R
Ross A. Okimoto
Researcher at University of California, San Francisco
Publications - 43
Citations - 15194
Ross A. Okimoto is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Cancer & Metastasis. The author has an hindex of 23, co-authored 39 publications receiving 14243 citations. Previous affiliations of Ross A. Okimoto include Tufts Medical Center & Harvard University.
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Journal ArticleDOI
Activating mutations in the epidermal growth factor receptor underlying responsiveness of non-small-cell lung cancer to gefitinib
Thomas J. Lynch,Daphne W. Bell,Raffaella Sordella,Sarada Gurubhagavatula,Ross A. Okimoto,Brian W. Brannigan,Patricia L. Harris,Sara M. Haserlat,Jeffrey G. Supko,Frank G. Haluska,David N. Louis,David C. Christiani,Jeff Settleman,Daniel A. Haber +13 more
TL;DR: A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib, and these mutations lead to increased growth factor signaling and confer susceptibility to the inhibitor.
Journal ArticleDOI
Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib
Kwak Eunice L,Raffaella Sordella,Daphne W. Bell,Godin-Heymann Nadia G,Ross A. Okimoto,Brian W. Brannigan,Patricia L. Harris,David R. Driscoll,Panos Fidias,Thomas J. Lynch,Sridhar K. Rabindran,John P. McGinnis,Allan Wissner,Sreenath V. Sharma,Kurt J. Isselbacher,Jeffrey Settleman,Daniel A. Haber +16 more
TL;DR: These findings suggest that one of these, HKI-272, may prove highly effective in the treatment of EGFR-mutant NSCLCs, including tumors that have become resistant to gefitinib or erlotinib.
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Epidermal Growth Factor Receptor Mutations and Gene Amplification in Non–Small-Cell Lung Cancer: Molecular Analysis of the IDEAL/INTACT Gefitinib Trials
Daphne W. Bell,Thomas J. Lynch,Sara M. Haserlat,Patricia L. Harris,Ross A. Okimoto,Brian W. Brannigan,Dennis C. Sgroi,Beth Muir,Markus J. Riemenschneider,Renee Iacona,Annetta D. Krebs,David H. Johnson,Giuseppe Giaccone,Roy S. Herbst,Christian Manegold,Masahiro Fukuoka,Mark G. Kris,José Baselga,Judith S. Ochs,Daniel A. Haber +19 more
TL;DR: EGFR mutations and, to a lesser extent, amplification appear to identify distinct subsets of NSCLC with an increased response to gefitinib, and the combination of gefithinib with chemotherapy does not improve survival in patients with these molecular markers.
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Amplification of MET may identify a subset of cancers with extreme sensitivity to the selective tyrosine kinase inhibitor PHA-665752
Gromoslaw A. Smolen,Raffaella Sordella,Beth Muir,Gayatry Mohapatra,Anne Barmettler,Heidi Archibald,Woo J. Kim,Ross A. Okimoto,Daphne W. Bell,Dennis C. Sgroi,James G. Christensen,Jeffrey Settleman,Daniel A. Haber +12 more
TL;DR: It is shown that gastric cancer cells with high-level stable chromosomal amplification of the growth factor receptor MET are extraordinarily susceptible to the selective inhibitor PHA-665752, which may identify a subset of epithelial cancers that are uniquely sensitive to disruption of this pathway.
Journal ArticleDOI
Inherited susceptibility to lung cancer may be associated with the T790M drug resistance mutation in EGFR
Daphne W. Bell,Ira Gore,Ross A. Okimoto,Godin-Heymann Nadia G,Raffaella Sordella,Roseann Mulloy,Sreenath V. Sharma,Brian W. Brannigan,Gayatry Mohapatra,Jeff Settleman,Daniel A. Haber +10 more
TL;DR: A family with multiple cases of non-small cell lung cancer associated with germline transmission of a specific secondary somatic mutation, EGFR T790M, is described, implicate altered EGFR signaling in genetic susceptibility to lung cancer.