Benjamin Huang, MD
Dr. Benjamin Huang is a physician-scientist whose research program focuses on mouse cancer modeling, molecular therapeutics, and functional genomics. He is a contributing member within the UCSF Helen Diller Family Comprehensive Cancer Center, the Children's Oncology Group Myeloid Committee, and the Leukemia and Lymphoma Society Pediatric Acute Leukemia Initiative.
Fellowship, 2016 - Pediatric Hematology/Oncology, University of California, San Francisco
Residency, 2013 - Pediatrics, University of California, San Francisco
M.D., 2010 - Medicine, University of California, San Francisco
B.S., 2005 - Electrical Engineering and Computer Sciences, University of California, Berkeley
Honors and Awards
- Rally Foundation Career Development Award, 2020
- St. Baldrick’s Foundation Scholar Award, 2020
- Hyundai Hope on Wheels Scholar Award, 2019
- UCSF Bleecher Young Investigator Award, 2017
- St. Baldrick's Foundation Fellowship Award, 2016
- UCSF School of Medicine Essential Core Teaching Award, 2010
- Alpha Omega Alpha, Medical Honor Society, 2009
- UC Berkeley Outstanding Graduate Student Instructor Award, 2006
- Eta Kappa Nu, Electrical Engineering and Computer Sciences Honor Society, 2001
- Inhibition of the Sec61 translocon overcomes cytokine-induced glucocorticoid resistance in T-cell acute lymphoblastic leukaemia.
- Integrated genomic analysis identifies UBTF tandem duplications as a recurrent lesion in pediatric acute myeloid leukemia.
- CBFB-MYH11 Fusion Transcripts Distinguish Acute Myeloid Leukemias with Distinct Molecular Landscapes and Outcomes.
- Single-cell DNA sequencing reveals complex mechanisms of resistance to quizartinib.
- Genetic disruption of N-RasG12D palmitoylation perturbs hematopoiesis and prevents myeloid transformation in mice.
- Loss of glucocorticoid receptor expression mediates in vivo dexamethasone resistance in T-cell acute lymphoblastic leukemia.
- Glucocorticoids paradoxically facilitate steroid resistance in T cell acute lymphoblastic leukemias and thymocytes.
- Convergent genetic aberrations in murine and human T lineage acute lymphoblastic leukemias.
- JAK/STAT pathway inhibition overcomes IL7-induced glucocorticoid resistance in a subset of human T-cell acute lymphoblastic leukemias.
- KRAS Allelic Imbalance Enhances Fitness and Modulates MAP Kinase Dependence in Cancer.
- Resistant T-Cell Acute Lymphoblastic Leukemias That Emerge after In Vivo Treatment with Dexamethasone Frequently Down-Regulate Glucocorticoid Receptor Protein Expression. Blood (ASH Annual Meeting Abstracts)
- Response and Resistance to Bromodomain Inhibition in AML Driven By Hyperactive Ras Signaling. Blood (ASH Annual Meeting Abstracts)
- Mutant Ikzf1, KrasG12D, and Notch1 cooperate in T lineage leukemogenesis and modulate responses to targeted agents.