Trends and Associations of Past-30-Day Cigar Smoking in the U.S. by Age, Race/Ethnicity, and Sex, NSDUH 2002-2020.

Cigar smoking remains a public health issue in the United States (U.S.), with a heterogeneous prevalence based on sociodemographic characteristics. Nationally representative data suggest changes in cigar smoking over time, with some evidence for sociodemographic differences. Using data from the 2002-2019 National Survey on Drug Use and Health (NSDUH), the prevalence of past-30-day cigar smoking was examined overall and stratified by sociodemographic characteristics; joinpoint regression examined the trends. Logistic regression analyses identified the correlates of cigar smoking using 2020 NSDUH data. From 2002 to 2004, the prevalence of cigar smoking remained stable (5.33-5.73%), but declined from 2004 to 2019 (5.73-4.29%). Cigar smoking declined in some periods between 2002-2019 among the non-Hispanic White, Hispanic, ages 12-17, ages 18-20, ages 21-25, age ≥ 35, and male subgroups, but remained unchanged among the non-Hispanic Other, ages 26-34, and female subgroups. Cigar smoking increased among non-Hispanic Black persons overall from 2002 to 2019 (6.67-8.02%). Past-30-day cigarette smoking and drug or alcohol use disorder was associated with an increased likelihood of cigar use, while female sex was associated with a decreased likelihood of cigar use, across all age groups. Though a decline in the prevalence of past-30-day cigar smoking is seen in the general population, the same is not evident among all sociodemographic subgroups. Our findings have the potential to inform tobacco cessation efforts within clinical practice, as well as regulatory efforts to reduce cigar use.

National longitudinal tobacco product cessation rates among US adults from the PATH Study: 2013-2019 (waves 1-5).

OBJECTIVE: To report on longitudinal tobacco product cessation rates, by product type, among adults (ages 18+ years) in the USA between 2013 and 2019. METHODS: The Population Assessment of Tobacco and Health Study, a nationally representative, longitudinal cohort study was used to report on annual and biennial rates of the following three cessation behaviours across 2013-2019: (1) discontinuing tobacco product use (ie, transition from past 30-day use to no past 30-day use), (2) attempting to quit tobacco product use and (3) quitting tobacco product use among those who attempted to quit. Each cessation behaviour was evaluated separately for cigarettes, electronic nicotine delivery systems (ENDS), cigars, hookah and smokeless tobacco. Generalised estimating equations were used to evaluate linear and nonlinear trends in cessation rates across the study period. RESULTS: Between 2013 and 2019, rates of discontinuing cigarette smoking among adults in the USA statistically increased from 16% to 18%, though these were consistently lower than rates of discontinuing use of other tobacco products. Similarly, quit attempt rates and rates of quitting among attempters increased for cigarette smokers. However, rates of discontinuing ENDS use sharply declined across the study period, from 62% to 44%. CONCLUSIONS: Findings show that tobacco product cessation rates have been changing in recent years in the USA alongside the changing tobacco product marketplace and regulatory environment, though rates of discontinuing cigarette smoking remain relatively low. Findings can serve as a benchmark against which future cessation rates can be compared with evaluate the impacts of future tobacco regulatory policies.

Predictors of Colorectal Cancer Screening in Two Underserved U.S. Populations: A Parallel Analysis.

BACKGROUND: Despite declining colorectal cancer (CRC) incidence and mortality rates in the U.S., significant geographic and racial disparities in CRC death rates remain. Differences in guideline-concordant CRC screening rates may explain some of these disparities. We aim to assess individual and neighborhood-level predictors of guideline-concordant CRC screening within two cohorts of individuals located within CRC mortality geographic hotspot regions in the U.S. METHODS: A total of 36,901 participants from the Southern Community Cohort Study and 4,491 participants from the Ohio Appalachia CRC screening study were included in this study. Self-reported date of last CRC screening was used to determine if the participant was within guidelines for screening. Logistic regression models were utilized to determine the association of individual-level predictors, neighborhood deprivation, and residence in hotspot regions on the odds of being within guidelines for CRC screening. RESULTS: Lower household income, lack of health insurance, and being a smoker were each associated with lower odds of being within guidelines for CRC screening in both cohorts. Area-level associations were less evident, although up to 15% lower guideline adherence was associated with residence in neighborhoods of greater deprivation and in the Lower Mississippi Delta, one of the identified CRC mortality hotspots. CONCLUSION: These results reveal the adverse effects of lower area-level and individual socioeconomic status on adherence to CRC guideline screening.

The obesity epidemic and rising diabetes incidence in a low-income racially diverse southern US cohort.

