New Hire: Nora Heisterkamp, Ph.D.
October 11, 2017 | by City of Hope
Dr. Heisterkamp is a pioneer in cancer genetics and uncovered the structure of the so-called “Philadelphia chromosome” (Ph), the first known genetic lesion that was discovered as a cause of cancer in humans. After graduate training at the University of Groningen and the Erasmus University in Rotterdam, the Netherlands, Dr. Heisterkamp joined the lab of John Stephenson, first at the Laboratory of Viral Carcinogenesis, a division of the National Cancer Institute (NCI).
Together with lab partner John Groffen, Ph.D., Dr. Heisterkamp identified the chromosomal translocation breakpoint of the Ph chromosome characteristic of chronic myeloid leukemia (CML) and Ph+ acute lymphoblastic leukemia (ALL). She cloned and named the Breakpoint Cluster Region (BCR) gene and subsequently demonstrated that the BCR and ABL1 genes are rearranged in CML to form the BCR-ABL1 oncogene in Ph+ leukemias. The first BCR-ABL1 transgenic mouse model, generated by Dr. Heisterkamp demonstrated that BCR-ABL1 is indeed the causative genetic lesion in Ph+ leukemias. In 2016, Drs. Heisterkamp and Groffen received the Janet Rowley Prize from the International CML Foundation for their outstanding lifetime contributions to the understanding of the biology of CML.
Dr. Heisterkamp is a permanent member of the National Institutes for Health (NIH) Tumor Microenvironment Study Section. Her studies are supported by two R01 grants from the NCI.
Her lab is currently investigating molecular mechanisms through which precursor B-lineage ALL cells are protected against eradication by therapy when they interact with non-leukemia cells in their environment. One recent new area of interest involves determining how carbohydrates attached to proteins and lipids on the surface of pre-B ALL cells mediate the reciprocal communication between the leukemia cells and their protective environment. Dr. Heisterkamp intends to capitalize on the knowledge obtained from these studies to design treatments that interfere with the cross-talk, making the leukemia cells more vulnerable to eradication.