Paola Betancur, PhD

Assistant Professor In RES
Radiation Oncology
+1 415 514-1084
Research Overview: 

We are interested in understanding the mechanisms encoded in the DNA by which cancerous cells avoid being detected and destroyed by the host’s immune system. Toward this goal, we examine the interactions between epigenetic modifiers, transcription factors and the genomic enhancers of target genes that in response to inflammation abnormally activate the immune escape program within tumor or damaged cells during aging, after radiation and in response to infectious diseases. To accomplish our goal, we have long lasting collaborations across campus, at Stanford University and other recognized national and international institutions.

With patients in mind, we are a research group dedicated to finding methods for improving the treatment of cancer by analyzing the DNA of individual patients. In the era of personalized medicine, this information is critical for understanding which therapy will be more effective for each patient, and for targeting specific cancer types, including cancer of the breast.

Primary Thematic Area: 
Cancer Biology & Cell Signaling
Secondary Thematic Area: 
Human Genetics
Research Summary: 
Gene regulation in health and disease

Websites

Publications: 

Abstract 4402: A genomic insertion/deletion variant activates immune escape and tumor promoting programs in breast cancer.

Cancer research

Paola Betancur, Carolina DiBenedetto, Daniza Diane Acenas, Anthony Rodriguez, Alysia Thach

High-resolution Inference of Multiplexed Anti-HIV Gene Editing using Single-Cell Targeted DNA Sequencing.

bioRxiv : the preprint server for biology

Bouzidi MS, Dossani ZY, Benedetto CD, Raymond KA, Desai S, Chavez LR, Betancur P, Pillai SK

Enhancer Clusters Drive Type I Interferon-Induced TRAIL Overexpression in Cancer, and Its Intracellular Protein Accumulation Fails to Induce Apoptosis.

Cancers

Di Benedetto C, Khan T, Serrano-Saenz S, Rodriguez-Lemus A, Klomsiri C, Beutel TM, Thach A, Walczak H, Betancur P

Activation of JUN in fibroblasts promotes pro-fibrotic programme and modulates protective immunity.

Nature communications

Cui L, Chen SY, Lerbs T, Lee JW, Domizi P, Gordon S, Kim YH, Nolan G, Betancur P, Wernig G