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Abstract Background Diagnosis of a chronic illness, such as cancer may influence health behavior changes, such as smoking cessation. The present analyses examine associations between a cancer diagnosis (i.e., yes or no) and response to an opt‐out smoking cessation bedside intervention provided to hospitalized patients. It was hypothesized that patients with a past or present cancer diagnosis would report higher motivation and engagement with quitting smoking, and higher rates of smoking abstinence after hospital discharge, compared to those without a cancer diagnosis. Methods Chart review was conducted on 5287 inpatients who accepted bedside treatment from a counselor and opted‐in to automated follow‐up calls from July 2014 to December 2019. Results At the time of inpatient assessment, those with a past or present cancer diagnosis (n = 419, 7.9%) endorsed significantly higher levels of importance of quitting than those without a cancer diagnosis (3.92/5 vs. 3.77/5), and were more likely to receive smoking cessation medication upon discharge (17.9% vs. 13.3%). Follow‐up data from 30‐days post‐discharge showed those with a cancer diagnosis endorsed higher rates of self‐reported abstinence (20.5%) than those without a cancer diagnosis (10.3%; p

Hospital-based tobacco treatment programs provide tobacco cessation for a diverse array of admitted patients. Person-centered approaches to classifying subgroups of individuals within large datasets are useful for evaluating the characteristics of the sample. This study categorized patients who received tobacco treatment while hospitalized and determined whether demographics and smoking-related health conditions were associated with group membership. Chart review data was obtained from 4854 patients admitted to a large hospital in South Carolina, USA, from July 2014 through December 2019 who completed a tobacco treatment visit. Smoking characteristics obtained from the visit interview were dichotomized, and then latent class analysis (LCA) was conducted to categorize patients based on smoking history and interest in stopping smoking. Finally, logistic regressions were used to evaluate demographics and smoking-related health conditions as predictors of class membership. LCA generated 5 classes of patients, differentiated by heaviness of smoking and motivation to quit. Patients who were black/African American were more likely to be lighter smokers compared to white patients. Hospitalized patients with a history of hypertension, diabetes, and congestive heart failure were more likely to be motivated to quit and also were more likely to be lighter smokers at the time of hospitalization. Hospitalized patients who smoke and receive tobacco treatment are heterogeneous in terms of their smoking histories and motivation to quit. Understanding latent categories of patients provides insight for tailoring interventions and potentially improving tobacco treatment outcomes.

We previously reported successful classification of breast cancer versus benign tissue using the Cole relaxation frequency measured on tissue excised during breast surgery as part of a study at two urban hospitals in the U.S. Midwest. Using that health system’s cancer registry, we have discovered retrospectively that outcomes for patients who participated in the initial study can be classified correctly in 3 well-differentiated categories: nonrecurrent (NR); recurrent with no metastasis (RNM); and recurrent with metastasis (RM). As Cole relaxation frequency increases, the classification moves from NR to RNM and finally to RM. Multivariate analysis showed a significant association of “time-cancer-free” for all patients in these recurrent categories, with P-values ranging between 0.0001 to 0.0047. Thus, this follow-up report shows the potential feasibility of using Cole relaxation frequency as a prognostic parameter in a larger prospective study.

Androgen Receptor (AR) signaling is a critical driver of hormone-dependent prostate cancer and has also been proposed to have biological activity in female hormone-dependent cancers, including type I endometrial carcinoma (EMC). In this study, we evaluated the preclinical efficacy of a third-generation AR antagonist, enzalutamide, in a genetic mouse model of EMC, Sprr2f-Cre;Ptenfl/fl. In this model, ablation of Pten in the uterine epithelium leads to localized and distant malignant disease as observed in human EMC. We hypothesized that administering enzalutamide through the diet would temporarily decrease the incidence of invasive and metastatic carcinoma, while prolonged administration would result in development of resistance and loss of efficacy. Short-term treatment with enzalutamide reduced overall tumor burden through increased apoptosis but failed to prevent progression of invasive and metastatic disease. These results suggest that AR signaling may have biphasic, oncogenic and tumor suppressive roles in EMC that are dependent on disease stage. Enzalutamide treatment increased Progesterone Receptor (PR) expression within both stromal and tumor cell compartments. Prolonged administration of enzalutamide decreased apoptosis, increased tumor burden and resulted in the clonal expansion of tumor cells expressing high levels of p53 protein, suggestive of acquired Trp53 mutations. In conclusion, we show that enzalutamide induces apoptosis in EMC but has limited efficacy overall as a single agent. Induction of PR, a negative regulator of endometrial proliferation, suggests that adding progestin therapy to enzalutamide administration may further decrease tumor burden and result in a prolonged response.

