Biography

Junhao Mao received his Ph.D. degree from the University of Rochester in 2002. He did his postdoctoral research at Harvard University from 2003 to 2008, where he was supported by the fellowships from Damon Runyon Cancer Research Foundation and Charles A. King Trust.   Dr. Mao was also a recipient of the Charles H. Hood Foundation Child Health Research Award in 2009.   He joined the Department of Cancer Biology at the University of Massachusetts Medical School in fall 2008.

The Hedgehog (Hh) Signaling Pathway in Development and Cancer

The Hedgehog (Hh) signaling pathway, initially identified by its patterning activity in Drosophila embryos, plays many distinct roles in vertebrate development. Deregulation of Hh signaling has also been implicated in the etiology of a wide range of human cancers.  The overall goal of our research is to understand the mechanisms underlying molecular and cellular control of Hh signaling in mammalian organogenesis and tumorigenesis, with an emphasis on stem cell and progenitor cell function.  Our current efforts consist of two separate projects.

1.  Hh signaling, stem cells, and childhood rhabdomyosarcoma
Rhabdomyosarcoma (RMS) is a fast-growing, highly malignant skeletal muscle tumor and the most common soft-tissue sarcoma in children.  Genetic evidence from both human and mouse has demonstrated a clear link between RMS and Hh signaling.  To facilitate the study of Hh signaling in tumorigenesis, we have generated a novel, inducible somatic mouse model of Hh-related sporadic RMS.  Using a combination of cell biological and mouse transgenic approaches, we are now examining the role of Hh signaling in muscle stem cell transformation and tumor initiation.  We are also interested in exploring the possibility of Hh regulation of RMS cancer stem cells and in characterizing Gli-mediated transcriptional networks in Hh-related tumors. 

2.  Hh-mediated mesenchymal regulation in gastrointestinal development and cancer
Recent studies have revealed extensive involvement of Hh signaling in many tumors arising from the gastrointestinal (GI) tract, including carcinomas of the stomach, colon, and pancreas.  Despite the significance of Hh in GI tumorigenesis, the exact function of Hh signaling in GI development remains unclear.  We have identified a primary role for Hh proteins as mitogens for mesenchymal progenitor cells in the developing gut.  We will examine the genetic and cellular interactions between the Hh signaling pathway and other critical pathways, such as BMP, Notch, IGF and Wnt in GI mesenchymal cell growth and differentiation.   Such interactions might form the developmental and mechanistic basis for Hh participation in GI tumorigenesis.