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      Chlamydia trachomatis and Mycoplasma genitalium Plasma Antibodies in Relation to Epithelial Ovarian Tumors

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          Abstract

          Objective. To assess associations of Chlamydia trachomatis and Mycoplasma genitalium antibodies with epithelial ovarian tumors. Methods. Plasma samples from 291 women, undergoing surgery due to suspected ovarian pathology, were analyzed with respect to C. trachomatis IgG and IgA, chlamydial Heat Shock Protein 60-1 (cHSP60-1) IgG and M. genitalium IgG antibodies. Women with borderline tumors ( n = 12), ovarian carcinoma ( n = 45), or other pelvic malignancies ( n = 11) were matched to four healthy controls each. Results. Overall, there were no associations of antibodies with EOC. However, chlamydial HSP60-1 IgG antibodies were associated with type II ovarian cancer ( P = .002) in women with plasma samples obtained >1 year prior to diagnosis ( n = 7). M. genitalium IgG antibodies were associated with borderline ovarian tumors ( P = .01). Conclusion. Chlamydial HSP60-1 IgG and M. genitalium IgG antibodies are in this study associated with epithelial ovarian tumors in some subsets, which support the hypothesis linking upper-genital tract infections and ovarian tumor development.

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          Worldwide burden of gynaecological cancer: the size of the problem.

          R. Sankaranarayanan, J Ferlay (2006)
          The estimation of cancer burden is valuable to set up priorities for disease control. The comprehensive global cancer statistics from the International Agency for Research on Cancer indicate that gynaecological cancers accounted for 19% of the 5.1 million estimated new cancer cases, 2.9 million cancer deaths and 13 million 5-year prevalent cancer cases among women in the world in 2002. Cervical cancer accounted for 493 000 new cases and 273 000 deaths; uterine body cancer for 199 000 new cases and 50 000 deaths; ovarian cancer for 204 000 new cases and 125 000 deaths; cancers of the vagina, vulva and choriocarcinoma together constituted 45 900 cases. More than 80% of the cervical cancer cases occurred in developing countries and two-thirds of corpus uteri cases occurred in the developed world. Political will and advocacy to invest in healthcare infrastructure and human resources to improve service delivery and accessibility are vital to reduce the current burden in low- and medium-resource countries.
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            Pathogenesis of ovarian cancer: lessons from morphology and molecular biology and their clinical implications.

            Chuen-Ming Shih, Robert Kurman (2008)
            The accepted view of ovarian carcinogenesis is that carcinoma begins in the ovary, undergoes progressive "dedifferentiation" from a well to a poorly differentiated tumor, and then spreads to the pelvic and abdominal cavities before metastasizing to distant sites. It has therefore been reasoned that survival for this highly lethal disease could be improved by developing screening methods that detect disease when it is confined to the ovary. To date, however, no prospective randomized trial of any ovarian cancer screening test(s) has demonstrated a decrease in mortality. We believe that one of the main reasons for this is that the dogma underlying ovarian carcinogenesis is flawed. Based on studies performed in our laboratory during the last decade, we have proposed a model of ovarian carcinogenesis that takes into account the diverse nature of ovarian cancer and correlates the clinical, pathological, and molecular features of the disease. In this model, ovarian tumors are divided into 2 groups designated type I and type II. Type I tumors are slow growing, generally confined to the ovary at diagnosis, and develop from well-established precursor lesions that are termed "borderline" tumors. Type I tumors include low-grade micropapillary serous carcinoma, mucinous, endometrioid, and clear cell carcinomas. They are genetically stable and are characterized by mutations in a number of different genes including KRAS, BRAF, PTEN, and beta-catenin. Type II tumors are rapidly growing highly aggressive neoplasms for which well-defined precursor lesions have not been described. Type II tumors include high-grade serous carcinoma, malignant mixed mesodermal tumors (carcinosarcomas), and undifferentiated carcinomas. This group of tumors has a high level of genetic instability and is characterized by mutation of TP53. The model helps to explain why current screening techniques, aimed at detecting stage I disease, have not been effective. Tumors that remain confined to the ovary for a long period belong to the type I group, but they account for only 25% of the malignant tumors. Most of what is considered ovarian cancer belongs to the type II category, and these are only rarely confined to the ovary. Although the reasons for this are not entirely clear, possible explanations include rapid spread from the ovary early in carcinogenesis and development of carcinoma in extra ovarian sites, notably, the peritoneum and fallopian tube, with secondary involvement of the ovary. The latter tumors are advanced stage at their inception. Therefore, a more realistic end point for the early detection of ovarian cancer is volume and not stage of disease. The model does not replace the histopathologic classification but, by drawing attention to the molecular genetic events that play a role in tumor progression, sheds light on new approaches to early detection and treatment.
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              Chlamydial persistence: beyond the biphasic paradigm.

              Richard Hogan, Sarah Mathews, Sanghamitra Mukhopadhyay … (2004)
              Article 0 comments Cited 113 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Infect Dis Obstet Gynecol
                Journal ID (publisher-id): IDOG
                Title: Infectious Diseases in Obstetrics and Gynecology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1064-7449
                ISSN (Electronic): 1098-0997
                Publication date (Print): 2011
                Publication date (Electronic): 28 July 2011
                Volume: 2011
                Electronic Location Identifier: 824627
                Affiliations
                1Department of Clinical Science/Obstetrics & Gynecology, Umeå University, SE-901 87 Umeå, Sweden
                2Department of Medical Biosciences/Pathology, Umeå University, SE-901 87 Umeå, Sweden
                3Public Health and Clinical Medicine, Nutritional Research, Umeå University, SE-901 87 Umeå, Sweden
                4Clinical Research Centre, Örebro University Hospital, SE-701 85 Örebro, Sweden
                5Department of Clinical Microbiology/Virology, Umeå University, SE-901 87 Umeå, Sweden
                Author notes

                Academic Editor: Gregory T. Spear

                Article
                DOI: 10.1155/2011/824627
                PMC ID: 3147007
                PubMed ID: 21811380
                SO-VID: 57246ea2-9320-4d5b-b9a6-506241b09970
                Copyright © Copyright © 2011 Annika Idahl et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 March 2011
                Date revision received : 28 April 2011
                Date accepted : 9 May 2011
                Categories
                Subject: Clinical Study

                ScienceOpen disciplines: Obstetrics & Gynecology
                Data availability:
                ScienceOpen disciplines: Obstetrics & Gynecology

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