Li Ma, PhD

  • Recruited to: The University of Texas MD Anderson Cancer Center
  • Recruited from: Whitehead Institute for Biomedical Research, Massachusetts Institute of Technology
  • Award: First-Time, Tenure-Track Faculty Member

Dr. Li Ma received her PhD from the Sloan-Kettering Institute and the Weill Graduate School of Medical Sciences of Cornell University in May 2006. She did her postdoctoral training at the Whitehead Institute for Biomedical Research and MIT in 2006-2010. In September 2010, Dr. Ma will join The University of Texas MD Anderson Cancer Center as an Assistant Professor in the Department of Experimental Radiation Oncology.

The central theme of Dr. Ma’s graduate and postdoctoral research is mouse models and molecular mechanisms of cancer. In graduate school, she worked with Dr. Pier Paolo Pandolfi on the role of tuberous sclerosis complex 2 (TSC2) in tuberous sclerosis (TSC) and cancer pathogenesis. She determined the genetic relationship between mammalian Pten and Tsc2 in tumor suppression in Pten+/−Tsc2+/− compound mouse mutants; this study provided an explanation for the differential cancer susceptibility observed in TSC patients and in patients suffering from PTEN heterozygous deficiency. In another study, she discovered that activation of ERK enhances mTOR activity through phosphorylation of TSC2 at specific residues, which illuminated an important connection between the growth factor-stimulated MAPK pathway and the TSC1/TSC2 complex. These findings have advanced our understanding of how TSC2 is inactivated through post-translational modification in the tuberous sclerosis syndrome, and more in general, how aberrant RAS-ERK signaling can lead to tumorigenesis in human cancers.

To pursue postdoctoral training, Dr. Ma joined Bob Weinberg’s lab at Whitehead. As PI on a Life Sciences Research Foundation Postdoctoral Fellowship and the K99 phase of an NIH/NCI Pathway to Independence Award, Dr. Ma carried out research to identify metastasis-regulating microRNAs. She identified miR-10b as a microRNA that is highly expressed specifically in metastatic breast cancer cells and tissues. Subsequent functional experiments demonstrated that overexpression of miR-10b induced tumor invasion and distant metastasis in two orthotopic models of breast cancer. Conversely, therapeutic silencing of miR-10b with ‘antagomirs’ suppressed metastasis in a mouse mammary tumor model. These studies provided the first functional evidence that overexpression of a specific microRNA can contribute to the development of metastasis, which can be exploited therapeutically in treating metastasis in animal models. In addition, she identified a second metastasis-promoting microRNA that functions to suppress the critical metastasis suppressor E-cadherin.

At MD Anderson, Dr. Ma will investigate the roles and mechanisms of microRNAs in regulating tumor metastasis, epithelial-mesenchymal transition and stem cels, and will develop new candidate therapies for malignant diseases.