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  • 1.
    Jonsson, Sarah
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology. Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Pelvic inflammatory disease and epithelial ovarian tumors2023Doctoral thesis, comprehensive summary (Other academic)
    Abstract [en]

    Background: Epithelial ovarian cancer and borderline ovarian tumors consist of several histotypes in which high-grade serous carcinoma is the most common. The majority of epithelial ovarian tumors are considered to originate in the fimbriated end of the fallopian tubes. What initiates these tumors is far from completely understood. Pelvic inflammatory disease has been proposed as a modifiable risk factor for epithelial ovarian tumors. A major cause of pelvic inflammatory disease is Chlamydia trachomatis which has been shown to have cancer-causing potential. The overall purpose of this thesis was to study associations of pelvic inflammatory disease and C. trachomatis with risk of epithelial ovarian tumors.

    Methods: In a cross-sectional study (Paper I) we collected ovarian tissue and corresponding blood samples from 69 women undergoing surgery due to suspected ovarian pathology. C. trachomatis specific protein (immunohistochemistry) and C. trachomatis DNA (qPCR) in ovarian tissue were analyzed (Paper I). In a nested case-control study (Paper II) prospective blood samples from 92 women diagnosed with high-grade serous ovarian cancer were matched to four controls each for age and date of plasma sampling. C. trachomatis specific plasma antibodies were analyzed by commercial Enzyme-Linked ImmunoSorbent Assay (ELISA) and Micro-ImmunoFluorescence (MIF) (Paper I and Paper II). We performed a nationwide register-based case-control study where we included 15 072 women diagnosed with epithelial ovarian cancer (Paper III), 4782 women diagnosed with borderline ovarian tumors (Paper IV), and ten controls each matched for age and residential district. Using national Swedish registers, we retrieved data on historyof pelvic inflammatory disease and the potential confounding factors parity, educational level, previous gynecological surgery, and hormonal therapy.

    Results: We found C. trachomatis DNA in ovarian tissue of eight women with ovarian carcinoma, but not in ovarian tissue from women with borderline ovarian tumors or benign disease (Paper I). The prevalence of the C. trachomatis specific protein did not differ in benign and malignant tissue (Paper I). Prevalence of C. trachomatis specific plasma antibodies was similar in cases and controls at diagnosis (Paper I) and prospectively (Paper II). A history of clinically verified pelvic inflammatory disease was associated with an increased risk of epithelial ovarian cancer overall (Paper III) and borderline ovarian tumors overall (Paper IV). Histotype-specific analyses showed an increased risk of serous carcinoma (Paper III), high-grade serous carcinoma (Paper III), clear cell carcinoma (Paper III), and serous borderline ovarian tumors (Paper IV) but not significantly with other histotypes. A dose-response relationship was seen between an increased number of pelvic inflammatory disease episodes and epithelial ovarian cancer (Paper III), as well as borderline ovarian tumors (Paper IV).

    Conclusions: This thesis contributes to an improved understanding of the association between pelvic inflammatory disease and epithelial ovarian tumors. The results regarding C. trachomatis are inconclusive and suggests that the association of pelvic inflammatory disease with epithelial ovarian tumors acts through mechanisms other than Chlamydia alone.

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  • 2.
    Jonsson, Sarah
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology. Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Umeå University, Faculty of Medicine, Department of Epidemiology and Global Health.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Inflammatory disease and epithelial ovarian cancer risk: a national population-based case-control study in SwedenManuscript (preprint) (Other academic)
  • 3.
    Jonsson, Sarah
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Radiation Sciences, Oncology. Umeå University, Faculty of Medicine, Department of Epidemiology and Global Health.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Biobank Research. Umeå University, Faculty of Medicine, Department of Surgical and Perioperative Sciences, Urology and Andrology. Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Nutritional Research.
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Pelvic inflammatory disease and risk of borderline ovarian tumors: a national population-based case-control study in SwedenManuscript (preprint) (Other academic)
  • 4.
    Jonsson, Sarah
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Jonsson, Håkan
    Umeå University, Faculty of Medicine, Department of Epidemiology and Global Health.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Häggström, Christel
    Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine.
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Pelvic inflammatory disease and risk of epithelial ovarian cancer: a national population-based case-control study in Sweden2023In: American Journal of Obstetrics and Gynecology, ISSN 0002-9378, E-ISSN 1097-6868, Vol. 230, no 1, p. 75.e1-75.e15Article in journal (Refereed)
    Abstract [en]

    Background: Epithelial ovarian cancer is an insidious disease, and women are often diagnosed when the disease is beyond curative treatment. Accordingly, identifying modifiable risk factors is of paramount importance. Inflammation predisposes an individual to cancer in various organs, but whether pelvic inflammatory disease is associated with an increased risk of epithelial ovarian cancer has not been fully determined.

    Objective: This study aimed to investigate a possible association between clinically verified pelvic inflammatory disease and the risk of epithelial ovarian cancer.

