H
Hillary E. Mulvey
Researcher at Harvard University
Publications - 6
Citations - 2140
Hillary E. Mulvey is an academic researcher from Harvard University. The author has contributed to research in topics: EGFR inhibitors & T790M. The author has an hindex of 5, co-authored 6 publications receiving 1680 citations.
Papers
More filters
Journal ArticleDOI
Tumor cells can follow distinct evolutionary paths to become resistant to epidermal growth factor receptor inhibition
Aaron N. Hata,Matthew J. Niederst,Hannah L. Archibald,Maria Gomez-Caraballo,Faria M. Siddiqui,Hillary E. Mulvey,Yosef E. Maruvka,Yosef E. Maruvka,Fei Ji,Hyo-eun C. Bhang,Viveksagar Krishnamurthy Radhakrishna,Giulia Siravegna,Haichuan Hu,Sana Raoof,Elizabeth L. Lockerman,Anuj Kalsy,Dana Lee,Celina L. Keating,David A. Ruddy,Leah J. Damon,Adam S. Crystal,Carlotta Costa,Zofia Piotrowska,Alberto Bardelli,Anthony J. Iafrate,Ruslan I. Sadreyev,Frank Stegmeier,Gad Getz,Lecia V. Sequist,Anthony C. Faber,Jeffrey A. Engelman +30 more
TL;DR: Findings provide evidence that clinically relevant drug-resistant cancer cells can both pre-exist and evolve from drug-tolerant cells, and they point to therapeutic opportunities to prevent or overcome resistance in the clinic.
Journal ArticleDOI
RB loss in resistant EGFR mutant lung adenocarcinomas that transform to small-cell lung cancer
Matthew J. Niederst,Lecia V. Sequist,John T. Poirier,Craig H. Mermel,Elizabeth L. Lockerman,Angel R. Garcia,Ryohei Katayama,Carlotta Costa,Kenneth N. Ross,Teresa Moran,Emily Howe,Linnea Fulton,Hillary E. Mulvey,Lindsay A. Bernardo,Farhiya Mohamoud,Norikatsu Miyoshi,Paul A. VanderLaan,Daniel B. Costa,Pasi A. Jänne,Darrell R. Borger,Sridhar Ramaswamy,Toshi Shioda,Anthony J. Iafrate,Gad Getz,Charles M. Rudin,Mari Mino-Kenudson,Jeffrey A. Engelman +26 more
TL;DR: Analysis of tumour samples and cell lines derived from resistant EGFR mutant patients revealed that Retinoblastoma (RB) is lost in 100% of these SCLC transformed cases, but rarely in those that remain NSCLC.
Journal ArticleDOI
The allelic context of the C797S mutation acquired upon treatment with third generation EGFR inhibitors impacts sensitivity to subsequent treatment strategies
Matthew J. Niederst,Haichuan Hu,Hillary E. Mulvey,Elizabeth L. Lockerman,Angel R. Garcia,Zofia Piotrowska,Lecia V. Sequist,Jeffrey A. Engelman +7 more
TL;DR: The results demonstrate that the allelic context in which C797S was acquired may predict responsiveness to alternative treatments, and are a novel mechanism of acquired resistance to third-generation TKIs.
Journal ArticleDOI
Heterogeneity Underlies the Emergence of EGFRT790 Wild-Type Clones Following Treatment of T790M-Positive Cancers with a Third-Generation EGFR Inhibitor
Zofia Piotrowska,Matthew J. Niederst,Chris Karlovich,Heather A. Wakelee,Joel W. Neal,Mari Mino-Kenudson,Linnea Fulton,Aaron N. Hata,Elizabeth L. Lockerman,Anuj Kalsy,Subba R. Digumarthy,Alona Muzikansky,Mitch Raponi,Angel R. Garcia,Hillary E. Mulvey,Melissa Parks,Richard H. DiCecca,Dora Dias-Santagata,A. John Iafrate,Alice T. Shaw,Andrew R. Allen,Jeffrey A. Engelman,Lecia V. Sequist +22 more
TL;DR: It is documents that half of T790M-positive EGFR-mutant lung cancers treated with rociletinib are T790-wild-type upon progression, suggesting that T790, wild-type clones can emerge as the dominant source of resistance.
Journal ArticleDOI
Three subtypes of lung cancer fibroblasts define distinct therapeutic paradigms.
Haichuan Hu,Zofia Piotrowska,Patricia J. Hare,Huidong Chen,Huidong Chen,Hillary E. Mulvey,Aislinn Mayfield,Sundus Noeen,Krystina E. Kattermann,Max Greenberg,August Williams,Amanda K. Riley,Jarad J. Wilson,Ying-Qing Mao,Ruo-Pan Huang,Mandeep Banwait,Jeffrey Ho,Giovanna Stein Crowther,Lida P. Hariri,Rebecca S. Heist,David P. Kodack,Luca Pinello,Luca Pinello,Alice T. Shaw,Mari Mino-Kenudson,Aaron N. Hata,Lecia V. Sequist,Cyril H. Benes,Matthew J. Niederst,Jeffrey A. Engelman +29 more
TL;DR: In this article, the authors established a living biobank of CAFs derived from biopsies of patients' non-small lung cancer (NSCLC) that encompasses a broad molecular spectrum of CAF in clinical NSCLC.