J
John C. Wain
Researcher at Harvard University
Publications - 270
Citations - 26192
John C. Wain is an academic researcher from Harvard University. The author has contributed to research in topics: Lung cancer & Genotype. The author has an hindex of 84, co-authored 268 publications receiving 24667 citations.
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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.
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Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers
Ryohei Katayama,Alice T. Shaw,Alice T. Shaw,Tahsin M. Khan,Tahsin M. Khan,Mari Mino-Kenudson,Benjamin Solomon,Balazs Halmos,Nicholas A. Jessop,John C. Wain,Alan Tien Yeo,Cyril H. Benes,Lisa Drew,Jamal Carlos Saeh,Katherine Crosby,Lecia V. Sequist,A. John Iafrate,Jeffrey A. Engelman +17 more
TL;DR: Findings from a series of lung cancer patients with acquired resistance to the ALK TKI crizotinib reinforce the need to tailor therapeutic strategies to the specific underlying drug resistance mechanisms in the tumors to improve clinical outcomes.
Journal ArticleDOI
Inhaled nitric oxide. A selective pulmonary vasodilator reversing hypoxic pulmonary vasoconstriction.
TL;DR: Breathing 80 ppm NO for 3 hours did not increase either methemoglobin or extravascular lung water levels or modify lung histology compared with those in control lambs.
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Lymphatic metastasis in the absence of functional intratumor lymphatics.
Timothy P. Padera,Ananth Kadambi,Emmanuelle di Tomaso,Carla Mouta Carreira,Edward B. Brown,Yves Boucher,Noah C. Choi,Douglas J. Mathisen,John C. Wain,Eugene J. Mark,Lance L. Munn,Rakesh K. Jain +11 more
TL;DR: Functional lymphatics associated with mouse tumors expressing normal or elevated levels of vascular endothelial growth factor–C (VEGF-C) are examined to suggest that the functional lymphatics in the tumor margin alone are sufficient for lymphatic metastasis and should be targeted therapeutically.
Journal ArticleDOI
The lysophosphatidic acid receptor LPA1 links pulmonary fibrosis to lung injury by mediating fibroblast recruitment and vascular leak.
Andrew M. Tager,Peter LaCamera,Barry S. Shea,Gabriele S. V. Campanella,Moisés Selman,Zhenwen Zhao,Vasiliy V. Polosukhin,John C. Wain,Banu A. Karimi-Shah,Nancy D. Kim,William K. Hart,Annie Pardo,Timothy S. Blackwell,Yan Xu,Jerold Chun,Andrew D. Luster +15 more
TL;DR: It is shown that lysophosphatidic acid levels increase in bronchoalveolar lavage fluid following lung injury in the bleomycin model of pulmonary fibrosis, and that mice lacking one of its receptors, LPA1, are markedly protected from fibrosis and mortality in this model.