Cole Laboratory

Ongoing research by the Cole Lab has shown that pediatric cancers rely upon a cell's normal repair mechanisms to overcome the cellular stress that results from continued growth caused by cellular mutations and oncogenic stimuli, particularly by the MYC and MYCN oncogenes. Among these repair genes are signaling mediated by the CHK1, ATR and Wee1 kinases, which when inhibited halt cancer cell growth. From this work, a clinical trial is currently underway to evaluate the safety and efficacy of combining a Wee1 inhibitor and chemotherapy as treatment for relapsed neuroblastoma and medulloblastoma.

Other research in the laboratory involves identifying the proteins required for malignant gliomas with alternative lengthening of telomeres (ALT) to continue to proliferate. To do these studies the Cole laboratory is performing high-throughput screening of patient-derived cell lines from tumors of children with malignant glioma with and without ALT in collaboration with the multi-institution Children's Brain Tumor Tissue Consortium.

The Cole Laboratory is also interested in understanding how the non-coding genome is involved in pediatric cancer development and progression. In collaboration with members of the Maris Lab, the Cole Lab discovered both short (miR-34a) and long (CASC15) noncoding RNAs that contribute to neuroblastoma tumorigenesis. In the future, Kristina Cole, MD, PhD, and her laboratory team hope to identify treatments that will improve the survival of children with malignant brain tumors.