Wei Wei,
Assistant Professor, Department of Molecular and Medical Pharmacology,
UCLA David Geffen School of Medicine
Dr. Wei Wei is an Assistant Professor in Department of Molecular & Medical Pharmacology at UCLA School of Medicine. He received his Ph.D. in Materials Science at California Institute of Technology under the supervision of Dr. James R. Heath. Wei's research interests include developing and employing a unique suite of single cell tools to cultivate new understanding and address significant questions in cancer research. Specifically, 1) Develop multi-omics single cell tools for interrogating the heterogeneous tumor cells and immune cells at multiple bimolecular levels. 2) Information theoretical and computational approaches for dissecting the high-dimensional single cell data with a particular focus on resolving tumor heterogeneity and dynamics of the signal transduction network for anticipating therapy resistance and identifying effective combination therapies. 3) Isolation, molecular characterization, and neoantigen identification of rare tumor cells in body fluids for cancer diagnosis and immunotherapy.
Kinetics of Cellular De-differentiation Transition in Metastatic Melanoma
Friday, 6 October 2017 at 14:30
Add to Calendar ▼2017-10-06 14:30:002017-10-06 15:30:00Europe/LondonKinetics of Cellular De-differentiation Transition in Metastatic MelanomaRNA-Seq, Single Cell Analysis and Single Molecule Analysis 2017 in Coronado Island, CaliforniaCoronado Island, CaliforniaSELECTBIOenquiries@selectbiosciences.com
Targeted therapies blocking BRAF and MEK have demonstrated high rates of responses. However, after an initial tumor regression, almost all BRAF-mutant melanoma tumors acquire resistance against BRAF inhibitors, but with highly variable kinetics. The general relationship between the phenotypic transition and drug-induced adaptation is not well known. Further, the detailed kinetics of the transition, especially at the early stage of treatment when the cancer cells are beginning to adapt to the drug, is also not clear. I will talk about how to harness single cell proteomic methods, bulk transcriptomic profiling, and mathematical modeling, to investigate the kinetics of the phenotypic adaptation of a panel of BRAFV600 mutated patient-derived melanoma cell lines and patient biopsies upon BRAF inhibition, with an eye towards identifying strategies for halting the adaptive response so as to lead to prolonged tumor growth inhibition.
