Christine M. Heske, M.D.
Assistant Clinical Investigator
Pediatric Oncology Branch
Building 10-CRC, Room 1-3816
Bethesda, MD 20892-1104
Dr. Heske's focus is on translational and clinical research in the area of pediatric sarcomas as it relates to the identification and evaluation of new therapeutic targets and overcoming mechanisms of resistance. Patients with metastatic or relapsed rhabdomyosarcoma, Ewing sarcoma and osteosarcoma continue to have poor outcomes, despite advances in therapy. Hence, finding new targets for these diseases and understanding the potential mechanisms of resistance relating to those targets is essential to improving outcomes for patients.
Her current laboratory projects include the identification of novel combination therapies in Ewing sarcoma, understanding the metabolic vulnerabilities of Ewing sarcoma, and exploiting DNA repair pathways in rhabdomyosarcoma and Ewing sarcoma..
In addition to conducting preclinical research, Dr. Heske is invested in translating promising laboratory findings into clinical trials. She is currently running a phase I/II trial for patients with rhabdomyosarcoma using combination therapy with an IGF-1 antibody and a Src family kinase inhibitor, and is an investigator for a phase I/II trial investigating PEN-866, an HSP90-SN-38 drug conjugate in sarcomas, which is based on work from her lab.
After completing her undergraduate work at Harvard University, Dr. Heske received her M.D. from The George Washington University School of Medicine and Health Sciences in 2008. She completed her pediatric internship and residency at Brown University/Hasbro Children's Hospital, followed by her fellowship training at the combined National Cancer Institute-Johns Hopkins University Pediatric Hematology and Oncology program, where she served as Chief Fellow.
Dr. Heske is board certified in General Pediatrics (2011) and Pediatric Hematology/Oncology (2015) and is currently an Assistant Clinical Investigator in the POB.
Wan X, Yeung C, Heske C, Mendoza A, Helman LJ. IGF-1R Inhibition Activates a YES/SFK Bypass Resistance Pathway: Rational Basis for Co-Targeting IGF-1R and Yes/SFK Kinase in Rhabdomyosarcoma. Neoplasia. 2015;17(4):358-66.
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This page was last updated on October 25th, 2019