Synergy between Cigarette Smoking and Human Papillomavirus Type 16 in Cervical Cancer In situ Development

Abstract

Background: A majority of studies have implicated the involvement of cigarette smoking in cervical cancer development, although its mechanism of action remains unclear. We conducted a large population-based case-control study to address the potential interaction between smoking and human papillomavirus type 16 (HPV-16) in development of cervical cancer in situ (CIS). Methods: Information on risk factors for CIS was collected via interview, and archival cervical smears were tested for HPV-16 DNA presence in cases (n = 375) and controls (n = 363). Adjusted odds ratios (OR) for the effects of smoking, HPV-16 presence/absence, and load at first smear (taken, on average, 9 years before diagnosis) were calculated. Results: The risk for CIS among current smokers who were HPV-16 positive at time of first smear was >14-fold [adjusted OR, 14.4; confidence interval (95% CI), 5.6-36.8] compared

Smoking as a major risk factor for cervical cancer and pre-cancer: Results from the EPIC cohort

“…These analyses showed similar patterns of statistically significant associations between smoking factors and CIN3/CIS and ICC risk to those found in the full cohort analyses. The fact that the significant excess risk of CC associated with smoking was not reduced by adjustment for HPV L1 serostatus suggests, as other studies did, 3,12,21,22,34 that smoking may indeed have an independent role in cervical carcinogenesis. In contrast, two retrospective case-control studies and two pooled analyses suggested that this association may be due to residual confounding by HPV or sexual behavior as a surrogate of HPV exposure.…”

“…20 Other studies conducted in the US and Sweden did not find a synergistic effect between smoking status and serological markers of HPV16 on the risk of CIN2-3 and ICC. 17,18,21 However, all of these studies found significantly increased risks of CIN2-3 and ICC in women who had ever smoked and were HPV seropositive as compared with women who were nonsmokers and HPV seronegative (ORs between 5.2 and 7.2 for CIN2-3 and 15.3 for ICC). Stratification by HR HPV serology instead of any HPV serology yielded virtually the same associations.…”

The Prevalence of Human Papilloma Virus Infection Among Women who Admitted to Çukurova University Faculty of Medicine Hospital

“…Ya pı lan bir ça lış ma da in si tu ser vi kal kan ser ge li şi min de si ga ra ve HPV 16 arasın da ki po tan si yel iliş ki yi in ce le miş ler ve si ga ra ile hem HPV 16 po zi tif li ği hem de HPV 16 vi ral yü kü ara sın da si ner jik bir et ki ol du ğu nu gös ter miş lerdir. 31 Si ga ra ve on ko je nik HPV enfeksiyonu ara sın -da ki iliş ki yi de ğer len dir mek için ya pı lan bir baş ka ça lış ma da ise si ga ra içen ler de HPV enfeksiyonu nun önem li şekil de da ha uzun sür dü ğü ve si ga ra iç meyen ka dın lar la kı yas lan dı ğın da on ko je nik HPV enfeksiyonu nun te miz len me ih ti ma li nin da ha dü şük ol du ğu tes pit edil di. 32 Ya pı lan baş ka bir ça lış ma da HPV DNA pre va lan sı nın si ga ra kul la nı mı ile art tı -ğı fa kat OKS kul la nı mı ile azal dı ğı bil di ril di.…”

“…Yük sek risk li tip ler için pU-1M ve pU-2R primer le ri kul la nı la rak po zi tif bu lu nan ör nek ler da ha son ra HPV 16,18,31, [12][13][14] İsta tis tik sel ana liz ola rak ki -ka re ve Fis her 'in ke sin tes ti kul la nıl mış tır. Ana liz ler Epi In fo 6.0 prog ra mı ile ya pıl mış tır.…”

Descriptive epidemiology of vaginal cancer incidence and survival by race, ethnicity, and age in the United States

“…[33][34][35] It is unknown whether there is synergism between cigarette smoking and HPV infection in the development of vaginal cancer, as there is for cervical cancer. 36 Because of the limited literature about HPV prevalence and other risk factors in API women, it is not clear why the incidence rate of vaginal SCC was lower among API women than among women of other races.…”