Sarah Naomi Olsen, PhD

Dr. Olsen is investigating new therapeutic options to treat acute myeloid leukemia (AML), an aggressive form of childhood cancer. One subtype of AML is characterized by a chromosomal translocation involving the MLL (KMT2A) and the AF9 gene, resulting in an abnormal MLL-AF9 fusion protein. Dr. Olsen is targeting the MLL-AF9 fusion protein using a newly developed protein degradation approach.

Adam D. Durbin, MD, PhD

Dr. Durbin is developing new ways to target neuroblastoma, using chemical inhibitors and genetic techniques to disrupt small RNA species and enzymes that neuroblastoma cells require for survival. These new factors will also be inhibited in animal models of human neuroblastoma, alone and in combination with drugs similar to those entering clinical trials. These studies aim to identify new levels of gene regulation and methods to inhibit the genes involved in formation of neuroblastoma, with minimal side effects.

Whitney Johnson, PhD

Dr. Johnson is studying how genome rearrangements occur in cancer, using artificial pancreatic cancer organoids—clusters of cells that act as a model system. Cancer cells have unstable genomes that mutate and rearrange at a high rate compared to normal cells. Ultimately, Dr. Johnson hopes to understand how genome instability may be exploited to improve cancer treatments, including immunotherapy.

Lillian M. Guenther, MD

Ewing sarcoma is an aggressive bone tumor that occurs in children and young adults. Cure rates, particularly when disease has spread, are low with currently available treatments. Dr. Guenther aims to identify critical genes on which Ewing sarcoma cells are dependent for survival, with the goal of discovering weaknesses in these cancer cells that may be exploited to stop cancer growth. CITED2 is of particular interest as a Ewing sarcoma-specific dependency gene based on a genome-wide screen in hundreds of cancer cell lines.

David Liu, MD

The treatment of metastatic melanoma has been transformed over the past decade with the development of (1) targeted therapies that target a very common gene mutation (BRAF mutations in 50-60% of tumors) in melanoma and (2) two different types of immune therapies that induce the immune system to attack the cancer (CTLA-4 and PD-1 inhibition). However, not all patients respond to either targeted or immune therapy, and there is evidence suggesting that patients who quickly develop resistance on the initial therapy (whether targeted or immune) have worse outcomes (e.g.

Harshabad Singh, MBBS

Cancers involving the lower esophagus (esophageal adenocarcinomas) have dramatically increased in number over the last several decades. The reason for rise in this cancer is not completely understood. However, long before these esophageal cancers arise the normal esophageal multilayered squamous lining (or epithelium) is replaced by a single layered columnar epithelium which has features similar to the lining of the intestine and is known as Barrett’s esophagus. Dr.

Eric S. Fischer, PhD

Cancer therapies that target a specific gene product (targeted therapies), for example the oncogenic BCR-ABL by Gleevec, are now a very successful paradigm in cancer treatment. However, many known cancer-driving proteins are recalcitrant to the development of traditional small molecule inhibitors. In recent years, novel pharmacologic strategies have been proposed and developed to tackle this pervasive problem in drug development.

Tikvah K. Hayes, PhD

Dr. Hayes is focused on understanding and identifying mechanisms of resistance to cancer therapies.  Why some cancers respond to some therapies at first, but later become unresponsive, is not well understood. Small cell lung cancer is an ideal cancer to investigate how and why chemotherapy, the oldest and most prescribed cancer regimen, initially causes tumor reduction but ultimately fails after some period of time. She will use a multifaceted approach to interrogate chemotherapeutic resistance with the goal of identifying new methods to enhance patient treatment.

Phillip A. Dumesic, MD, PhD

Dr. Dumesic seeks to understand how physical exercise promotes health. In addition to strengthening skeletal muscle, exercise also benefits distant organ systems, providing protection from metabolic disorders and chronic diseases including cancer. These widespread effects highlight muscle’s ability to communicate via secreted signals.