<i>Chlamydia trachomatis</i>Serology in Women with and without Ovarian Cancer

Ness, Roberta B.; Shen, Caixia; Bass, Debra C.; Jackson, Carlynn; Moysich, K.B.; Edwards, Robert P.; Brunham, Robert C.

doi:10.1155/2008/219672

Cited by 24 publications

(26 citation statements)

References 10 publications

(15 reference statements)

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“…In the analysis considering "high" and "low" positive antibody levels to C. trachomatis cHSP60-1 antibodies and EOC risk, women with high positive antibody levels had higher risk of EOC only among women <60 at blood collection (P het = 0.04; <60 years, Our findings of positive associations between select C. trachomatis antibodies and EOC risk are in line with the results of three previous studies 18,19,25 ; however, others have observed no association. 20,22,24 Previous studies have predominantly analyzed ovarian cancer as a single disease, with small sample size precluding analyses by subtype beyond serous vs nonserous disease. [18][19][20]22,24,25 In the current study, we provide a detailed investigation by histotype, observing suggestive heterogeneity by tumor histology.…”

Section: Sensitivity and Subgroup Analysesmentioning

confidence: 99%

“…20,22,24 Previous studies have predominantly analyzed ovarian cancer as a single disease, with small sample size precluding analyses by subtype beyond serous vs nonserous disease. [18][19][20]22,24,25 In the current study, we provide a detailed investigation by histotype, observing suggestive heterogeneity by tumor histology. Pgp3 serology indicating current or past infection with C. trachomatis was not associated with EOC risk overall in contrast to two recent studies, 18,25 but was associated with significantly higher risk of mucinous EOC; this has not previously been described.…”

Section: Sensitivity and Subgroup Analysesmentioning

confidence: 99%

“…16 Similarly, the distal end of the fallopian tubes harbors the potentially vulnerable junction of the fallopian tubal epithelium and the peritoneal mesothelium. 17 Epidemiologic data on STIs and EOC risk are limited and the results divergent, [18][19][20][21][22][23][24][25] and few studies are prospective. 18,22,25,26 The largest and most recent prospective study (n = 337 cases) observed a twofold higher risk of EOC among women seropositive to chlamydial Pgp3 antibodies, 25 with similar associations between relatively high circulating antibodies in another recent prospective study 18 ; no associations were observed for M. genitalium, the investigated HPV types (L1 proteins of types 16, 18 and 45), or HSV-2.…”

Section: Introductionmentioning

confidence: 99%

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Serologic markers of Chlamydia trachomatis and other sexually transmitted infections and subsequent ovarian cancer risk: Results from the EPIC cohort

Idahl

Cornet

Maldonado

et al. 2020

Intl Journal of Cancer

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A substantial proportion of epithelial ovarian cancer (EOC) arises in the fallopian tube and other epithelia of the upper genital tract; these epithelia may incur damage and neoplastic transformation after sexually transmitted infections (STI) and pelvic inflammatory disease. We investigated the hypothesis that past STI infection, particularly Chlamydia trachomatis, is associated with higher EOC risk in a nested case‐control study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort including 791 cases and 1669 matched controls. Serum antibodies against C. trachomatis, Mycoplasma genitalium, herpes simplex virus type 2 (HSV‐2) and human papillomavirus (HPV) 16, 18 and 45 were assessed using multiplex fluorescent bead‐based serology. Conditional logistic regression was used to estimate relative risks (RR) and 95% confidence intervals (CI) comparing women with positive vs. negative serology. A total of 40% of the study population was seropositive to at least one STI. Positive serology to C. trachomatis Pgp3 antibodies was not associated with EOC risk overall, but with higher risk of the mucinous histotype (RR = 2.30 [95% CI = 1.22‐4.32]). Positive serology for chlamydia heat shock protein 60 (cHSP60‐1) was associated with higher risk of EOC overall (1.36 [1.13‐1.64]) and with the serous subtype (1.44 [1.12‐1.85]). None of the other evaluated STIs were associated with EOC risk overall; however, HSV‐2 was associated with higher risk of endometrioid EOC (2.35 [1.24‐4.43]). The findings of our study suggest a potential role of C. trachomatis in the carcinogenesis of serous and mucinous EOC, while HSV‐2 might promote the development of endometrioid disease.

