Aaron Hata, M.D., Ph.D. & Heidie Frisco Cabanos, Ph.D.

Funded in Collaboration With Stand Up To Cancer (SU2C)

The last two decades have seen the development of increasingly effective cancer therapies that target different aspects of tumors cells, including uncontrolled growth/survival, evasion of the immune system, hyper-activated signaling pathways and dysregulated gene expression programs. In a subset of cancers, including non-small cell lung cancer (NSCLC) with mutations in the epidermal growth factor receptor (EGFR), these therapies can lead to dramatic tumor regressions in a significant number of patients.  However, in the majority of EGFR mutant lung cancer patients who respond to anti-cancer therapies, relapse usually occurs preventing long-term cures. We propose to investigate the reasons why cancer cells become resistant to treatment. We believe a tumor is made up of a number of different types of cells that can each respond differently to treatment. We hope to uncover and understand these differences by looking at genomic data taken from patients who are biopsied before treatment, during response to treatment, and when resistance emerges. We are also interested in understanding the role the immune system plays during cancer treatment. We’d like to understand if the tumor has developed ways to evade the immune system, and how we can promote the patient’s own immune system to fight back against the cancer. It is our hope that combining traditional drug treatment with newer immunotherapies will provide greater tumor regressions. Our goal is to create a deeper understanding of the make-up of a tumor in order to identify novel therapies to expand the survival of patients with NSCLC.

Location: Massachusetts General Hospital Cancer Center - Massachusetts
Proposal: Sequential profiling of acquired resistance in EGFR mutant non-small cell lung cancers
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