D
Daniel B. Costa
Researcher at Beth Israel Deaconess Medical Center
Publications - 221
Citations - 22063
Daniel B. Costa is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Lung cancer & Erlotinib. The author has an hindex of 49, co-authored 211 publications receiving 19246 citations. Previous affiliations of Daniel B. Costa include Harvard University & University of Manchester.
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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
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
Crizotinib in ROS1-Rearranged Non–Small-Cell Lung Cancer
Alice T. Shaw,Sai-Hong Ignatius Ou,Yung-Jue Bang,D. Ross Camidge,Benjamin Solomon,Ravi Salgia,Gregory J. Riely,Marileila Varella-Garcia,Geoffrey I. Shapiro,Daniel B. Costa,Robert C. Doebele,Long P. Le,Zongli Zheng,Zongli Zheng,Weiwei Tan,Patricia Stephenson,S. Martin Shreeve,L. Tye,James G. Christensen,Keith D. Wilner,Jeffrey W. Clark,A. John Iafrate +21 more
TL;DR: Crizotinib showed marked antitumor activity in patients with advanced ROS1-rearranged NSCLC, and ROS1 rearrangement defines a second molecular subgroup of NSCLCs for which crizotin ib is highly active.
Journal ArticleDOI
Activity and safety of crizotinib in patients with ALK-positive non-small-cell lung cancer: updated results from a phase 1 study.
D. Ross Camidge,Yung-Jue Bang,Eunice L. Kwak,A. John Iafrate,Marileila Varella-Garcia,Stephen B. Fox,Gregory J. Riely,Benjamin Solomon,Sai-Hong Ignatius Ou,Dong Wan Kim,Ravi Salgia,Panagiotis Fidias,Jeffrey A. Engelman,Leena Gandhi,Pasi A. Jänne,Daniel B. Costa,Geoffrey I. Shapiro,Patricia LoRusso,Katherine Ruffner,Patricia Stephenson,Yiyun Tang,Keith D. Wilner,Jeffrey W. Clark,Alice T. Shaw +23 more
TL;DR: Crizotinib is well tolerated with rapid, durable responses in patients with ALK-positive NSCLC and there seems to be potential for ongoing benefit after initial disease progression in this population, but a more formal definition of ongoing benefit in this context is needed.
Journal ArticleDOI
Adaptive resistance to therapeutic PD-1 blockade is associated with upregulation of alternative immune checkpoints.
Shohei Koyama,Esra A. Akbay,Yvonne Y. Li,Grit S. Herter-Sprie,Kevin A. Buczkowski,William G. Richards,Leena Gandhi,Amanda J. Redig,Scott J. Rodig,Hajime Asahina,Robert E. Jones,Meghana M. Kulkarni,Mari Kuraguchi,Sangeetha Palakurthi,Peter E. Fecci,Bruce E. Johnson,Pasi A. Jänne,Jeffrey A. Engelman,Sidharta P. Gangadharan,Daniel B. Costa,Gordon J. Freeman,Raphael Bueno,F. Stephen Hodi,Glenn Dranoff,Kwok-Kin Wong,Peter S. Hammerman,Peter S. Hammerman +26 more
TL;DR: Analysis of the tumour immune microenvironment in the context of anti-PD-1 therapy in two fully immunocompetent mouse models of lung adenocarcinoma suggests that upregulation of TIM-3 and other immune checkpoints may be targetable biomarkers associated with adaptive resistance to PD-1 blockade.