Willingness to Take PrEP for HIV Prevention: The Combined Effects of Race/Ethnicity and Provider Trust.

Blacks and Hispanics/Latinos are disproportionately burdened by HIV compared to non-Hispanic Whites, as evidenced by higher HIV incidence, prevalence, and deaths attributable to AIDS. Increasing the use of novel prevention techniques such as Truvada for pre-exposure prophylaxis (PrEP) could greatly help in reducing these disparities by lowering HIV incidence among these higher risk groups. Trust in providers, which may differ by race and ethnicity, may influence willingness to take PrEP. This study explores the moderating effect of race/ethnicity on trust in one's primary care provider (PCP) on PrEP willingness. This study found a significant association between PCP trust and PrEP willingness, with those with greater trust having 3.24 times the adjusted odds of being willing to try PrEP. Results regarding the effects of race and ethnicity on these outcomes, however, were inconclusive. Results indicate the importance of fostering trust between PrEP-prescribing PCPs and their patients.

Loss of PDCD4 contributes to enhanced chemoresistance in Glioblastoma multiforme through de-repression of Bcl-xL translation.

Glioblastoma multiforme (GBM) is the most common and aggressive form of tumor of the central nervous system. Despite significant efforts to improve treatments, patient survival rarely exceeds 18 months largely due to the highly chemoresistant nature of these tumors. Importantly, misregulation of the apoptotic machinery plays a key role in the development of drug resistance. We previously demonstrated that Bcl-xL, an important anti-apoptotic protein, is regulated at the level of translation by the tumor suppressor programmed cell death 4 (PDCD4). We report here a strong correlation between low expression of PDCD4 and high expression of Bcl-xL in adult de novo GBM, GBM tumor initiating cells, and established GBM cell lines. Importantly, high Bcl-xL expression correlated significantly with poor progression and patient survival. We demonstrate that re-expression of PDCD4 in GBM cells down-regulated Bcl-xL expression and decreased cell viability. Finally, we show that direct inhibition of Bcl-xL by small molecule antagonist ABT-737 sensitizes GBM cells to doxorubicin. Our results identify Bcl-xL as a novel marker of GBM chemoresistance and advocate for the combined use of Bcl-xL antagonists and existing chemotherapeutics as a treatment option for this aggressive tumor.