BACKGROUND: Obesity is known to be a major risk factor for diabetes, but the magnitude of risk and variation between blacks and whites are less well documented in populations heavily affected by obesity. Herein we assess rates and risks of incident diabetes in a diverse southern population where obesity is common. METHODS: A total of 24,000 black and 14,064 white adults aged 40-79 in the Southern Community Cohort Study with no self-reported diabetes at study enrollment during 2002-2009 was followed for up to 10 (median 4.5) years. Incidence rates, odds ratios (OR) and accompanying 95% confidence intervals (CI) for medication-treated incident diabetes were determined according to body mass index (BMI) and other characteristics, including tobacco and alcohol consumption, healthy eating and physical activity indices, and socioeconomic status (SES). RESULTS: Risk of incident diabetes rose monotonically with increasing BMI, but the trends differed between blacks and whites (pinteraction < .0001). Adjusted ORs (CIs) for diabetes among those with BMI≥40 vs 20-25 kg/m2 were 11.9 (8.4-16.8) for whites and 4.0 (3.3-4.8) for blacks. Diabetes incidence was more than twice as high among blacks than whites of normal BMI, but the racial difference became attenuated as BMI rose, with estimated 5-year probabilities of developing diabetes approaching 20% for both blacks and whites with BMI≥40 kg/m2. Diabetes risk was also associated with low SES, significantly (pinteraction≤.02) more so for whites, current cigarette smoking, and lower healthy eating and physical activity indices, although high BMI remained the predominant risk factor among both blacks and whites. From baseline prevalence and 20-year projections of the incidence trends, we estimate that the large majority of surviving cohort participants with BMI≥40 kg/m2 will be diagnosed with diabetes. CONCLUSIONS: Even using conservative criteria to ascertain diabetes incidence (i.e., requiring diabetes medication use and ignoring undiagnosed cases), rates of obesity-associated diabetes were exceptionally high in this low-income adult population. The findings indicate that effective strategies to halt the rising prevalence of obesity are needed to avoid substantial increases in diabetes in coming years.

Weight change in breast cancer survivors compared to cancer-free women: a prospective study in women at familial risk of breast cancer.

BACKGROUND: This study prospectively examines weight gain in breast cancer survivors compared with cancer-free women from a familial risk cohort. METHODS: Absolute and percent weight change over 4 years was compared among 303 breast cancer survivors and 307 cancer-free women matched on age and menopausal status, from the same familial risk cohort. Linear and logistic regression was used to estimate the association between survivor status and weight gain. RESULTS: Overall, breast cancer survivors gained significantly more weight [ß = 3.06 pounds; 95% confidence intervals (CI), 0.94-5.17] than cancer-free women. Significant weight gain was observed in survivors diagnosed less than 5 years prior to baseline (ß = 3.81 pounds; 95% CI, 1.22-6.29) and women with estrogen receptor (ER)-negative tumors (ß = 7.26 pounds; 95% CI, 2.23-12.30). Furthermore, survivors treated with chemotherapy were 2.1 times more likely to gain at least 11 pounds during follow-up compared with cancer-free women (OR, 2.10; 95% CI, 1.21-3.63). Weight gain was even greater among survivors who took statins while undergoing chemotherapy treatment (Pinteraction = 0.01). CONCLUSION: This is the first study to demonstrate that weight gain is an important issue in breast cancer survivors with a familial risk. In the first five years posttreatment, breast cancer survivors gain weight at a faster rate than cancer-free women, particularly after chemotherapy and statin use but not after hormone therapy alone. IMPACT: Our findings provide support for the development of weight gain interventions for young breast cancer survivors with a familial risk.

Adipocytokines, inflammation, and breast cancer risk in postmenopausal women: a prospective study.

Obesity is a known risk factor for postmenopausal breast cancer; it has been postulated that adipocytokines may mediate this association. We explored the relationship between three markers altered by obesity: leptin, adiponectin, and soluble tumor necrosis factor receptor 2 (sTNF-R2), an inflammatory marker, with breast cancer risk in postmenopausal women. A nested case-control study of postmenopausal women was conducted within CLUE II, a prospective population-based cohort. Baseline plasma levels of leptin, adiponectin, and sTNF-R2 were assayed in 272 female breast cancer cases and 272 controls matched on age, date, and hour of blood draw. Conditional logistic regression was used to estimate matched odds ratios (OR) and 95% confidence intervals (CI). sTNF-R2 and leptin were independently positively associated with breast cancer risk in adjusted models. The OR for breast cancer comparing the highest to lowest tertile was 2.44 (95% CI: 1.30-4.58) for sTNF-R2 and 1.98 (95% CI: 1.20-3.29) for leptin. While higher levels of adiponectin were protective (OR for the lowest tertile = 1.63; 95% CI: 1.02-2.60), there was no dose response. A 20% reduction in the breast cancer risk associated with overweight/obesity was observed when sTNF-R2 alone was included in multivariable models. Including both sTNF-R2 and adiponectin in the models resulted in a 29% reduction in the OR. Adipocytokines and sTNF-R2 are important factors in the etiology of postmenopausal breast cancer due to adiposity. This study informs our understanding of the relationship between obesity, inflammation, and postmenopausal breast cancer and identifies potential biomarkers.

Mutation of a single allele of the cancer susceptibility gene BRCA1 leads to genomic instability in human breast epithelial cells.

