• 2019-07
  • 2019-08
  • 2019-09
  • 2019-10
  • 2019-11
  • 2020-03
  • 2020-07
  • 2020-08
  • The epidemiological evidence for a relationship between toba


    The epidemiological evidence for a relationship between tobacco and cervical carcinogenesis is supported by a number of biological studies. Several of these demonstrated malignant transformations of papilloma and cervical tissue from exposure to chemical carcinogens contained in tobacco smoke [11,37]. Other studies have reported that smoking appears to additionally increase the risks of HPV infection and the likelihood of infection persistence through the suppression of Acarbose [38,39]. In a recent study on progression of HPV infections in adult women, those who smoked were significantly less likely to clear an infection than non-smokers [40]. The plausibility of a causal link between smoking and cervical carcinogenesis is also strengthened by evidence of tobacco-specific carcinogens in the cervical mucus of smokers [41].
    Conclusions This population-based case-control study indicates that among Australian women 30–44 years of age, current users of hormonal contraceptives and current-smokers were at increased risk of developing CIN 2/3, and that longer duration of use and increasing intensity of exposure, respectively, lead to further increase in risk. The evidence from this study also indicates that these increased risks are generally reversible, with risks returning to similar levels as those for never-users and never-smokers within 5 years of stopping/quitting. Our findings support smoking cessation in users to decrease their risk of pre-cancerous lesions. Although we found that contraceptives increase the risk of CIN2/3, combined oral contraceptives have been shown to be protective in the long term against endometrial and ovarian cancers [42,43] in addition to their effective contraceptive properties. Overall, our study reinforces the continuing need and importance of routine cervical screening for cancer prevention in both vaccinated and unvaccinated populations.
    Data statement
    Authors contributions
    Funding Funding for the study was provided by the National Health and Medical Research Council (NHMRC) Grant no. 337600. The funding body had no role in the design, collection, analysis or interpretation of data; in writing of the manuscript or the decision to submit the manuscript for publication. r> Conflict of interest statement KC is a co-PI of an investigator-initiated trial of cytology and primary HPV screening in Australia (‘Compass’) (ACTRN12613001207707 and NCT02328872), which is conducted and funded by the Victorian Cytology Service (VCS) Inc Ltd., a government-funded health promotion charity. The VCS Inc Ltd. have received equipment and a funding contribution for the Compass trial from Roche Molecular Systems and Ventana Inc USA. KC is also a PI on Compass in New Zealand, (‘Compass NZ’) (ACTRN12614000714684) which is conducted and funded by Diagnostic Medlab (DML), now Auckland District Health Board. DML received an equipment and a funding contribution for the Compass trial from Roche Molecular Systems. However neither KC nor her institution on her behalf (Cancer Council NSW) receive direct or indirect funding from industry for Compass Australia or NZ or any other project. KC, EB, FS, and DO’C have received grants from the NHMRC. KC and EB currently receive salary support from the NHMRC. KC, SE, LSV, and DO’C receive salary support from Cancer Council NSW. HX has no competing interests to declare.
    Introduction Liver cancer is the sixth most commonly occurring cancer in the world and the second leading cause of cancer mortality [1]. In almost all areas of the world, the incidence of liver cancer is three- to four-fold higher among men than women [2]. Men also have higher recurrence rates and poorer survival after diagnosis of liver cancer than do women [3,4]. Reasons for this gender disparity are not clear. While some major risk factors, such as infection with hepatitis B virus (HBV) or hepatitis C virus (HCV), excessive alcohol consumption, and cigarette smoking, are more common among men, these factors do not fully account for the gender differences in liver cancer incidence and survival [2].