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Nada Y. Kalaany, PhD

Assistant Professor, Department of Pediatrics, Harvard Medical School

Associate in Medicine, Medicine/Endocrinology, Boston Children's Hospital

Contact Info

Nada Kalaany
Boston Children's Hospital
3 Blackfan Circle
Boston, MA, 02115
Mailstop: CLS-16067
Phone: 617-919-4896
Fax: 617-730-0856
nada.kalaany@childrens.harvard.edu

Assistant

Meghan Foster
Program Coordinator
Endocrinology/Center for Basic and Translational Obesity Research
Boston Children's Hospital
3 Blackfan Circle
CLS-16065.1
Boston, MA, 02115
Phone: 617-919-2133
Fax: 617-730-0856
meghan.foster@childrens.harvard.edu

DF/HCC Program Affiliation

Gastrointestinal Malignancies

Lab Website

Nada Kalaany Faculty Page

Research Abstract

The goal of our laboratory is to identify the mechanisms underlying the association of obesity/type2 diabetes and cancer.
Evidence for a robust correlation between systemic metabolism and cancer incidence and progression has been accumulating for over a century. Indeed, the anti-tumorigenic effects of dietary restriction that are known to delay cancer incidence and decrease tumor growth in laboratory rodents, have been recognized since the early 1900s. Moreover, the last quarter of the twentieth century has witnessed a worldwide epidemic surge of obesity and its associated metabolic syndrome (dyslipidemia, hypertension, hyperglycemia, insulin resistance and type2 diabetes). Recent epidemiological studies demonstrate a linear correlation between the observed increase in obesity as well as type2 diabetes and mortality from cancers of a wide variety of tissues. This correlation has been estimated to account, in the United States, for 14% and 20% of all deaths from cancer in men and women, respectively.

Our recent work has unveiled a key role for the PTEN/PI3K pathway in determining tumor sensitivity to dietary restriction at early stages of tumor formation. This signaling pathway, known to integrate extracellular hormonal/growth factor stimuli to regulate cell survival, proliferation, and motility, is frequently mutated in a broad array of human cancers and has therefore been extensively studied. However, the role of PTEN/PI3K pathway in modulating the response of tumors to body metabolism is just starting to emerge.

Our laboratory aims at understanding how signaling pathways, such as PI3K/PTEN, influence tumor initiation and maintenance in the context of obesity and its metabolic syndrome and whether such an effect can be exploited therapeutically.

Publications

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