James Cusack, MD, FACS is a graduate of Dartmouth College and Emory University Medical School and trained in surgery at Tufts New England Medical Center. He also was a research fellow in Surgery at the Brigham and Women's Hospital and spent three years as a fellow in Surgical Oncology at the M. D. Anderson Cancer Center. Since 2000, he has been on staff at Massachusetts General Hospital and the Dana-Farber Cancer Institute and on the faculty of Harvard Medical School. In 2008, he became associate professor of surgery at Harvard Medical School, associate visiting surgeon at Massachusetts General Hospital, and director of the Division of Surgical Oncology Laboratories.
Dr. Cusack chairs the Scientific Program Committee of the Society of Surgical Oncology (SSO), and has served on several other SSO Committees including the Fellowship and Research Grants Committee, the Continuing Medical Education Committee, the SSO Planning Task Force, and the Clinical Affairs Committee, which he chaired in 2003. In 2009, he was appointed to the American Society of Clinical Oncology (ASCO) review subcommittee for the Advanced Clinical Research Award (ACRA) in Colorectal Cancer. He was also appointed in 2010 to the ASCO GI Program Committee and the Program Committee for the International Conference on Colon and Rectal Surgery - Colorectal Cancer to be held in Shanghai in March 2011.
Dr. Cusack has made landmark contributions to the understanding of cancer treatment resistance and the development of novel targeted therapies to enhance treatment response. His bibliography lists over 60 publications. He is section editor of the journals ANNALS OF SURGICAL ONCOLOGY and CANCER and serves on the editorial board of the WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY. Dr. Cusack also works in Bangladesh, Liberia, and Kazakhstan to improve the delivery of surgical and cancer care in the developing world.
The Cusack Laboratory focuses on cancer resistance mechanisms and has been NIH funded since 1997. Findings from the Laboratory have shown that radiation and chemotherapy induce resistance mechanisms. Blocking these responses with targeted agents augments the effectiveness of anti-cancer therapies. Dr. Cusack is co-inventor of the patent that describes this therapeutic strategy, now licensed for novel drug development.
Dr. Cusack is Director of the MGH Surgical Oncology Laboratories and Chair of the 2010 Scientific Program Committee for the Society of Surgical Oncology. He is a member of the Program Committee for the American Society of Clinical Oncology (ASCO) Gastrointestinal Cancers Symposium and the ASCO Advanced Clinical Research Awards subcommittee. He is Section Editor of Translational Research and Biomarkers Section of the ANNALS OF SURGICAL ONCOLOGY, Section Editor of the Translational Reviews section of CANCER and a Member of the Editorial Staff of the WORLD JOURNAL OF GASTROINTESTINAL ONCOLOGY.
Dr. Cusack recently defined the role of HB-EGF in cancer resistance. Based on this work, he is developing a new cancer treatment with scientists in Japan. Ongoing research is investigating biomarkers in rectal cancer and Merkel Cell carcinoma.
Cusack JC, Giacco GG, Cleary K, Davidson BS, Izzo F, Skibber J, Yen J, Curley SA. Survival factors in 186 patients younger than 40 years old with colorectal adenocarcinoma. J Am Coll Surg 1996 Aug;183(2):105-12.
Wang C-Y, Cusack JC, Liu R, Baldwin AS. Control of inducible chemoresistance: enhanced anti-tumor therapy through increased apoptosis by inhibition of NF-kB. Nat Med 1999 Apr;5(4):412-7.
Curley SA, Cusack JC Jr, Tanabe KK, Stoelzing O, Ellis LM. Advances in the treatment of liver tumors. Curr Probl Surg 2002 May; 39(5): 449-571.
Regenbogen S, Cusack JC. Advances in the surgical technique for primary rectal cancer. In: Ajani J, editor. Therapeutic approaches to localized rectal cancer: current colorectal cancer reports. Bangalore, India: Current Science; 2005; vol. 1(1): 43-50.
Wang F, Sloss C, Zhang X, Lee SW, Cusack JC. Membrane-bound heparin-binding epidermal growth factor-like growth factor (HB-EGF) regulates E-cadherin expression in pancreatic carcinoma cells. Cancer Res 2007 Sept 15;67:8486-93.
Sloss C, Wang F, Liu R, Xia L, Houston M, Ljungman, D, Palladino MA, Cusack JC. Proteasome inhibition activates epidermal growth factor receptor (EGFR) and EGFR-independent mitogenic kinase signaling pathways in pancreatic cancer cells. Clin Cancer Res 2008 Aug 15; 14:5116-23.
Sloss CM, Wang F, Palladino, MA, Cusack JC. Activation of EGFR by proteasome inhibition requires heparin-binding EGF-like growth factor (HB-EGF) in pancreatic cancer cells. (Pub online, Oncogene 2010 Mar 8).
MGH Hotline 12/05/08: A multidisciplinary team from the MGH Cancer Center recently traveled to Kazakhstan’s capitol Astana to work with the city’s Department of Health to improve the oncology services at a local hospital.
Massachusetts General Hospital is partnering with the American Society of Colon and Rectal Surgeons, and Coaches vs. Cancer to promote screening and treatment for colorectal cancer.
Phone 2: 617-724-4000