Researcher | Research Overview
A main focus of the Kalaany lab is to investigate the correlation between systemic metabolism and cancer incidence and progression, with the goal of identifying metabolic dependencies that could be targeted therapeutically in cancer patients.
Altered metabolism is a hallmark of cancer. It is however, not only driven by cell-autonomous genetic alterations in oncogenes and tumor suppressor genes, but also by the surrounding tissue microenvironment, as well as the systemic macroenvironment of the host. Evidence for a robust correlation between systemic metabolism and cancer incidence and progression has been accumulating for over a century. For instance, the anti-tumorigenic effects of dietary restriction have been recognized since the early 1900s. Moreover, recent epidemiological studies demonstrate a linear correlation between obesity, type 2 diabetes and mortality from cancers of a wide variety of tissues. Conversely, cancer-associated cachexia, or the organismal energy-wasting syndrome that degrades muscle and fat, can be detrimental to many cancer patients, negatively impacting their quality of life and shortening survival.
Using different models of lung and pancreatic cancer, the Kalaany lab aims at identifying metabolic dependencies in tumors growing under distinct systemic metabolic states, with the goal of targeting them therapeutically in cancer patients, while minimizing toxicity in normal tissues.
In particular, the Kalaany lab aims at understanding:
- How tumors survive and thrive in a nutrient-limiting microenvironment
- How tumor growth and metabolism can be affected by the systemic metabolic state of the host (e.g. dietary restriction, obesity, insulin resistance)
- How the host systemic metabolic state can, itself, get affected by tumor growth and metabolism (e.g. cancer-associated cachexia, or energy-wasting syndrome)
Researcher | Research Background
Nada Kalaany received her PhD from UT Southwestern Medical Center where she studied the role of nuclear hormone receptors in diet-induced obesity. As a postdoctoral fellow, she worked at the Whitehead Institute at MIT where she uncovered a role for oncogenic signaling in modulating the sensitivity of tumors to dietary restriction. She has since joined the faculty of Boston Children's Hospital, Division of Endocrinology. She is also an Associate Member at the Broad Institute of MIT and Harvard, and a member of the Dana-Farber/Harvard Cancer Center.