Michael T. Lewis, Ph.D.

Assistant Professor, Baylor College of Medicine

Michael T. Lewis, Ph.D.Phone: 713-798-3296
Fax: 713-798-1659
Email: mtlewis@breastcenter.tmc.edu

Funding
Publications
Research

Education:
1982-1986 - B.S. Biology, College of William and Mary
1989-1995 - Ph.D. Biology, University of California
1995-1998 - Post-doc. Biology, University of California
1999 - Post-doc. Physiology and Biophysics, University of Colorado

Positions:
7/01-present - Assistant Professor – Baylor College of Medicine Breast Center and the
     Department of Molecular and Cellular Biology, Houston , TX 77030 .
6/99-6/01 - Instructor – University of Colorado School of Medicine , Denver , CO 80262 .
      Department of Physiology and Biophysics.
1/99-6/99 - Postdoctoral Research Associate – University of Colorado School of Medicine ,
      Denver , CO 80262 . Department of Physiology and Biophysics. Laboratory of
      Dr. Peggy Neville.
7/95-12/98 - Post Graduate Researcher – University of California , Santa Cruz , CA 95064 .
      Department of Biology. Laboratory of Dr. Charles Daniel .
9/89-6/95 Teaching Assistant – University of California , Santa Cruz . Department of Biology. 9/89-6/95 Graduate Researcher – University of California , Santa Cruz . Department of
      Biology. Laboratory of Dr. Jerry Feldman.
7/88-8/89 Research Scientist – National Biomedical Research Foundation – Protein
      Information Resource (NBRF-PIR). 3900 Reservoir Rd., N.W. , Washington , D.C. , 20007 . 10/86-7/88 Biologist – National Biomedical Research Foundation

Professional Activities, Awards and Honors:
1989 University of California Regents Fellowship
1992-Present Charter member - Sigma Xi ( Santa Cruz chapter)
1996 University of California Breast Cancer Research Program Postdoctoral Research Award 2000 Department of Defense IDEA Award
2001 Organizer – Gordon Research Conference in Mammary Gland Biology Workshops 2001-2002 Member - Pathogenesis Study Section – Univ. California Breast Cancer
      Research Program
2001-Present Member - San Antonio Breast Cancer Symposium Organization Committee 2003 Organizer – NIH Workshop on Homeobox genes in mammary gland development
2003-Present Member - Tumor Progression Study Section – Univ. California Breast Cancer
      Research Program
2003-Present Member – Molecular Biology Genetics 2 Study Section - Dept. Defense Breast
     Cancer Research Program
2003 Susan Love M.D. Breast Cancer Research Foundation Grant Award
2003 Department of Defense CONCEPT Award

Research:
Our laboratory studies the developmental biology of the mammary gland as it relates to both normal breast function and breast cancer progression. Current laboratory research is centered on the role of hedgehog signal transduction in mammary gland development and breast cancer using the mouse as a model organism.

During embryonic development, the hedgehog signal transduction network mediates cell-cell communication and is required for normal organ formation. However, genetic mutation of hedgehog network genes can cause severe birth defects, basal cell carcinoma of the skin, and other tumors including lethal medulloblastomas of the brain.

Our work has demonstrated that loss-of-function mutations in two hedgehog network genes, Patched-1 (Ptc-1) and Gli-2, cause cancer-like lesions that closely resemble human ductal carcinoma in situ (DCIS). More recently, hedgehog signaling has been found to be required for functional differentiation of the gland at the onset of lactation.

The specific mechanism by which mutations in the hedgehog network lead to differentiation failure and mammary lesions is not known. Our data lead us to ask several fundamental questions, among which are: 1) Which genes in the hedgehog signaling network are required for different phases of mammary gland development. 2) In which tissue compartment(s) do these genes function? 3) What genes regulate, or are regulated by hedgehog signaling? 4) How does the hedgehog network interact with other hormone- and growth factor-dependent regulatory networks (e.g. estrogen, progesterone and TGFß-1)? And 5) Do hedgehog signaling disruptions lead to neoplasia in the human breast?