Expectations of Racism and Carotid Intima-Media Thickness in African American Women.

OBJECTIVE: Several researchers have argued that racism-related stressors play an important role in adverse cardiovascular outcomes among African American women. However, studies have primarily focused on experiences of racism; thus, the role of expectations of racism is insufficiently understood. The current proof-of-concept study was designed to examine associations among expectations of racism, self-reported experiences of racism, and carotid intima-media thickness (IMT), a marker of cardiovascular risk, in African American women. METHODS: Participants were 52 healthy African American women, aged 30 to 50 years (M (SD) = 40.8 (4.3)). Expectations of racism were assessed with a modified version of the Race-Based Rejection Sensitivity Questionnaire, experiences of racism were assessed with the Schedule of Racist Events, and carotid IMT was measured using B-mode ultrasound. RESULTS: In linear regression analyses adjusted for age, expectations of racism were associated with higher levels of carotid IMT (b = .04, SE = .014, p = .013), after adjusting for experiences of racism. Findings remained significant after additional adjustments for cardiovascular risk factors (b = .03, SE = .014, p = .032). Associations were not confounded by additional stressors, hostility, or negative affect (depressive symptoms). CONCLUSIONS: Independent of actual reports of racism, "expectations" of racism may be associated with increased cardiovascular risk in African American women. In addition, although experiences of discrimination were associated with depressive symptoms, expectations of racism were not, suggesting that other negative emotions likely play a role. Future studies are needed to replicate these results in larger samples and to explore the psychological and physiological pathways through which expectations of racism might affect cardiovascular disease risk across a range of populations.

The human papillomavirus type 16 E7 oncoprotein activates the Fanconi anemia (FA) pathway and causes accelerated chromosomal instability in FA cells.

Fanconi anemia (FA) patients have an increased risk for squamous cell carcinomas (SCCs) at sites of predilection for infection with high-risk human papillomavirus (HPV) types, including the oral cavity and the anogenital tract. We show here that activation of the FA pathway is a frequent event in cervical SCCs. We found that FA pathway activation is triggered mainly by the HPV type 16 (HPV-16) E7 oncoprotein and is associated with an enhanced formation of large FANCD2 foci and recruitment of FANCD2 as well as FANCD1/BRCA2 to chromatin. Episomal expression of HPV-16 oncoproteins was sufficient to activate the FA pathway. Importantly, the expression of HPV-16 E7 in FA-deficient cells led to accelerated chromosomal instability. Taken together, our findings establish the FA pathway as an early host cell response to high-risk HPV infection and may help to explain the greatly enhanced susceptibility of FA patients to squamous cell carcinogenesis at anatomic sites that are frequently infected by high-risk HPVs.