The purpose of this period prevalence study is to compare the prevalence of cardiovascular disease (CVD) in current/former established smokeless tobacco (SLT) users (ever SLT users who have used the product fairly regularly) to those who were: 1) never established cigarette smokers and SLT users, and 2) current/former established exclusive cigarette smokers (have smoked at least a 100 or more cigarettes in lifetime) only, adjusting for known risk factors for CVD. Analyses included 4,703 men ≥ 40 years of age who participated in the Population Assessment of Tobacco and Health (PATH) Study, Waves: 1–4, conducted between 2013 and 2017. Current users were those using SLT products daily or on some days, whereas former users had not used SLT and/or cigarettes in the past 12 months. CVD prevalence was defined as a self-reported diagnosis of congestive heart failure, stroke, or myocardial infarction. Among current/former established SLT users, years of use defined exposure history, while pack-years defined exposure history for smokers. Adjusted odds ratios (AOR) and 95% confidence intervals (CI) were reported with trend tests to examine dose–response associations. Current/former established exclusive SLT users were not significantly more likely to have had any CVD compared to never established cigarette and SLT users (OR = 1.7 [0.8–3.7]), or current/former established exclusive cigarette smokers (OR = 0.9 [0.5–1.8]). Current/former established exclusive cigarette smokers were more likely to have had any CVD compared to those who were never established cigarette and SLT users (OR = 1.6 [1.1–2.3]).

Summary: The SARS-CoV-2 viral pandemic has induced a global health crisis, which requires more in-depth investigation into immunological responses to develop effective treatments and vaccines. To understand protective immunity against COVID-19, we screened over 60,000 asymptomatic individuals in the Southeastern United States for IgG antibody positivity against the viral Spike protein, and approximately 3% were positive. Of these 3%, individuals with the highest anti-S or anti-RBD IgG level showed a strong correlation with inhibition of ACE2 binding and cross-reactivity against non-SARS-CoV-2 coronavirus S-proteins. We also analyzed samples from 94 SARS-CoV-2 patients and compared them with those of asymptomatic individuals. SARS-CoV-2 symptomatic patients had decreased antibody responses, ACE2 binding inhibition, and antibody cross-reactivity. Our study shows that healthy individuals can mount robust immune responses against SARS-CoV-2 without symptoms. Furthermore, IgG antibody responses against S and RBD may correlate with high inhibition of ACE2 binding in individuals tested for SARS-CoV-2 infection or post vaccination.

BackgroundAfrican Americans (AAs) have higher colorectal cancer (CRC) incidence and mortality rate than Caucasian Americans (CAs). Recent studies suggest that immune responses within CRCs contribute to the disparities. If racially distinct immune signatures are present in the early phases of carcinogenesis, they could be used to develop interventions to prevent or slow disease.MethodsWe selected a convenience sample of 95 patients (48 CAs, 47 AAs) with preinvasive colorectal adenomas from the surgical pathology laboratory at the Medical University of South Carolina. Using immunofluorescent-conjugated antibodies on tissue slides from the lesions, we quantified specific immune cell populations: mast cells (CD117+), Th17 cells (CD4+RORC+), and NK cell ligand (MICA/B) and inflammatory cytokines, including IL-6, IL-17A, and IFN-γ. We compared the mean density counts (MDCs) and density rate ratios (RR) and 95% CI of immune markers between AAs to CAs using negative binomial regression analysis. We adjusted our models for age, sex, clinicopathologic characteristics (histology, location, dysplasia), and batch.ResultsWe observed no racial differences in age or sex at the baseline endoscopic exam. AAs compared to CAs had a higher prevalence of proximal adenomas (66% vs. 40%) and a lower prevalence of rectal adenomas (11% vs. 23%) (p =0.04) but no other differences in pathologic characteristics. In age, sex, and batch adjusted models, AAs vs. CAs had lower RRs for cells labeled with IFNγ (RR 0.50 (95% CI 0.32-0.81); p=0.004) and NK cell ligand (RR 0.67 (0.43-1.04); p=0.07). In models adjusted for age, sex, and clinicopathologic variables, AAs had reduced RRs relative to CAs for CD4 (p=0.02), NK cell ligands (p=0.01), Th17 (p=0.005), mast cells (p=0.04) and IFN-γ (p< 0.0001).ConclusionsOverall, the lower RRs in AAs vs. CAs suggests reduced effector response capacity and an immunosuppressive (‘cold’) tumor environment. Our results also highlight the importance of colonic location of adenoma in influencing these differences; the reduced immune responses in AAs relative to CAs may indicate impaired immune surveillance in early carcinogenesis. Future studies are needed to understand the role of risk factors (such as obesity) in influencing differences in immune responses by race.