The UT Health San Antonio, with missions of teaching, research and healing, is one of the country’s leading health sciences universities.
Principal Investigator(s)
Huang, Hui-Ming
Funded by
NIH-NATIONAL CANCER INSTITUTE
Collaborating Institutions
OSMULSKI OSU BAYLOR DUKE UTSA VERMONT
OverallSystems Analysis of Epigenomic Architecture in Cancer ProgressionDespite anti-hormone therapies in patients, the cognate receptors ER? and AR can remain functional tosupport oncogenic signaling for advanced progression of breast and prostate cancers. Intensive studies haveuncovered cellular and biochemical changes underlying the development of hormone resistance. However,epigenetic mechanisms for establishing and maintaining a hormone-resistant phenotype remain to beexplored.
The UT Health San Antonio, with missions of teaching, research and healing, is one of the country’s leading health sciences universities.
Principal Investigator(s)
Risinger, April L
Funded by
NIH-NATIONAL CANCER INSTITUTE
Collaborating Institutions
Oklahoma
Microtubule stabilizing agents (MSAs) are some of the most widely used and effective therapies availablefor the treatment of solid tumors. However, their utility is compromised by innate and acquired drugresistance. The taccalonolides (taccas) are a mechanistically unique class of MSAs that circumventmultiple clinically relevant forms of drug resistance. Multiple potent taccas identified by our laboratorieshave effective antitumor activity in drug sensitive and resistant in vivo models but suffer from a narrowtherapeutic window.
The UT Health San Antonio, with missions of teaching, research and healing, is one of the country’s leading health sciences universities.
Principal Investigator(s)
Boyer, Thomas G
Funded by
NIH-NATIONAL INSTITUTE ON AGING
Alzheimer's disease (AD) is a profoundly debilitating neurodegenerative disorder without effective treatment or determinative antemortem diagnostics. Improvements in diagnostic and treatment options will require a better understanding of the biological processes that drive AD onset and progression. The prevailing model to explain AD pathogenesis holds that neuronal degeneration and clinical demise are precipitated by the gradual accumulation, in brain centers controlling memory and cognition, of amyloid-? (A?) peptide, a catabolite of the transmembrane Amyloid Precursor Protein (APP).