Welcome to the lab of
Research in the Turner laboratory is focused on two areas:
Cancer Health Disparities
Despite significant declines in cancer morbidity, racial health disparities in death rates still exist for many cancers. For example, in our state of South Carolina (SC), mortality rates between African American (AA) and European American (EA) prostate cancer patients are the highest rate in the country. AA prostate cancer patients in SC are three times more likely to die of prostate cancer than their European counterparts (EA). It is becoming increasingly apparent that racial disparity in cancer exists due to molecular and genetic differences in tumor biology as well as socioeconomic and standard of care issues. Though many molecular factors may cause racial specific differences in tumor biology, a potential role is provided by the mechanistic link between dietary sugars and cancer. Advanced glycation end products (AGE’s) are reactive metabolites produced by the uncontrolled reaction between sugars and proteins in a process known as glycation. AGE’s accumulate within our bodies as we grow older with pathogenic effects. Because proteins, lipids and DNA are present throughout the body, the destructive capacity of AGE’s is enormous and their accumulation is a major factor contributing to the aging process. Accumulated AGE levels are implicated in most of the diseases associated with growing older such diseases include hyperglycemia, diabetes, neurodegenerative disorders, stroke and heart disease. Apart from normal metabolism, a major source of AGE accumulation in our bodies is through the ingestion of unhealthy and processed foods. This is racially significant as:
Due to these socioeconomic and environmental factors our research group investigates if increases in advanced glycation end products in African American cancer patients make them susceptible to the development of aggressive disease and contribute to health disparity.
Prostate Cancer Biomarkers
Prostate cancer is the most commonly diagnosed and the second leading cause of cancer death among men in the western world. Advanced disease accounts for the majority of prostate cancer related deaths and is a result of lymphatic, local or contiguous spread. Patients with early stage prostate cancer may have slow growing tumors which are unlikely to cause any problems in the patient’s lifetime or they may have tumors that progress to advanced disease and require immediate definitive therapy. Current markers for stratifying prostate cancer patients are unreliable so we therefore need to identify additional biomarkers that can aid in the stratification of early stage prostate cancer patients. This would allow the immediate treatment of patients with potentially aggressive tumors and save patients with indolent tumors from undergoing needless therapy with significant side effects. Androgen deprivation therapy (ADT) (medical castration, bilateral orchiectomy, or both) targets androgen receptor (AR) transcriptional activity by reducing available ligand (the hormone androgen) and is the standard of care for men with advanced prostate cancer. However, many patients undergoing ADT become resistant to its effects and progress to castrate (androgen/hormone) resistant prostate cancer (CRPC). Despite the recent additions of several new agents, treatment strategies for patients with CRPC are inadequate, with progression-free survival rates as low as 2 months. CRPC is dependent upon the reactivation of AR function after ADT. One mechanism thought to promote restoration of AR function in CRPC is increased co-factor recruitment to target gene promoters which can negate the requirement of ligand.
Mounting evidence associates members of the ETS (v-ets erythroblastosis virus E26 oncogene) family of transcription factors with AR transcriptional co-regulation and prostate cancer progression.
Our research examines if Elevated ETS1 expression is a potential biomarker for advanced prostate cancer and its increased activity is a critical co-regulatory factor restoring AR function in CRPC.
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