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Molecular and Cellular Biology

Houston, Texas

Image 1: Ovulated mouse cumulus cell oocyte complex immunostained for matrix proteins hyaluronan and versican. By JoAnne Richards, Ph.D.; Image 2: By Yi LI, Ph.D.; Image 3: Mouse oocyte at meiosis I immunostained  for tubulin (red) phosphop38MAPK (green) and DNA (blue). By JoAnne Richards,  Ph.D.;  Image 4: Expanded cumulus cell ooctye ocmplex  immunostained for hyaluronan (red), TSG6 (green) and DAN (blue). By JoAnne  Richards, Ph.D.;  Image 5: Epithelial cells taken from a mouse  mammary gland were cultured in a dish and transduced with a retrovirus  expressing two genes. The green staining shows green fluorescent protein and the red  staining shows progesterone receptor expression. The nucleus of each cell is  stained blue. Photomicrograph taken at 200X magnification.  By Sandra L. Grimm,  Ph.D.; Image 6: Ovarian vasculature (red) is excluded from the granulosa cells (blue) within growing follicles (round structures); Image 7:  Ovulated mouse cumulus cell oocyte  complex immunostained for matrix proteins hyaluronan and versican. By JoAnne Richards, Ph.D.
Department of Molecular and Cellular Biology
not shown on screen

Sean E. McGuire M.D., Ph.D.

Assistant Professor
Department of Molecular & Cellular Biology

Assistant Professor of Radiation Oncology
University of Texas MD Anderson Cancer Center


M.D.: Baylor College of Medicine
Ph.D.: Baylor College of Medicine
Residency: University of Texas MD Anderson Cancer Center

Research Interest

Cross-talk between DNA Damage Response and Growth Signaling in the Cell
A critical task for the proliferating cell is to coordinate its response to mitotic signals with mechanisms that ensure genomic integrity. The inability to integrate these processes can result in the inappropriate progression through the cell cycle in the presence of DNA damage, leading to the accumulation of mutations and chromosomal aberrations which can ultimately give rise to cancer. Indeed, a number of cancers have now been shown to arise from the inheritance of mutations that alter the ability to detect or repair DNA damage. For example, inherited breast cancer has been associated with germline mutations in BRCA1, BRCA2, CHEK2, ATM, NBS1, RAD50, BRIP1, PALB2, p53, and PTEN. An intriguing feature of these mutations is their tendency to give rise to cancers with a strong predilection for specific tissues in the body. For example, germ-line mutations in BRCA1 and BRCA2 confer an extremely high risk of cancers in steroid hormone responsive tissues such as the breast and ovary. The mechanisms underlying the tissue specificity of these tumors is currently unknown, but they strongly implicate an interaction between the molecular machinery of DNA damage repair and the specific growth signals to which these tissues normally respond.

The family of steroid receptor coactivators (SRC’s) are important molecules that coordinate steroid receptor signaling in a number of tissues including the breast and prostate. Currently, the laboratory is investigating the role of steroid receptor coactivators in mediating cellular responses to DNA damage-induced kinase signaling. Understanding these events will lend insight into both tumorigenesis and treatment of steroid responsive cancers.

Contact Information

Baylor College of Medicine
One Baylor Plaza, DeBakey M822
Houston, TX 77030

Phone: 713-798-9174

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