Photo of Nada Y. Kalaany,  PhD

Nada Y. Kalaany, PhD

Boston Children's Hospital

Boston Children's Hospital
Phone: (617) 919-4896
Fax: (617) 730-0856

Nada Y. Kalaany, PhD

Boston Children's Hospital


  • Assistant Professor, Pediatrics, Harvard Medical School
  • Associate in Medicine, Medicine/Endocrinology, Boston Children's Hospital


Research Abstract

The goal of our laboratory is to identify the mechanisms underlying the association of systemic metabolism and cancer, particularly that of the lung, pancreas and colon.

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.


Powered by Harvard Catalyst
  • Karsli-Uzunbas G, Guo JY, Price S, Teng X, Laddha SV, Khor S, Kalaany NY, Jacks T, Chan CS, Rabinowitz JD, White E. Autophagy is Required for Glucose Homeostasis and Lung Tumor Maintenance. 2014. PubMed
  • Curry NL, Mino-Kenudson M, Oliver TG, Yilmaz OH, Yilmaz VO, Moon JY, Jacks T, Sabatini DM, Kalaany NY. Pten-null tumors cohabiting the same lung display differential AKT activation and sensitivity to dietary restriction. 2013; 3:908-21. PubMed
  • Possemato R, Marks KM, Shaul YD, Pacold ME, Kim D, Birsoy K, Sethumadhavan S, Woo HK, Jang HG, Jha AK, Chen WW, Barrett FG, Stransky N, Tsun ZY, Cowley GS, Barretina J, Kalaany NY, Hsu PP, Ottina K, Chan AM, Yuan B, Garraway LA, Root DE, Mino-Kenudson M, Brachtel EF, Driggers EM, Sabatini DM. Functional genomics reveal that the serine synthesis pathway is essential in breast cancer. Nature 2011. PubMed
  • Kalaany NY, Sabatini DM. Tumours with PI3K activation are resistant to dietary restriction. Nature 2009; 458:725-31. PubMed
  • Guertin DA, Stevens DM, Thoreen CC, Burds AA, Kalaany NY, Moffat J, Brown M, Fitzgerald KJ, Sabatini DM. Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1. Dev Cell 2006; 11:859-71. PubMed
  • Kalaany NY, Mangelsdorf DJ. LXRS and FXR: the yin and yang of cholesterol and fat metabolism. Annu Rev Physiol 2006; 68:159-91. PubMed
  • Kalaany NY, Gauthier KC, Zavacki AM, Mammen PP, Kitazume T, Peterson JA, Horton JD, Garry DJ, Bianco AC, Mangelsdorf DJ. LXRs regulate the balance between fat storage and oxidation. Cell Metab 2005; 1:231-44. PubMed
  • El-Sabban ME, Sfeir AJ, Daher MH, Kalaany NY, Bassam RA, Talhouk RS. ECM-induced gap junctional communication enhances mammary epithelial cell differentiation. J Cell Sci 2003; 116:3531-41. PubMed