Giada Bianchi, MD

Multiple myeloma (MM) is an incurable cancer of blood cells. It evolves from monoclonal gammopathy of undetermined significance (MGUS), a pre-malignant condition affecting 3-5% of individuals older than 50 years. MGUS patients progress to MM at a rate of 1% per year and the mechanisms underlying such transformation are unknown. No genetic driver mutations have been identified in MM to date, thus limiting our therapeutic options. Signaling through the transmembrane receptor Roundabout1 (ROBO1) is important in solid tumors, particularly gastrointestinal cancer.

Neil T. Umbreit, PhD

Dr. Umbreit [HHMI Fellow] studies chromosome segregation, the process by which the genetic information on chromosomes is duplicated and the copies are segregated equally into two new cells. Cancer cell proliferation is marked by frequent errors in chromosome segregation, resulting in abnormal genetic content in the progeny. He is investigating one type of chromosome segregation error, called a “chromosome bridge,” a major mechanism through which genetic information can be amplified and/or rearranged to distort gene function in cancer cells.

Mark W. Zimmerman, PhD

Dr. Zimmerman studies neuroblastoma, a tumor of the peripheral sympathetic nervous system. In high-risk neuroblastoma tumors, which account for 15% of all childhood cancer deaths, the chromatin remodeling gene CHD5 is often deleted and its loss is associated with poor prognosis. The gene expression program regulated by CHD5 has strong tumor suppressive effects and has thus emerged as a very attractive target for potential anti-cancer therapeutics. CHD5 expression is also altered in other cancer types, indicating a potential role in many different adult and pediatric malignancies.

Scott Haihua Chu, PhD

Dr. Chu focuses on a promising new class of therapy that inhibits epigenetic regulators, proteins that control the expression and activity of genes through DNA sequence-independent chemical modifications. Much remains unknown about how these new drugs induce specific changes in tumors upon treatment or what their efficacy is in sustaining long-term, durable responses in patients. He plans to characterize the changes induced with the use of such inhibitors in animal and human models of leukemia.

Amanda Balboni Iniguez, PhD

Dr. Balboni Iniguez studies Ewing sarcoma, a rare pediatric solid tumor containing a characteristic chromosomal translocation that fuses the EWSR1 gene to the FLI1 gene. The resulting EWS/FLI fusion protein initiates an oncogenic gene expression program, thus promoting tumorigenesis. EWS/FLI represents an attractive tumor-specific therapeutic target; however, it has been difficult to pharmacologically inhibit. Her work will focus on elucidating a novel approach to selectively target EWS/FLI by utilizing a small-molecule inhibitor against the transcriptional regulator proteins CDK12/13.

Eliezer M. Van Allen, MD

Many cancers are treated with chemotherapies that affect DNA repair, such as platinum chemotherapy, and some patients derive significant benefit from these agents. However, the underlying genomic features that drive selective response to these treatments is incompletely characterized. Dr. Van Allen aims to blend precision cancer medicine principles with DNA repair treatments and enhance cancer care. He will do so by studying the genomics of response to existing and emerging DNA repair therapies in preclinical models as well as patients across different tumor types.