Inhibition of oncogenic MAPK signaling in combination with neutralizing the anti-apoptotic BCL-2 repertoire leads to the killing of cancer cells. Here, human melanoma cells are treated with PLX-4032 (BRAF V600E inhibitor) and ABT-263 (BCL-2 antagonist) to promote apoptosis (yellow). PMIDs: 24608435, 23152056, and 22268005

Our current research interests are divided into three areas, but adopt a unified theme to decipher the interplay between mitochondria and cell death signaling:

I. What are the biochemical, physiological, and structural consequences of protein·protein interactions within the BCL-2 family?

II. How does the mitochondrial environment influence BCL-2 family function and the core cell death machinery?

III. How do oncogenic and tumor suppressor signals intersect with the core cell death machinery and metabolic pathways to regulate tumorigenesis and chemosensitivity?

We explore the above questions using state-of-the-art apoptosis, metabolism, and cancer biology model systems — usually focusing on hematological malignancies and melanoma.

The laboratory is a highly collaborative group on the Mount Sinai campus, which has enriched our scientific impact and experimental skill set — along with creating an ideal atmosphere for mentoring students and post-doctoral fellows.