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PURPOSE: More than half of individuals with serious mental illness (SMI) smoke, contributing to premature cancer mortality. A cancer diagnosis provides an opportunity to assist with smoking cessation; however, supportive oncology trials frequently exclude patients with SMI. To fill this gap, we examined differences in engagement and tobacco cessation in a pragmatic clinical trial. METHODS: We recruited 303 participants from two National Cancer Institute–designated Comprehensive Cancer Centers, of which 10% had prior diagnoses of SMI (major depressive disorder, bipolar disorder, and schizophrenia spectrum disorders). We compared self-reported smoking behaviors, patient attitudes and beliefs about cessation, and rates of trial completion, engagement, and smoking abstinence among recently diagnosed patients with cancer with and without SMI. Six months after trial completion, we completed qualitative interviews on barriers and facilitators to tobacco cessation in a random sample of participants with SMI. RESULTS: Trial participants with SMI had similar motivation to quit smoking as those without SMI. Additionally, participants with SMI had a similar ability to engage in a tobacco treatment trial (6.5 counseling sessions completed v 7.3 sessions) and benefit from tobacco treatment as those without SMI (32.3% v 27.8% 6-month quit rates). CONCLUSION: Patients with cancer and SMI were able to engage in and benefit from a tobacco cessation trial integrated into cancer care. A cancer diagnosis provides an opportunity to assist patients with SMI with smoking cessation referrals and treatment. Pragmatic supportive oncology trials that include a diverse population of adults with SMI are needed to inform care delivery and improve cancer outcomes for patients with SMI and cancer.

Objective:Individuals with schizophrenia experience increased lung cancer mortality and decreased access to cancer screening and tobacco cessation treatment. To promote screening among individuals ...

Stroke is a sexually dimorphic disease. Elderly women not only have higher stroke incidence than age-matched men, but also have poorer recovery and higher morbidity and mortality after stroke. In older, post-menopausal women, gonadal hormone levels are similar to that of men. This suggests that tissue damage and functional outcomes are influenced by biologic sex (XX vs. XY) rather than the hormonal milieu at older ages. We employed the Four Core Genotype (FCG) mouse model to study the contribution of sex chromosome complement and gonadal hormones to stroke sensitivity in aged mice in which the testis determining gene (Sry) is removed from the Y chromosome, allowing for the generation of XX males and XY females. XXF, XXM, XYF, XYM and XYwt aged mice were subjected to middle cerebral artery occlusion (MCAO). XXF and XXM mice had significantly larger infarct volumes than XYF and XYM cohorts respectively. There was no significant difference in hormone levels among aged FCG mice. XXF/XXM mice also had more robust microglial activation and higher serum levels of pro-inflammatory cytokines than XYF/XYM cohort respectively. We concluded that the sex chromosome complement contributes to ischemic sensitivity in aged animals and leads to sex differences in innate immune responses.

Introduction: Aging is the most important non-modifiable risk factor for ischemic stroke; modeling stroke in aged animals is of clinical relevance and translational value. Stroke is a sexually dimorphic disease. Elderly women not only have higher stroke incidence than age-matched men, but also have poorer recovery, higher morbidity and mortality once a stroke occurs. Much of this has been attributed to the loss of estrogen with menopause. However, stroke incidence does not begin to climb until well after natural menopause, suggesting there are hormone independent effects on ischemic sensitivity. As hormone levels are relatively equivalent between sexes at the age post-menopausal, tissue damage and functional outcomes must be influenced by biologic sex (XX vs. XY) in addition to the hormonal milieu. Hypothesis: We hypothesized that sex differences in ischemic stroke in aged brains are shaped by the sex chromosome complement. Methods: The Four Core Genotype (FCG) mouse model was utilized to dissociate the effects of sex chromosome compliment from hormone exposure on ischemic sensitivity. XXF, XXM, XYF, and XYM aged mice (18-20 months) were subjected to 90-minute middle cerebral artery occlusion (MCAO). Stroke outcomes were examined at 24h and 7d of stroke. Inflammatory responses were also evaluated by flow cytometry, immunohistochemistry, and multiplex cytokine analysis. Results: At 24h and 7d of stroke, more microglial activation and higher levels of pro-inflammatory cytokines (IL-1β and IL-6) were seen in XXF and XXM than in XYF and XYM mice respectively. Accordingly, XXF and XXM mice had significantly larger infarct volumes than XYF and XYM cohorts respectively (XXF vs.XYF: 43.26 ± 5.63% vs. 24.22 ± 3.48%; XXM vs. XYM: 50.44 ± 6.11% vs. 26.24 ± 3.91%; P Conclusions: The sex chromosome complement contributes to ischemic sensitivity in aged animals, which is likely mediated in part by innate immune responses.