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Fei Huang

Researcher at Bristol-Myers Squibb

Publications -  34
Citations -  2045

Fei Huang is an academic researcher from Bristol-Myers Squibb. The author has contributed to research in topics: Receptor tyrosine kinase & Cancer. The author has an hindex of 17, co-authored 34 publications receiving 1952 citations.

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Journal ArticleDOI

Identification of Candidate Molecular Markers Predicting Sensitivity in Solid Tumors to Dasatinib: Rationale for Patient Selection

TL;DR: It is implicate that dasatinib may represent a valuable treatment option in this difficult-to-treat population of patients with resistance or intolerance to prior therapy and to test this hypothesis, clinical studies are under way to determine the activity of d asatinib in these patients.
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The mechanisms of differential sensitivity to an insulin-like growth factor-1 receptor inhibitor (BMS-536924) and rationale for combining with EGFR/HER2 inhibitors.

TL;DR: A strategy for testing combinations of IGF-IR inhibitors with other targeted therapies in clinical studies to achieve improved patient outcomes is provided and further exploration of mechanisms for intrinsic and acquired drug resistance by these preclinical studies may lead to more rationally designed drugs that target multiple pathways for enhanced antitumor efficacy.
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High IGF-IR activity in triple-negative breast cancer cell lines and tumorgrafts correlates with sensitivity to anti-IGF-IR therapy

TL;DR: The IGF signature was present in triple-negative breast cancers and TNBC cell lines, which were especially sensitive to BMS-754807, and sensitivity was significantly correlated to the expression of the IGF gene signature.
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Differential Mechanisms of Acquired Resistance to Insulin-like Growth Factor-I Receptor Antibody Therapy or to a Small-Molecule Inhibitor, BMS-754807, in a Human Rhabdomyosarcoma Model

TL;DR: This is the first study to define and compare acquired resistance mechanisms for IGF-IR/IR small-molecule inhibitor versus anti-IGF-IR antibody and provides insights into the differential acquired Resistance mechanisms.