William Razzell, PhD

Dr. Razzell [HHMI Fellow] is using cell biological, molecular genetic, and biophysical approaches to understand how cell-derived mechanical forces contribute to tumorigenesis through the modulation of cellular signaling pathways. One pathway that is responsive to mechanical forces is the Hippo pathway, which prevents excessive tissue growth during development. Characterizing how cell-derived forces control normal Hippo signaling will provide insight into the mechanisms by which Hippo pathway misregulation contributes to tumor progression.

Bryan C. King, PhD

Dr. King (Berger Foundation Fellow) is studying mechanisms by which nutrient-deprived cancer cells utilize extracellular proteins as a source of amino acids to promote their growth and survival. The bulk uptake of extracellular material, through a process called macropinocytosis, is a major means of nutrient uptake in single-celled, amoeboid organisms. Recent evidence suggests that mutations prevalent in cancer cells can activate this ancient scavenging mechanism.

Aaron D. Viny, MD

Dr. Viny [William Raveis Charitable Fund Fellow] is studying the oncogenic role of abnormalities in the cohesin complex-a group of proteins that function to align and stabilize sister chromatids (copies of the chromosomes) during cell division.  Mutations within several proteins in this complex have been identified in solid tumors and hematologic malignancies, particularly acute myeloid leukemia, the most common adult leukemia. Although it was presumed these mutations would result in unbalanced chromosomal breaks, this outcome has not yet been observed.

Ly P. Vu, PhD

Dr. Vu is studying childhood acute myeloid leukemia (AML), a complex and heterogeneous disease. Despite exciting advances in our understanding of AML and the availability of more aggressive treatment regimens, ~30% of children still eventually relapse from this disease and there are yet no approved targeted therapies for children with AML. Her project aims to uncover the role of Syncrip, a novel RNA binding protein, in maintaining the leukemia stem cell in AML.

Christine Mayr, MD, PhD

[Island Outreach Foundation Innovator of the Damon Runyon-Rachleff Innovation Award]

Cancer is thought to arise through a series of genetic mutations in the DNA sequence. Depending on the location of these errors and the genes that are affected, these mutations lead to the many different features that characterize cancer cells such as uncontrolled proliferation, escape from cell death and metastasis.

Sarat Chandarlapaty, MD, PhD

The PI3K/AKT/mTOR signaling pathway normally conveys cues from the cell's environment into programs that promote cellular growth, division, and motility. Components of the PI3K signaling pathway are mutated in greater than 70% of all breast cancers and promote the persistent and exaggerated cell growth that is necessary for tumor formation and survival. This pathway is therefore a promising target for treating breast cancers; however, drugs designed to target the PI3K signaling pathway are initially effective but resistance rapidly develops. Dr.

Zsofia K. Stadler, MD

Heritable factors are an important determinant of cancer risk. At present, only a small fraction of this genetic risk is explained by known cancer predisposition genes. Our preliminary data suggests that in pediatric cancers or cancers that occur in early adulthood, de novo or "new" genetic mutations may be identified that contribute to cancer causation. As such, the aim of our study is to study children with specific types of cancer (leukemia and neuroblastoma) without a family history of the disease to determine if we can identify the genetic cause of their cancer.

Luc G. Morris, MD

Head and neck cancer is a lethal malignancy that can arise in the mouth, throat, voice box, and related areas. These tumors are squamous cell cancers that are, in many cases, caused by tobacco use or human papillomavirus (HPV) infection. Head and neck cancers have many molecular similarities with squamous cell cancers of the lung and esophagus. Dr. Morris is studying a poorly understood gene called FAT1, which is frequently altered in head and neck cancer (as well as lung and esophageal cancer). He has found that this gene, in its normal state, prevents tumor development.