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Section: Sensitivity and Subgroup Analysesmentioning

confidence: 99%

Section: Sensitivity and Subgroup Analysesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Serologic markers of Chlamydia trachomatis and other sexually transmitted infections and subsequent ovarian cancer risk: Results from the EPIC cohort

Idahl

Cornet

Maldonado

et al. 2020

Intl Journal of Cancer

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“…There are several studies, which attempted to find an association between C. trachomatis and ovarian cancer (Idahl et al, 2010;Ness et al, 2003;Ness et al, 2008;Shanmughapriya et al, 2012). However, these studies employ analysis of IgG antibodies in patients or bacterial genetic material in the tumour samples.…”

Section: Downregulation Of P53 Duringmentioning

confidence: 99%

Chlamydia trachomatis impairs host base excision repair by downregulating polymerase β

Gulve

Prusty

Rudel

2019

Cellular Microbiology

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Chlamydia trachomatis infections have been associated with ovarian cancer by several epidemiological studies. Here, we show that C. trachomatis‐infected primary human ovarian epithelial cells display elevated oxidative DNA damage. Base excision repair, an important cellular mechanism to repair oxidative DNA lesions, was impaired in infected primary ovarian and in several other types of cells. Polymerase β was downregulated in infected cells associated with upregulation of microRNA‐499a (miR‐499a). Stabilising polymerase β by inhibiting miR‐499a significantly improved repair. Moreover, downregulation of tumour suppressor p53 also resulted in attenuated repair in these cells. Thus, our data show that downregulation of polymerase β by direct inhibition through miR‐499a and downregulation of p53 debilitate the host‐cell base excision repair during C. trachomatis infection.

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“…Ness and colleagues [59] reported a significant difference in IgG antibody titers against Ctr elementary bodies and heat shock proteins (CHSP) in the serum of ovarian cancer patients compared to the control group, but failed to validate the finding in a larger, population-based group [60]. In a more recent patient cohort analyzed by Idahl et al .…”

Section: The Tumorigenic Effects Of Oxidative Stress and Inflammatmentioning

confidence: 99%

The Molecular Fingerprint of High Grade Serous Ovarian Cancer Reflects Its Fallopian Tube Origin

Kessler

Fotopoulou

Meyer

2013

IJMS

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High grade serous ovarian cancer (HGSC), the most lethal and frequent type of epithelial ovarian cancer (EOC), has poor long term prognosis due to a combination of factors: late detection, great metastatic potential and the capacity to develop resistance to available therapeutic drugs. Furthermore, there has been considerable controversy concerning the etiology of this malignancy. New studies, both clinical and molecular, strongly suggest that HGSC originates not from the surface of the ovary, but from the epithelial layer of the neighboring fallopian tube fimbriae. In this paper we summarize data supporting the central role of fallopian tube epithelium in the development of HGSC. Specifically, we address cellular pathways and regulatory mechanisms which are modulated in the process of transformation, but also genetic changes which accumulate during disease progression. Similarities between fallopian tube mucosa and the malignant tissue of HGSC warrant a closer analysis of homeostatic mechanisms in healthy epithelium in order to elucidate key steps in disease development. Finally, we highlight the importance of the cancer stem cell (CSC) identification and understanding of its niche regulation for improvement of therapeutic strategies.

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Chlamydia trachomatisSerology in Women with and without Ovarian Cancer

Cited by 24 publications

References 10 publications

Serologic markers of Chlamydia trachomatis and other sexually transmitted infections and subsequent ovarian cancer risk: Results from the EPIC cohort

Serologic markers of Chlamydia trachomatis and other sexually transmitted infections and subsequent ovarian cancer risk: Results from the EPIC cohort

Chlamydia trachomatis impairs host base excision repair by downregulating polymerase β

The Molecular Fingerprint of High Grade Serous Ovarian Cancer Reflects Its Fallopian Tube Origin

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