutant tumor cells, it is shown that the Hippo pathway effector YAP acts as a parallel survival input to promote resistance to RAF and MEK inhibitor therapy.
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Evolution and clinical impact of co-occurring genetic alterations in advanced-stage EGFR-mutant lung cancers
Collin M. Blakely,Thomas B.K. Watkins,Wei Wu,Beatrice Gini,Jacob J. Chabon,Caroline E. McCoach,Nicholas McGranahan,Gareth A. Wilson,Nicolai Juul Birkbak,Victor Olivas,Julia K Rotow,Ashley Maynard,Victoria E. Wang,Matthew A. Gubens,Kimberly C. Banks,Richard B. Lanman,Aleah F. Caulin,John St. John,Anibal Cordero,Petros Giannikopoulos,Andrew Simmons,Philip C. Mack,David R. Gandara,Hatim Husain,Robert C. Doebele,Jonathan W. Riess,Maximilian Diehn,Charles Swanton,Trever G. Bivona +28 more
TL;DR: This study calls for revisiting the prevailing single-gene driver-oncogene view and links clinical outcomes to co-occurring genetic alterations in patients with advanced-stage EGFR-mutant lung cancer.
Journal ArticleDOI
RAS nucleotide cycling underlies the SHP2 phosphatase dependence of mutant BRAF-, NF1- and RAS-driven cancers.
Robert J. Nichols,Franziska Haderk,Carlos Stahlhut,Christopher J. Schulze,Golzar Hemmati,David Wildes,Christos Tzitzilonis,Kasia Mordec,Abby Marquez,Jason Romero,Tientien Hsieh,Aubhishek Zaman,Victor Olivas,Caroline E. McCoach,Collin M. Blakely,Zhengping Wang,Gert Kiss,Elena S. Koltun,Adrian Liam Gill,Mallika Singh,Mark A. Goldsmith,Jacqueline Smith,Trever G. Bivona +22 more
TL;DR: It is shown that targeting the SHP2 phosphatase (encoded by PTPN11) with RMC-4550, a small-molecule allosteric inhibitor, is effective in human cancer models bearing RAS–GTP-dependent oncogenic BRAF, NF1 loss or nucleotide-cycling oncogenesis RAS.
Journal ArticleDOI
RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer.
Gorjan Hrustanovic,Victor Olivas,Evangelos Pazarentzos,Asmin Tulpule,Saurabh Asthana,Collin M. Blakely,Ross A. Okimoto,Luping Lin,Dana S. Neel,Amit J. Sabnis,Jennifer Flanagan,Elton Chan,Marileila Varella-Garcia,Dara L. Aisner,Aria Vaishnavi,Sai-Hong Ignatius Ou,Eric A. Collisson,Eiki Ichihara,Philip C. Mack,Christine M. Lovly,Niki Karachaliou,Rafael Rosell,Jonathan W. Riess,Robert C. Doebele,Trever G. Bivona +24 more
TL;DR: It is demonstrated in models of lung adenocarcinoma harboring the oncogenic fusion of ALK and EML4 that the GTPase RAS–mitogen-activated protein kinase (MAPK) pathway, but not other known ALK effectors, is required for tumor-cell survival.