About David Sykes, MD, PhD

David completed his undergraduate training in Biochemistry at the University of Alberta in Edmonton, Canada. He entered the Medical Scientist Training Program (M.D., Ph.D.) at the University of California San Diego and carried out his Ph.D. research with Dr. Mark Kamps where he became interested in the problems that arise during white blood cell development.

David did his internship and residency at the Massachusetts General Hospital as well as a year as a Chief Medical Resident in the Department of Internal Medicine. He was a Hematology and Oncology fellow in the combined Dana-Farber Cancer Institute, MGH Cancer Center fellowship program.

David joined the MGH Cancer Center as an attending in benign hematology. He splits his time between the laboratory (80% research) and clinic (20% direct patient care).

David has a special interest in rare hematologic conditions. In 2011 he defined a new syndrome - the TEMPI syndrome - which affects approximately 20 patients worldwide (https://www.nejm.org/doi/full/10.1056/NEJMc1106670).

David completed his post-doctoral research training in the laboratory of Dr. David Scadden, working to identify new therapies for patients with acute myeloid leukemia. 

David transitioned to his own lab as an assistant professor in 2017 (http://sykeslab.com/). 

He continues to see patients in clinic on Fridays and see patients in the hospital on the inpatient hematology consult service. 

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Locations

Mass General Cancer Center: Hematology Oncology
55 Fruit St.
Boston, MA 02114
Phone: 617-724-4000
Fax: 617-724-6801

Medical Education

  • MD, UCSD
  • Residency, Massachusetts General Hospital
  • Fellowship, Dana Farber Cancer Institute

American Board Certifications

  • Hematology, American Board of Internal Medicine
  • Internal Medicine, American Board of Internal Medicine
  • Medical Oncology, American Board of Internal Medicine

Accepted Insurance Plans

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Research

The Sykes Lab is interested in a variety of topics, all centered around white blood cell development and how this development can be corrupted in the setting of infection, cancer or inherited disorders.

1. Acute myeloid leukemia represents a defect in white blood cell development where the white blood cells are frozen at an immature (called undifferentiated) stage of maturation. We are working to develop 'differentiation therapy' for patients with AML -- therapy designed to trick the immature leukemia cells into resuming their normal process of maturation.

2. The Barth Syndrome is a rare inherited X-linked disorder in which children do not have the enzyme tafazzin, and therefore develop both cardiomyopathy and neutropenia. We are working to understand the mechanism that links the lack of tafazzin activity to the development of neutropenia.

3. Metastatic prostate cancer almost always targets the bone and bone marrow. We are working to understand this specific relationship between prostate cancer and why it preferentially targets the bone marrow and how to stimulate the immune cells to eradicate the tumor cells. 

Publications

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