Biallelic inactivation of cancer susceptibility gene BRCA1 leads to breast and ovarian carcinogenesis. Paradoxically, BRCA1 deficiency in mice results in early embryonic lethality, and similarly, lack of BRCA1 in human cells is thought to result in cellular lethality in view of BRCA1's essential function. To survive homozygous BRCA1 inactivation during tumorigenesis, precancerous cells must accumulate additional genetic alterations, such as p53 mutations, but this requirement for an extra genetic "hit" contradicts the two-hit theory for the accelerated carcinogenesis associated with familial cancer syndromes. Here, we show that heterozygous BRCA1 inactivation results in genomic instability in nontumorigenic human breast epithelial cells in vitro and in vivo. Using somatic cell gene targeting, we demonstrated that a heterozygous BRCA1 185delAG mutation confers impaired homology-mediated DNA repair and hypersensitivity to genotoxic stress. Heterozygous mutant BRCA1 cell clones also showed a higher degree of gene copy number loss and loss of heterozygosity in SNP array analyses. In BRCA1 heterozygous clones and nontumorigenic breast epithelial tissues from BRCA mutation carriers, FISH revealed elevated genomic instability when compared with their respective controls. Thus, BRCA1 haploinsufficiency may accelerate hereditary breast carcinogenesis by facilitating additional genetic alterations.

Telomere length in different histologic types of ovarian carcinoma with emphasis on clear cell carcinoma.

Ovarian carcinoma is composed of a heterogeneous group of tumors with distinct clinico-pathological and molecular features. Alteration of telomerase activity has been reported in ovarian tumors but the pattern of telomere length in their specific histological subtypes has not been reported. In this study, we performed quantitative telomere fluorescence in situ hybridization on a total of 219 ovarian carcinomas including 106 high-grade serous carcinomas, 26 low-grade serous carcinomas, 56 clear cell carcinomas and 31 low-grade endometrioid carcinomas. The mean relative telomere length of carcinoma to stromal cells was calculated as a telomere index. This index was significantly higher in clear cell carcinoma compared with the other histologic types (P=0.007). Overall there was no association between the telomere index and mortality, but when stratified by histologic types, the hazard ratio for death among women with clear cell carcinoma with a telomere index >1 was significantly increased at 4.93 (95% CI 1.64-14.86, P=0.005) when compared with those with a telomere index ≤1. In conclusion, our results provide new evidence that telomere length significantly differs by histologic type in ovarian carcinoma. Specifically, clear cell carcinomas have longer mean relative telomere lengths compared with the other histologic types and longer telomeres in clear cell carcinoma are associated with increased mortality suggesting that aberrations in telomere length may have an important role in the development and progression of this neoplasm.

Shorter telomeres in luminal B, HER-2 and triple-negative breast cancer subtypes.

Telomeres are nucleoprotein structures that protect chromosome ends from degradation and recombination. Cancers often have critically shortened telomeres, contributing to genomic instability. Many of these tumors activate telomerase to stabilize telomeric ends and achieve a capacity for unlimited replication. Telomere shortening has been reported in in situ and invasive carcinomas, including breast, and has been associated with disease recurrence after surgical resection. However, previous studies have not evaluated breast cancer subtypes. The objective of this study was to evaluate telomere lengths in different subtypes of breast cancer. Breast carcinomas (n=103) identified between 2001 and 2010 from patients seen at the Johns Hopkins Hospital were categorized into luminal A (n=18), luminal B (n=28), HER-2-positive (n=20) and triple-negative carcinomas (n=37) based on tumor characteristics. Telomere lengths were assessed directly at the single cell level by fluorescence in situ hybridization, and patient groups were compared using Fisher's exact tests. ER-negative status (P=0.022), PR-negative status (P=0.008), HER-2-positive status (P=0.023) and p53-positive status (P=0.022) were associated with shorter telomere length. A larger proportion of luminal A cancers had normal or long telomere lengths as compared with luminal B cases (P=0.002), HER-2-positive cases (P=0.011) or triple-negative cases (P=0.0003). Luminal B, HER-2-positive and triple-negative cases did not differ significantly. Telomere length was shorter in more aggressive subtypes, such as luminal B, HER-2-positive and triple-negative tumors, suggesting that tumor telomere length may have utility as a prognostic and/or risk marker for breast cancer.

Precursor lesions of high-grade serous ovarian carcinoma: morphological and molecular characteristics.

The lack of proven screening tools for early detection and the high mortality of ovarian serous carcinoma (OSC), particularly high grade, have focused attention on identifying putative precursor lesions with distinct morphological and molecular characteristics. The finding of occult invasive and intraepithelial fallopian tube carcinomas in prophylactically removed specimens from asymptomatic high-risk BRCA 1/2-mutation carriers supports the notion of an origin for OSC in the fallopian tube. The intraepithelial carcinomas have been referred to as serous intraepithelial carcinomas (STICs) but our own findings (unpublished data) and recent reports have drawn attention to a spectrum of changes that fall short of STICs that we have designated serous tubal intraepithelial lesions (STILs).