Emma Watson, PhD

Dr. Watson [Suzanne and Bob Wright Fellow] is taking advantage of high-throughput genetic screens to map gene networks involved in the response to metabolic stress. Cancer cells tap into growth-promoting metabolic programs, enabling them to robustly proliferate using limited resources from the tissue microenvironment and bloodstream. The metabolic plasticity observed in cancer cells can be at least partly attributed to metabolic stress response pathways that enable the cancer to mobilize resources for growth.

Timothy D. Martin, PhD

Dr. MartinĀ [Marion Abbe Fellow] focuses on genomic instability, a hallmark of virtually all cancers that underlies the mutations and aneuploidy (incorrect chromosome number) changes that perturb oncogenes and tumor suppressor genes (TSGs). Patient tumor sequencing has unveiled common genomic alterations across different cancers. Recent work described how the cancer genome is shaped by the loss of many genes and gene clusters.

Ann Mullally, MD

Myeloproliferative neoplasms (MPN) are a type of blood cancer sometimes considered to be "pre-leukemias" which can progress to leukemia and are also lethal cancers in their own right. A population of rare hematopoietic stem cells (HSC), called MPN disease-propagating cells, typically harbor mutations that cause the cells to overproliferate. These mutated HSC produce abnormal cancerous blood cells that over time can eliminate the normal blood cells in the bone marrow.