    Study Design: In this national population-based case-control study, all women in Sweden diagnosed with epithelial ovarian cancer between 1999 and 2020 and 10 controls for each were identified, matched for age and residential district. Using several Swedish nationwide registers, data on previous pelvic inflammatory disease and potential confounding factors (age, parity, educational level, and previous gynecologic surgery) were retrieved. Adjusted odds ratios and 95% confidence intervals were estimated using conditional logistic regression. Histotype-specific analyses were performed for the subgroup of women diagnosed with epithelial ovarian cancer between 2015 and 2020. Moreover, hormonal contraceptives and menopausal hormone therapy were adjusted in addition to the aforementioned confounders.

    Results: This study included 15,072 women with epithelial ovarian cancer and 141,322 controls. Most women (9102 [60.4%]) had serous carcinoma. In a subgroup of cases diagnosed between 2015 and 2020, high-grade serous carcinoma (2319 [60.0%]) was identified. A total of 168 cases (1.1%) and 1270 controls (0.9%) were diagnosed with pelvic inflammatory disease. Previous pelvic inflammatory disease was associated with an increased risk of epithelial ovarian cancer (adjusted odds ratio, 1.39; 95% confidence interval, 1.17–1.66) and serous carcinoma (adjusted odds ratio, 1.46; 95% confidence interval, 1.18–1.80) for the entire study population. For the subgroup of women diagnosed in 2015–2020, pelvic inflammatory disease was associated with high-grade serous carcinoma (adjusted odds ratio, 1.43; 95% confidence interval, 1.01–2.04). The odds ratios of the other histotypes were as follows: endometrioid (adjusted odds ratio, 0.13; 95% confidence interval, 0.02–1.06), mucinous (adjusted odds ratio, 1.55; 95% confidence interval, 0.56–4.29), and clear cell carcinoma (adjusted odds ratio, 2.30; 95% confidence interval, 0.90–5.86). A dose-response relationship was observed between the number of pelvic inflammatory disease episodes and the risk of epithelial ovarian cancer (Ptrend<.001).

    Conclusion: A history of pelvic inflammatory disease is associated with an increased risk of epithelial ovarian cancer and a dose-response relationship is evident. Histotype-specific analyses show an association with increased risk of serous epithelial ovarian cancer and high-grade serous carcinoma and potentially also with clear cell carcinoma, but there is no significant association with other histotypes. Infection and inflammation of the upper reproductive tract might have serious long-term consequences, including epithelial ovarian cancer.

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  • 5.
    Jonsson, Sarah
    et al.
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Lundin, Eva
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Elgh, Fredrik
    Umeå University, Faculty of Medicine, Department of Clinical Microbiology.
    Ottander, Ulrika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Idahl, Annika
    Umeå University, Faculty of Medicine, Department of Clinical Sciences, Obstetrics and Gynecology.
    Chlamydia trachomatis and Anti-MUC1 Serology and Subsequent Risk of High-Grade Serous Ovarian Cancer: A Population-Based Case-Control Study in Northern Sweden2020In: Translational Oncology, ISSN 1944-7124, E-ISSN 1936-5233, Vol. 13, no 1, p. 86-91Article in journal (Refereed)
    Abstract [en]

    BACKGROUND: Chlamydia trachomatis salpingitis causes inflammatory damage to the fallopian tube and could potentially cause initiation and progression of high-grade serous ovarian cancer (HGSC). Furthermore, C. trachomatis infection may stimulate mucin 1 (MUC1) protein production, possibly affecting anti-MUC1 antibody levels. The aim of this study was to examine if serology indicating past infection with C. trachomatis as well as anti-MUC1 production was associated with subsequent risk of HGSC.

    MATERIALS AND METHODS: In a prospective nested case-control study within the Northern Sweden Health and Disease Study and the Northern Sweden Maternity Cohort, the prevalence of chlamydial and anti-MUC1 antibodies was analyzed in blood samples drawn more than one year before diagnosis from 92 women with HGSC and 359 matched controls. Matching factors were age, date at blood draw, and sampling cohort. Plasma C. trachomatis IgG was analyzed using commercial micro-immunofluorescence test; chlamydial Heat Shock Protein 60 IgG (cHSP60) and anti-MUC1 IgG were analyzed with ELISA technique.

    RESULTS: The prevalence of C. trachomatis IgG and cHSP60 IgG antibodies, as well as the level of anti-MUC1 IgG was similar in women with HGSC and controls (16.3% vs. 17.0%, P = 0.87; 27.2% vs. 28.5%, P = 0.80; median 0.24 vs. 0.25, P = 0.70). Anti-MUC1 IgG and cHSP60 IgG levels were correlated (r = 0.169; P < 0.001).

    CONCLUSIONS: The findings of this prospective nested case-control study did not support an association between C. trachomatis infection, as measured by chlamydial serology, or anti-MUC1 IgG antibodies, and subsequent risk of HGSC.

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