<i>Chlamydia trachomatis</i> and invasive cervical cancer: A pooled analysis of the IARC multicentric case‐control study

Smith, Jennifer S.; Bosetti, Cristina; Muñóz, Núbia; Herrero, Rolando; Bosch, F. Xavier; Eluf-Neto, José; Meijer, Chris J.L.M.; Brule, Adriaan J. C. van den; Franceschi, Silvia; Peeling, Rosanna W.

doi:10.1002/ijc.20257

Cited by 231 publications

(174 citation statements)

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“…Our finding suggests a plausible mechanism whereby C. trachomatis infection could be associated with increased risk for cervical cancer, as has been reported in several epidemiological studies. 7,[10][11][12]23,24 It has been reported that C. trachomatis infection may induce large local amounts of pro-inflammatory chemokines, including IL-1, IL-8 and granulocyte-macrophage colony-stimulating factor 25 producing a chronic inflammatory background that may conceivably contribute to HPV DNA persistence in the cervix.…”

Section: Discussionmentioning

confidence: 99%

“…Chlamydia (C.) trachomatis has been found repeatedly to associate with cervical neoplasia and invasive cancer in cross-sectional case-control studies, 7,8 although the association has commonly been thought to be the result of confounding by HPV. During recent years, an association with C. trachomatis has also been found in several biobank-based longitudinal studies with invasive cervical cancer as endpoint.…”

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confidence: 99%

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Chlamydia trachomatis infection and persistence of human papillomavirus

Silins

Ryd

Strand

et al. 2005

Intl Journal of Cancer

139

108

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Human papillomavirus (HPV) persistence is the major cause of cervical cancer, but most HPV infections will not persist and risk factors for HPV persistence are not well known. Chlamydia (C.) trachomatis infection seems to also be associated with cervical cancer. We investigated whether C. trachomatis infection is a risk factor for HPV persistence. In a cohort of 12,527 women participating in a population-based HPV screening trial in Sweden, 6,418 women completed testing for HPV DNA by general primer PCR and typing by reverse dot blot hybridization. On average 19 months later, 303 women that had been HPV-positive and had normal cytology at enrollment completed a new HPV test. Environmental exposures were assessed by an 87-item questionnaire. Previous sexually transmitted infections were also investigated by serology. At follow-up, 44% of the women were positive for the same type of HPV DNA as at enrollment. Persistence correlated with length of follow-up (p < 0.01) and condom use seemed to protect against HPV persistence (p < 0.05). The most significant risk factor for persistent presence of HPV DNA was self-reported history of previous C. trachomatis infection (relative risk in multivariate model = 2.09; 95% confidence interval = 1.05-4.18). We conclude that persistence of oncogenic HPV infections is more likely among women with a previous C. trachomatis infection. ' 2005 Wiley-Liss, Inc.Key words: HPV infection; HPV persistence; Chlamydia trachomatis; epidemiology Persistent oncogenic HPV infection is recognized as a necessary factor in development of high grade cervical intraepithelial neoplasia and invasive cervical cancer. 1 Genital infections with oncogenic HPV types are very common among sexually active women, but only a minority of infected women will have a persistent HPV infection. 2-4 Type-specific persistence of HPV (defined as repeated detectability of the same type of HPV DNA in serial samples) is a much stronger risk factor for high-grade CIN 5 and cervical cancer 6 than HPV infection per se.Chlamydia (C.) trachomatis has been found repeatedly to associate with cervical neoplasia and invasive cancer in cross-sectional case-control studies, 7,8 although the association has commonly been thought to be the result of confounding by HPV. During recent years, an association with C. trachomatis has also been found in several biobank-based longitudinal studies with invasive cervical cancer as endpoint. [9][10][11][12] The vexed question of whether the association could be due to confounding by HPV infection is, however, only possible to address in cohort studies comprising only HPV-infected women.A possible explanation for the association of C. trachomatis and cervical cancer might be that the C. trachomatis-induced inflammation results in an impaired ability to clear HPV infections.To investigate these issues, we carried out a prospective, population-based cohort study restricted to HPV-infected women with HPV persistence as the endpoint. Subjects and methods Study settingA population-based randomized mul...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Chlamydia trachomatis infection and persistence of human papillomavirus

Silins

Ryd

Strand

et al. 2005

Intl Journal of Cancer

139

108

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“…In contrast, moderate and borderline associations were found with CIN3/CIS. History of CT infection has also been associated with CC in several previous studies [2][3][4]6 and it is assumed it increases the probability that HPV infections will become persistent, increasing thus the risk of neoplasia. 29,30 In contrast, a large prospective study based on the placebo arms of two multinational clinical trials of HPV vaccination found a moderate association between CT PCR positivity and CIN2 but not with CIN3.…”

Section: Epidemiologymentioning

confidence: 99%

“…In addition to HPV, associations have been found with Chlamydia trachomatis (CT) and Human Herpes Virus 2 (HHV-2). [1][2][3][4][5][6] However, most of the evidence comes from retrospective case-control studies and little data are available from prospective designs.…”

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confidence: 99%

Prospective seroepidemiologic study on the role of Human Papillomavirus and other infections in cervical carcinogenesis: Evidence from the EPIC cohort

et al. 2014

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To evaluate prospectively the association between serological markers of selected infections, including HPV, and risk of developing cervical cancer (CC) and precancer, we performed a nested case–control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) study that included 184 cases of invasive CC (ICC), 425 cases of cervical intraepithelial neoplasia (CIN) grade 3 or carcinoma in situ (CIS), and 1,218 matched control women. At enrollment participants completed lifestyle questionnaires and provided sera. Subjects were followed‐up for a median of 9 years. Immunoassays were used to detect serum antibodies to Human Herpes Virus 2 (HHV‐2), Chlamydia trachomatis (CT), Chlamydia pneumoniae, L1 proteins of mucosal and cutaneous HPV types, E6/E7 proteins of HPV16/18, as well as to four polyomaviruses. Adjusted odds ratios (OR) [and 95% confidence intervals (CI)] for CIN3/CIS and ICC risk were respectively: 1.6 (1.2–2.0) and 1.8 (1.1–2.7) for L1 seropositivity to any mucosal HPV type, 1.0 (0.4–2.4) and 7.4 (2.8–19.7) for E6 seropositivity to HPV16/18, 1.3 (0.9–1.9) and 2.3 (1.3–4.1) for CT seropositivity, and 1.4 (1.0–2.0) and 1.5 (0.9–2.6) for HHV‐2 seropositivity. The highest OR for ICC was observed for HPV16 E6 seropositivity [OR = 10.2 (3.3–31.1)]. Increasing number of sexually transmitted infections (STIs) was associated with increasing risk. Non‐STIs were not associated with CC risk. In conclusion, this large prospective study confirms the important role of HPV and a possible contribution of CT and HHV‐2 in cervical carcinogenesis. It further identifies HPV16 E6 seropositivity as the strongest marker to predict ICC well before disease development.

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“…The amplified HPV-DNA is identified by sequencing or hybridization with a specific sequence of a DNA or RNA probe. The hybridized DNA-DNA or DNA-RNA complex is then detected by means of colorimetric or chemiluminence techniques [2,14].…”

Section: Introductionmentioning

confidence: 99%