Edward Paul Hasty
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Edward Paul Hasty, Ph.D., is Professor of Molecular Medicine at University of Texas Health Science Center San Antonio. Hasty works on DNA repair and cell cycle response to DNA damage and their impact on aging and cancer.
Dr. E. Paul Hasty's lab focuses on the impact chromatin metabolism has on cancer and aging in genetically altered cells mice using embryonic stem cell/gene targeting technology. Specifically, they study proteins important for the repair of DNA double-strand breaks by two different pathways. The first pathway is called recombinational repair by virtue that it utilizes a homologous template usually provided by the sister chromatid. To disrupt recombinational repair, they mutated Rad51 and found it to be essential for cellular proliferation and repair of DNA damaged by ionizing radiation. Rad51 - mutant embryos die shortly after implantation. Next, they determined that a cell cycle response contributed to embryonic lethality by crossing the rad51-mutant mice to p53-mutant mice. p53 is a tumor suppressor that is essential for stopping cellular proliferation after DNA damage. They also discovered that Rad51 functions by binding to a breast cancer susceptibility gene called Brca2 and mice with a subtle Brca2 mutation exhibit a shortened life span due to increased cancer incidence.
Dr. E. Paul Hasty's lab focuses on the impact chromatin metabolism has on cancer and aging in genetically altered cells mice using embryonic stem cell/gene targeting technology. Specifically, they study proteins important for the repair of DNA double-strand breaks by two different pathways. The first pathway is called recombinational repair by virtue that it utilizes a homologous template usually provided by the sister chromatid. To disrupt recombinational repair, they mutated Rad51 and found it to be essential for cellular proliferation and repair of DNA damaged by ionizing radiation. Rad51 - mutant embryos die shortly after implantation. Next, they determined that a cell cycle response contributed to embryonic lethality by crossing the rad51-mutant mice to p53-mutant mice. p53 is a tumor suppressor that is essential for stopping cellular proliferation after DNA damage. They also discovered that Rad51 functions by binding to a breast cancer susceptibility gene called Brca2 and mice with a subtle Brca2 mutation exhibit a shortened life span due to increased cancer incidence.