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      Trends in the Incidence of Human Papillomavirus-Associated Cancers by County-Level Income and Smoking Prevalence in the United States, 2000-2018

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          Abstract

          Human papillomavirus (HPV)-associated cancer burden is rising in the United States. Trends in the incidence by county-level income and smoking prevalence remain undescribed. We used the Surveillance, Epidemiology, and End Results 21 database to ascertain HPV-associated cancers during 2000-2018. Trends were estimated by county-level income and smoking prevalence quartiles. Anal and vulvar cancer incidence among women and anal cancer incidence among men increased markedly in the lowest-income counties, whereas the increases were slower in the highest-income counties (eg, for vulvar cancer, incidence increased 1.9% per year, 95% confidence interval [CI] = 0.9% to 2.9%, in the lowest-income counties vs 0.8% per year, 95% CI = 0.6% to 1.1%, in the highest-income counties). In recent years, cervical cancer incidence plateaued (0.0% per year [95% CI = −0.5% to 0.5%]) in the highest-income counties; in the lowest-income counties, the annual percentage change was 1.6% per year (95% CI = −0.7% to 4.0%). Counties with high smoking prevalence had marked increases in incidence compared with their counterparts (eg, anal cancer among men increased 4.4% per year [95% CI = 2.7% to 6.0%] for those living in counties with the highest smoking prevalence vs 1.2% per year [95% CI = 0.7% to 1.7%] for those living in counties with the lowest smoking prevalence). Improved and targeted prevention is needed to combat the widening disparities.

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          Estimating average annual per cent change in trend analysis

          Trends in incidence or mortality rates over a specified time interval are usually described by the conventional annual per cent change (cAPC), under the assumption of a constant rate of change. When this assumption does not hold over the entire time interval, the trend may be characterized using the annual per cent changes from segmented analysis (sAPCs). This approach assumes that the change in rates is constant over each time partition defined by the transition points, but varies among different time partitions. Different groups (e.g. racial subgroups), however, may have different transition points and thus different time partitions over which they have constant rates of change, making comparison of sAPCs problematic across groups over a common time interval of interest (e.g. the past 10 years). We propose a new measure, the average annual per cent change (AAPC), which uses sAPCs to summarize and compare trends for a specific time period. The advantage of the proposed AAPC is that it takes into account the trend transitions, whereas cAPC does not and can lead to erroneous conclusions. In addition, when the trend is constant over the entire time interval of interest, the AAPC has the advantage of reducing to both cAPC and sAPC. Moreover, because the estimated AAPC is based on the segmented analysis over the entire data series, any selected subinterval within a single time partition will yield the same AAPC estimate—that is it will be equal to the estimated sAPC for that time partition. The cAPC, however, is re-estimated using data only from that selected subinterval; thus, its estimate may be sensitive to the subinterval selected. The AAPC estimation has been incorporated into the segmented regression (free) software Joinpoint, which is used by many registries throughout the world for characterizing trends in cancer rates. Copyright © 2009 John Wiley & Sons, Ltd.
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            Human papillomavirus, smoking, and sexual practices in the etiology of anal cancer.

            The incidence of anal cancer has increased among both men (160%) and women (78%) from 1973 to 2000 in the U.S. The authors conducted a population-based case-control study of anal cancer to examine factors that may account for this increase. Men (n = 119 patients) and women (n = 187 patients) who were diagnosed with anal cancer between 1986 and 1998 in the Seattle area were ascertained through the local Surveillance, Epidemiology, and End Results registry. Control participants (n = 1700) were ascertained through random-digit telephone dialing. Participants were interviewed in person and provided blood samples. Archival tumor tissue was tested for human papilloma virus (HPV) DNA, and serum samples were tested for HPV type 16 (HPV-16). Overall, 88% of tumors (all histologies) in the study were found to be positive for HPV. HPV-16 was the most frequent HPV type detected (73% of all tumors), followed by HPV-18 (6.9%), regardless of gender. However, 97.7% of tumors from men who were not exclusively heterosexual contained HPV DNA. The risk of anal cancer increased among men (odds ratio [OR], 5.3; 95% confidence interval [95% CI], 2.4-12.0) and women (OR, 11.0; 95% CI, 5.5-22.1) who had > or = 15 sexual partners during their lifetime. Among men who were not exclusively heterosexual and women, receptive anal intercourse was related strongly to the risk of anal cancer (OR, 6.8 [95% CI, 1.4-33.8] and OR, 2.2 [95% CI, 1.4-3.3], respectively). Current smokers among men and women were at particularly high risk for anal cancer, independent of age and other risk factors (OR, 3.9 [95% CI, 1.9-8.0] and OR, 3.8 [95% CI, 2.4-6.2], respectively). The high proportion of tumors with detectable HPV suggests that infection with HPV is a necessary cause of anal cancer, similar to that of cervical cancer. Increases in the prevalence of exposures, such as cigarette smoking, anal intercourse, HPV infection, and the number of lifetime sexual partners, may account for the increasing incidence of anal cancer in men and women. Copyright 2004 American Cancer Society.
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              Nicotine-mediated cell proliferation and tumor progression in smoking-related cancers.

