Massachusetts General Hospital

Boston, Massachusetts
Director of Thoracic Oncology and Attending Physician, Massachusetts General Hospital
Associate Professor Medicine, Harvard Medical School

Research

Dr. Alice Shaw’s research aims to provide viable treatments for lung cancer patients whose tumors have become resistant to their current drug therapy. With NFCR support since 2014, she seeks to develop new treatments for patients with anaplastic lymphoma kinase (ALK) mutations in non-small cell lung cancer. While only 5% of lung cancer patients are diagnosed with ALK-positive lung cancer (or ALK+ lung cancer), the ALK mutation leads to a high rate of cancer growth and spread to other parts of the body. Dr. Shaw was the lead investigator in the global registration studies for two drugs, which led to their FDA approval for advanced ALK+ lung cancer. These therapies have dramatically improved the outlook for patients, but, eventually, almost all patients will develop resistance.

By using multiple research models, Dr. Shaw and her team quickly identified new drug combinations for lung cancer patients who have developed resistance to their current therapy. Dr. Shaw demonstrated a marked regression of ALK+ lung cancer tumors in mice when treated with a combination of FDA-approved ALK+ lung cancer agents and inhibitors of SHP2 — a cancer gene that regulates cancer cell survival and growth and suppresses an immune system protein. In 2019, a first-in-human clinical trial led by Dr. Shaw began with this combination therapy. Hope is on the horizon with this new combination therapy for ALK+ lung cancer patients who have become resistant to standard targeted therapies.

Bio

Alice T. Shaw, M.D., Ph.D., received her B.A. in biochemistry at Harvard University and her M.D. and Ph.D. degrees from Harvard Medical School (where she is currently an Associate Professor). She then completed her residency at Massachusetts General Hospital and her postdoctoral work at Massachusetts Institute of Technology. Dr. Shaw was also a fellow at Massachusetts General Hospital and is currently the Director of Thoracic Oncology and an Attending Physician there.

In addition to her funding from NFCR, Dr. Shaw has been awarded other research grants throughout her career, including from the Damon Runyon Cancer Research Foundation, the Burroughs Welcome Fund, the V Foundation for Cancer Research, Uniting Against Lung Cancer and the National Institutes of Health.

Related Content

What is Genomic Sequencing, and Who Can Benefit?

NFCR In the News: Addressing Deadly Brain Cancer, GBM

Efficiently Eliminating Metastasized Melanoma Cells

The prevalence of skin cancer is rising at an alarming rate, with melanoma being the deadliest. Melanoma is renowned for quickly spreading to other organs (or metastasizing), drastically decreasing the likelihood of survival. Being able to stop the spread of melanoma cells is essential to save the lives of many patients; however, no researcher has been able to solve the puzzle – until now. With long-term support from the National Foundation for Cancer Research (NFCR), Dr. Daniel Haber and his team developed the CTC-iChip – a medical device to capture the few circulating tumor cells (CTCs) present in a standard blood sample from a patient. Circulating tumor cells are tumor cells that have become detached from the primary tumor and enter the blood circulation. While CTCs occur once in a billion cells and are extremely rare, they nevertheless may hold the key to metastasis—the stage responsible for most cancer deaths. Dr. Haber and his team developed methods to analyze the genes in CTCs, providing a liquid biopsy and an invaluable window into a patient’s cancer in real-time. Doctors may efficiently obtain critical information from their patient’s CTCs for life-saving treatment decisions in advanced cancer with the liquid biopsy. Though this significant breakthrough sparked excitement throughout the oncology world, Dr. Haber continued digging for more pieces to the puzzle. He honed in on the unique makeup of CTCs to understand what fueled the spread of these deadly cells and what inhibited it. Using samples from melanoma patients, the team found that the unique lipogenesis regulator (referred to as SREBP2) held an important role in combating the growth of CTCs. SREBP2 directly induces transcription of the iron carrier, which kicks off a chain reaction at a cellular level. This chain reaction causes resistance to ferroptosis inducers, a type of programmed cell death. The ability to manufacture these chain reactions within CTCs opens up a realm of therapeutic opportunities for patients with metastatic melanoma. While this discovery is highly significant in the war on cancer, it is only just the beginning of understanding how to reduce melanoma metastasis. Dr. Haber remains committed to solving more pieces of the puzzle. To support the work of Dr. Haber and other world-renowned researchers, please make a gift today. Additional Reads You May Enjoy: New Drug Makes Unresectable or Metastatic Ocular Cancer Treatable Catching Cancer Cells on Their Way to Spreading Detecting Skin Cancer with Artificial Intelligence and Other Game-Changing Technologies in Cancer Stay connected with the cancer community! Receive NFCR’s monthly e-newsletter and blogs featuring stories of inspiration, support resources, cancer prevention tips, and more. Sign up here.