M
Mari Mino-Kenudson
Researcher at Harvard University
Publications - 521
Citations - 49078
Mari Mino-Kenudson is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & Medicine. The author has an hindex of 87, co-authored 462 publications receiving 40552 citations. Previous affiliations of Mari Mino-Kenudson include Vanderbilt University Medical Center & Emory University.
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Journal ArticleDOI
Anaplastic Lymphoma Kinase Inhibition in Non–Small-Cell Lung Cancer
Eunice L. Kwak,Yung-Jue Bang,D. Ross Camidge,Alice T. Shaw,Benjamin Solomon,Robert G. Maki,Sai-Hong Ignatius Ou,Bruce J. Dezube,Pasi A. Jänne,Daniel B. Costa,Marileila Varella-Garcia,Woo-Ho Kim,Thomas J. Lynch,Panos Fidias,Hannah Stubbs,Jeffrey A. Engelman,Lecia V. Sequist,Weiwei Tan,Leena Gandhi,Mari Mino-Kenudson,Greg C. Wei,S. Martin Shreeve,Mark J. Ratain,Jeffrey Settleman,James G. Christensen,Daniel A. Haber,Keith D. Wilner,Ravi Salgia,Geoffrey I. Shapiro,Jeffrey W. Clark,A. John Iafrate +30 more
TL;DR: The inhibition of ALK in lung tumors with the ALK rearrangement resulted in tumor shrinkage or stable disease in most patients, and the drug resulted in grade 1 or 2 gastrointestinal side effects.
Journal ArticleDOI
Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Lecia V. Sequist,Belinda A. Waltman,Dora Dias-Santagata,Subba R. Digumarthy,Alexa B. Turke,Panos Fidias,Kristin Bergethon,Alice T. Shaw,Scott N. Gettinger,Arjola K. Cosper,Sara Akhavanfard,Rebecca S. Heist,Jennifer S. Temel,James G. Christensen,John C. Wain,Thomas J. Lynch,Kathy Vernovsky,Eugene J. Mark,Michael Lanuti,A. John Iafrate,Mari Mino-Kenudson,Jeffrey A. Engelman +21 more
TL;DR: Detailed genetic and histological analysis of 37 patients with drug-resistant non–small cell lung cancers carrying EGFR mutations provides new insights into the shifting sands of drug resistance evolution in lung cancers and suggests that serial biopsies may be essential in the quest to reverse or even prevent the development ofdrug resistance.
Journal ArticleDOI
Clinical Features and Outcome of Patients With Non–Small-Cell Lung Cancer Who Harbor EML4-ALK
Alice T. Shaw,Beow Y. Yeap,Mari Mino-Kenudson,Subba R. Digumarthy,Daniel B. Costa,Rebecca S. Heist,Benjamin Solomon,Hannah Stubbs,Sonal Admane,Ultan McDermott,Jeffrey Settleman,Susumu Kobayashi,Eugene J. Mark,Scott J. Rodig,Lucian R. Chirieac,Eunice L. Kwak,Thomas J. Lynch,A. John Iafrate +17 more
TL;DR: EML4-ALK defines a molecular subset of NSCLC with distinct clinical characteristics and patients who harbor this mutation do not benefit from EGFR TKIs and should be directed to trials of ALK-targeted agents.
Journal ArticleDOI
ROS1 Rearrangements Define a Unique Molecular Class of Lung Cancers
Kristin Bergethon,Alice T. Shaw,Sai-Hong Ignatius Ou,Ryohei Katayama,Christine M. Lovly,Nerina T. McDonald,Pierre P. Massion,Christina Siwak-Tapp,Adriana Gonzalez,Rong Fang,Eugene J. Mark,Julie M. Batten,Haiquan Chen,Keith D. Wilner,Eunice L. Kwak,Jeffrey W. Clark,David P. Carbone,Hongbin Ji,Jeffrey A. Engelman,Mari Mino-Kenudson,William Pao,A. John Iafrate +21 more
TL;DR: ROS1 rearrangement defines a molecular subset of NSCLC with distinct clinical characteristics that are similar to those observed in patients with ALK-rearranged NSCLCs, and crizotinib shows in vitro activity and early evidence of clinical activity in ROS1- rearrangedNSCLC.
Journal ArticleDOI
Functional genomics reveal that the serine synthesis pathway is essential in breast cancer
Richard Possemato,Kevin Marks,Yoav D. Shaul,Michael E. Pacold,Dohoon Kim,Kıvanç Birsoy,Shalini Sethumadhavan,Hin-Koon Woo,Hyun Gyung Jang,Abhishek K. Jha,Walter W. Chen,Francesca G. Barrett,Nicolas Stransky,Zhi-Yang Tsun,Glenn S. Cowley,Jordi Barretina,Jordi Barretina,Nada Y. Kalaany,Peggy P. Hsu,Kathleen Ottina,Albert M. Chan,Bingbing Yuan,Levi A. Garraway,Levi A. Garraway,David E. Root,Mari Mino-Kenudson,Elena F. Brachtel,Edward M. Driggers,David M. Sabatini +28 more
TL;DR: Results reveal that certain breast cancers are dependent upon increased serine pathway flux caused by PHGDH overexpression and demonstrate the utility of in vivo negative-selection RNAi screens for finding potential anticancer targets.