Our group is interested in understanding the metabolic adaptations that allow cancer cells to grow and proliferate, causing tumor growth. To understand how cancer cell metabolism works to fuel tumor growth, we use metabolomics techniques to catalog what nutrients are in the microenvironment of tumors. This provides us with a "menu" of nutrients that cancer cells could potentially metabolize to fuel their growth. Once we know the "menu" for different tumor types, we then use a variety of experimental tools from metabolomics to CRISPR gene editing to determine which nutrients cancer cells actually consume from the "menu", and which metabolic pathways process these nutrients. From these experiments, we are delineating the biochemical underpinnings of cancer cell growth.
Massachusetts Institute of Technology
Cambridge, MA
Post-doctoral fellow - Tumor Metabolism
2019
University of California, Berkeley
Berkeley, CA
PhD - Biochemistry, Biophysics and Structural Biology
2015
University of Chicago
Chicago, IL
BA/BA - Biology/Romance Languages and Literature
2009
Microenvironmental arginine restriction sensitizes pancreatic cancers to polyunsaturated fatty acids by suppression of lipid synthesis.
Microenvironmental arginine restriction sensitizes pancreatic cancers to polyunsaturated fatty acids by suppression of lipid synthesis. Elife. 2026 Aug 05; 14.
PMID: 42554218
Isolation of Bacteria and Fungi from Human Pancreatic Tumors and Duodenum.
Isolation of Bacteria and Fungi from Human Pancreatic Tumors and Duodenum. Gut Microbes. 2026 Dec 31; 18(1):2695522.
PMID: 42411381
Tissue-specific tolerance mechanisms and lymph node co-drainage shape T cell immunity in the upper digestive system and pancreatic cancer progression.
Tissue-specific tolerance mechanisms and lymph node co-drainage shape T cell immunity in the upper digestive system and pancreatic cancer progression. Cell Rep. 2026 May 26; 45(5):117324.
PMID: 42090287
The HIF-2 transcription factor mediates resistance to ferroptosis in pancreatic cancer.
The HIF-2 transcription factor mediates resistance to ferroptosis in pancreatic cancer. Mol Cell. 2026 Apr 02; 86(7):1260-1274.e4.
PMID: 41932308
YIA26-005: Identification of FAD Biosynthesis As a Microenvironmental Synthetic Lethal Target of Pancreatic Adenocarcinomas.
YIA26-005: Identification of FAD Biosynthesis As a Microenvironmental Synthetic Lethal Target of Pancreatic Adenocarcinomas. J Natl Compr Canc Netw. 2026 Mar 31; 24(3.5).
PMID: 41911863
YIA26-005: Identification of FAD Biosynthesis As a Microenvironmental Synthetic Lethal Target of Pancreatic Adenocarcinomas.
YIA26-005: Identification of FAD Biosynthesis As a Microenvironmental Synthetic Lethal Target of Pancreatic Adenocarcinomas. J Natl Compr Canc Netw. 2026 Mar 31; 24(3.5).
PMID: 42055063
Catabolism of extracellular glutathione supplies cysteine to support tumours.
Catabolism of extracellular glutathione supplies cysteine to support tumours. Nature. 2026 May; 653(8115):933-941.
PMID: 41851454
Microglial fructose metabolism is essential for glioblastoma growth.
Microglial fructose metabolism is essential for glioblastoma growth. Proc Natl Acad Sci U S A. 2026 Mar 24; 123(12):e2521256123.
PMID: 41843684
The transcriptional repressor Fli1 inhibits proteostasis during nutrient stress to limit NK cell persistence in solid tumors.
The transcriptional repressor Fli1 inhibits proteostasis during nutrient stress to limit NK cell persistence in solid tumors. Immunity. 2026 Mar 10; 59(3):717-733.e10.
PMID: 41713422
Intraoperative arteriovenous patient sampling to assess in situ non-small cell lung cancer metabolism.
Intraoperative arteriovenous patient sampling to assess in situ non-small cell lung cancer metabolism. J Clin Invest. 2026 Mar 16; 136(6).
PMID: 41591824