Biological and Biomedical Science
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Nabeel Bardeesy

Department of Medicine
Massachusetts General Hospital
Richard B. Simches Research Center
185 Cambridge St., CPZN-4216
Boston, MA 02114
Tel: (617) 643-2579
Fax: (617) 643-3170
Email: bardeesy.nabeel@mgh.harvard.edu


Nabeel Bardeesy

Nabeel Bardeesy’s laboratory focuses on understanding the how the signature genetic changes in pancreatic adenocarcinoma influence the biology of this disease. Particular interests include defining the relationship between perturbed pancreatic differentiation and cancer initiation and progression, and elucidating the tumor suppressor functions of the TGFβ and Lkb1 pathways.

 

References:

  • Bardeesy N, Cheng KH, Berger JH, Chu GC, Pahler J, Olson P, Hezel AF, Horner J, Lauwers GY, Hanahan D, DePinho RA. Smad4 is dispensable for normal pancreas development yet critical in progression and tumor biology of pancreas cancer. Genes Dev. 2006 Nov 15;20(22):3130-46. PMID: 17114584 [PubMed - indexed for MEDLINE]
  • Bardeesy N, Aguirre AJ, Chu GC, Cheng KH, Lopez LV, Hezel AF, Feng B, Brennan C, Weissleder R, Mahmood U, Hanahan D, Redston MS, Chin L, Depinho RA. Related Articles, Links Both p16(Ink4a) and the p19(Arf)-p53 pathway constrain progression of pancreatic adenocarcinoma in the mouse. Proc Natl Acad Sci U S A. 2006 Apr 11;103(15):5947-52. Epub 2006 Apr 3. PMID: 16585505 [PubMed - indexed for MEDLINE]
  • Aguirre AJ, Bardeesy N, Sinha M, Lopez L, Tuveson DA, Horner J, Redston MS, DePinho RA. Activated Kras and Ink4a/Arf deficiency cooperate to produce metastatic pancreatic ductal adenocarcinoma. Genes Dev. 2003 Dec 15;17(24):3112-26. Epub 2003 Dec 17. PMID: 14681207 [PubMed - indexed for MEDLINE]
  • Bardeesy N, Sinha M, Hezel AF, Signoretti S, Hathaway NA, Sharpless NE, Loda M, Carrasco DR, DePinho RA. Loss of the Lkb1 tumour suppressor provokes intestinal polyposis but resistance to transformation. Nature. 2002 Sep 12;419(6903):162-7. PMID: 12226664 [PubMed - indexed for MEDLINE