              Tobacco smoke contains multiple classes of established carcinogens including benzo(a)pyrenes, polycyclic aromatic hydrocarbons, and tobacco-specific nitrosamines. Most of these compounds exert their genotoxic effects by forming DNA adducts and generation of reactive oxygen species, causing mutations in vital genes such as K-Ras and p53. In addition, tobacco-specific nitrosamines can activate nicotinic acetylcholine receptors (nAChR) and to a certain extent β-adrenergic receptors (β-AR), promoting cell proliferation. Furthermore, it has been demonstrated that nicotine, the major addictive component of tobacco smoke, can induce cell-cycle progression, angiogenesis, and metastasis of lung and pancreatic cancers. These effects occur mainly through the α7-nAChRs, with possible contribution from the β-ARs and/or epidermal growth factor receptors. This review article will discuss the molecular mechanisms by which nicotine and its oncogenic derivatives such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and N-nitrosonornicotine induce cell-cycle progression and promote tumor growth. A variety of signaling cascades are induced by nicotine through nAChRs, including the mitogen-activated protein kinase/extracellular signal-regulated kinase pathway, phosphoinositide 3-kinase/AKT pathway, and janus-activated kinase/STAT signaling. In addition, studies have shown that nAChR activation induces Src kinase in a β-arrestin-1-dependent manner, leading to the inactivation of Rb protein and resulting in the expression of E2F1-regulated proliferative genes. Such nAChR-mediated signaling events enhance the proliferation of cells and render them resistant to apoptosis induced by various agents. These observations highlight the role of nAChRs in promoting the growth and metastasis of tumors and raise the possibility of targeting them for cancer therapy. ©2014 AACR.
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                Author and article information

                Journal
                JNCI Cancer Spectr
                JNCI Cancer Spectr
                jncics
                JNCI Cancer Spectrum
                Oxford University Press
                2515-5091
                April 2022
                03 March 2022
                03 March 2022
                : 6
                : 2
                : pkac004
                Affiliations
                [1 ] Center for Health Services Research, Department of Management, Policy, and Community Health, UTHealth School of Public Health , Houston, TX, USA
                [2 ] Department of Biostatistics and Epidemiology, Graduate School of Public Health, Medical Sciences Campus, University of Puerto Rico , San Juan, Puerto Rico, USA
                [3 ] General Outbreak & Jail Team (GOJ), COVID-19 Contact Tracing & Contact Monitoring Unit (CTCMU) , Houston Health Department City of Houston, Houston, TX, USA
                [4 ] Center for Healthcare Data, Department of Management, Policy and Community Health, School of Public Health, UTHealth Science Center at Houston , Houston, TX, USA
                Author notes

                Yueh-Yun Lin, MS and Haluk Damgacioglu, PhD with equal contribution.

                Correspondence to: Ashish A. Deshmukh, PhD, MPH, Center for Health Services Research, Department of Management, Policy and Community Health, UTHealth School of Public Health, 1200 Pressler St, RAS-E 329, Houston, TX, USA (e-mail: ashish.a.deshmukh@uth.tmc.edu).
                Author information
                https://orcid.org/0000-0003-0649-9503
                https://orcid.org/0000-0001-8936-8108
                Article
                pkac004
                10.1093/jncics/pkac004
                8891496
                35603851
                87a6ddd5-bfd3-4321-bf3f-b052ddb4186e
                © The Author(s) 2022. Published by Oxford University Press.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 October 2021
                : 22 October 2021
                Page count
                Pages: 4
                Funding
                Funded by: National Cancer Institute, DOI 10.13039/100000054;
                Award ID: R01CA232888
                Award ID: U54CA096300
                Award ID: U54CA096297
                Funded by: National Institute on Minority Health and Health Disparities, DOI 10.13039/100006545;
                Award ID: K01MD016440
                Categories
                Brief Communications
                AcademicSubjects/MED00010

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