Houston Methodist. Leading Medicine.
Houston Methodist. Leading Medicine

Andrew Dannenberg M.D.

Andrew Dannenberg, M.D.

Andrew Dannenberg, M.D.

Full Affiliate Member 
Cancer Research Program
The Methodist Hospital Research Institute

Henry R. Erle, M.D.-Roberts Family Professor of Medicine
Weill Cornell Medical College of Cornell University

E-mail: ajdannen@med.cornell.edu
Phone: 212-746-4403



Tufts University, Boston, MA (Biology)


Washington University, St. Louis, MO 

Postdoctoral Training

Intern/Resident, The New York Hospital, Cornell Medical Center, New York, NY

Gastroenterology Fellow, The New York Hospital , Cornell Medical Center, New York, NY



Dr. Andrew Dannenberg is the Henry R. Erle, MD-Roberts Family Professor of Medicine at Weill Cornell Medical College.  He received his medical degree from Washington University in St. Louis and served as a medical resident and gastroenterology fellow at The New York Hospital-Cornell Medical Center. His research focuses on the mechanisms underlying the inflammation-cancer connection in multiple organs. Dr. Dannenberg has authored more than 150 scientific articles, and edited several books and journals. In 2011, he was awarded the American Association for Cancer Research-Prevent Cancer Foundation award for excellence in cancer prevention research. He is a member of the Association of American Physicians, the American Society for Clinical Investigation, and the American Association for Cancer Research. He previously chaired the Program Committee of the AACR "Frontiers in Cancer Prevention Research" meeting and serves on the editorial boards of several journals including Cancer Prevention Research and the Journal of Clinical Oncology

Description of Research

Dr. Dannenberg’s research is focused on the connection between chronic inflammation and cancer with an emphasis on prostaglandin (PG) biology.  The long-term goal of this research is to develop evidence-based strategies to decrease inflammation and reduce the risk of developing cancer. 

Human cancers, premalignant lesions and chronic inflammatory states (e.g. ulcerative colitis), are identified in which the expression of enzymes involved in PG biosynthesis (cyclooxygenase-2, COX-2), catabolism (15-hydroxyprostaglandin dehydrogenase) or transport (PGT) is deregulated. The signal transduction pathways that control the expression of these genes in normal and diseased tissues are then explored. In this way, the mechanisms by which PGs impact wound healing or stimulate the formation and progression of tumors are being defined. 

As second major focus of the research program is hormone receptor-positive breast cancer, and a key signaling pathway by which PGE2 induces cytochrome P450 aromatase, the enzyme that catalyzes the synthesis of estrogens from androgens.  Pharmacological and genetic studies are used to assess the impact of targeting specific molecules involved in PG synthesis on tumor formation and growth.  The contribution of body mass and diet to changes in PG levels, inflammation and the expression of genes implicated in carcinogenesis is also being explored.  Given the link between chronic colitis and colon cancer, a major goal is to identify PG-responsive genes that play key roles in colorectal mucosal homeostasis, and biomarkers that may reflect inflammation and cancer prognosis.

Major Areas of Research

Cancer, breast, prostaglandin, inflammation

Recent Publications

Subbaramaiah K, Morris PG, Zhou XK, Morrow M, Du B, Giri D, Kopelovich L, Hudis CA, Dannenberg AJ. Increased levels of COX-2 and prostaglandin E2 contribute to elevated aromatase expression in inflamed breast tissue of obese women. Cancer Discov. 2012 Apr;2(4):356-65. PMID: 22576212

Khan KM, Kothari P, Du B, Dannenberg AJ, Falcone DJ. Matrix metalloproteinase-dependent microsomal prostaglandin E synthase-1 expression in macrophages: role of TNF-α and the EP4 prostanoid receptor. J Immunol. 2012 Feb 15;188(4):1970-80. PMID: 22227567

Morris PG, Hudis CA, Giri D, Morrow M, Falcone DJ, Zhou XK, Du B, Brogi E, Crawford CB, Kopelovich L, Subbaramaiah K, Dannenberg AJ. Inflammation and increased aromatase expression occur in the breast tissue of obese women with breast cancer. Cancer Prev Res (Phila). 2011 Jul;4(7):1021-9. PMID: 21622727

Subbaramaiah K, Howe LR, Bhardwaj P, Du B, Gravaghi C, Yantiss RK, Zhou XK, Blaho VA, Hla T, Yang P, Kopelovich L, Hudis CA, Dannenberg AJ. Obesity is associated with inflammation and elevated aromatase expression in the mouse mammary gland. Cancer Prev Res (Phila). 2011 Mar;4(3):329-46. PMID: 21372033

Sinicrope FA, Dannenberg AJ. Obesity and breast cancer prognosis: weight of the evidence. J Clin Oncol. 2011 Jan 1;29(1):4-7. PMID: 21115867

Boyle JO, Gümüs ZH, Kacker A, Choksi VL, Bocker JM, Zhou XK, Yantiss RK, Hughes DB, Du B, Judson BL, Subbaramaiah K, Dannenberg AJ. Effects of cigarette smoke on the human oral mucosal transcriptome. Cancer Prev Res (Phila). 2010 Mar;3(3):266-78. PMID: 20179299

Duffield-Lillico AJ, Boyle JO, Zhou XK, Ghosh A, Butala GS, Subbaramaiah K, Newman RA, Morrow JD, Milne GL, Dannenberg AJ. Levels of prostaglandin E metabolite and leukotriene E(4) are increased in the urine of smokers: evidence that celecoxib shunts arachidonic acid into the 5-lipoxygenase pathway. Cancer Prev Res (Phila). 2009 Apr;2(4):322-9. PMID: 19336727

Kekatpure VD, Dannenberg AJ, Subbaramaiah K. HDAC6 modulates Hsp90 chaperone activity and regulates activation of aryl hydrocarbon receptor signaling. J Biol Chem. 2009 Mar 20;284(12):7436-45. PMID: 19158084

Subbaramaiah K, Benezra R, Hudis C, Dannenberg AJ. Cyclooxygenase-2-derived prostaglandin E2 stimulates Id-1 transcription. J Biol Chem. 2008 Dec 5;283(49):33955-68. PMID: 18842581 

Subbaramaiah K, Hudis C, Chang SH, Hla T, Dannenberg AJ. EP2 and EP4 receptors regulate aromatase expression in human adipocytes and breast cancer cells. Evidence of a BRCA1 and p300 exchange. J Biol Chem. 2008 Feb 8;283(6):3433-44. PMID: 18083712