Umeå University's logo

umu.sePublications
Change search
Link to record
Permanent link

Direct link
Lundin, Eva
Publications (10 of 137) Show all publications
Jonsson, S., Jonsson, H., Lundin, E., Häggström, C. & Idahl, A. (2025). Pelvic inflammatory disease and risk of borderline ovarian tumors: a national population-based case–control study in Sweden. International Journal of Cancer, 156(3), 529-537
Open this publication in new window or tab >>Pelvic inflammatory disease and risk of borderline ovarian tumors: a national population-based case–control study in Sweden
Show others...
2025 (English)In: International Journal of Cancer, ISSN 0020-7136, E-ISSN 1097-0215, Vol. 156, no 3, p. 529-537Article in journal (Refereed) Published
Abstract [en]

The resemblance between fallopian tube cells and serous borderline ovarian tumors (BOTs) suggests a potential origin link, with salpingitis proposed as a contributing factor in the pathogenesis of BOT. This study aimed to explore the potential association between pelvic inflammatory disease (PID) and the risk of developing BOT. A national population-based case–control study in Sweden included women with BOT between 1999 and 2020 and 10 matched controls. Data from nationwide registers were analyzed using conditional logistic regression, adjusting for age, residential district, educational level and parity. Among 4782 cases and 45,167 controls, 2.0% of cases and 1.3% of controls had a history of PID. Previous PID was associated with an increased risk of BOT overall (aOR, 1.48; 95% CI, 1.19–1.85). Significant association was observed with serous tumors (aOR, 1.76; 95% CI, 1.36–2.29), while not with mucinous tumors (aOR, 0.95; 95% CI, 0.60–1.49). A dose–response relationship between number of PID episodes and serous BOT risk was noted (Ptrend <.001). This study demonstrates that PID is associated with increased risk of serous BOT, with a dose response relationship. The study highlights the potential serious implications of upper reproductive tract infections and inflammation. This underscores the need for further investigation of biological mechanisms and possible impact of PID on serous BOT development.

Place, publisher, year, edition, pages
John Wiley & Sons, 2025
Keywords
borderline ovarian tumor, pelvic inflammatory disease, population-based case–control study
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-230606 (URN)10.1002/ijc.35180 (DOI)001319832700001 ()39319548 (PubMedID)2-s2.0-85205247420 (Scopus ID)
Funder
Lions Cancerforskningsfond i Norr, LP 23-2343Lions Cancerforskningsfond i Norr, LP 22-2315Lions Cancerforskningsfond i Norr, LP 21-2280Lions Cancerforskningsfond i Norr, LP 20-2233Lions Cancerforskningsfond i Norr, LP 18-2196
Available from: 2024-10-08 Created: 2024-10-08 Last updated: 2025-01-12Bibliographically approved
Björk, E., Israelsson, P., Nagaev, I., Nagaeva, O., Lundin, E., Ottander, U. & Mincheva-Nilsson, L. (2024). Endometriotic tissue-derived exosomes downregulate NKg2D-mediated cytotoxicity and promote apoptosis: mechanisms for survival of ectopic endometrial tissue in endometriosis. Journal of Immunology, 213(5), 567-576
Open this publication in new window or tab >>Endometriotic tissue-derived exosomes downregulate NKg2D-mediated cytotoxicity and promote apoptosis: mechanisms for survival of ectopic endometrial tissue in endometriosis
Show others...
2024 (English)In: Journal of Immunology, ISSN 0022-1767, E-ISSN 1550-6606, Vol. 213, no 5, p. 567-576Article in journal (Refereed) Published
Abstract [en]

Endometriosis, affecting 10% of women, is defined as implantation, survival, and growth of endometrium-like/endometriotic tissue outside the uterine cavity, causing inflammation, infertility, pain, and susceptibility to ovarian cancer. Despite extensive studies, its etiology and pathogenesis are poorly understood and largely unknown. The prevailing view is that the immune system of endometriosis patients fails to clear ectopically disseminated endometrium from retrograde menstruation. Exosomes are small extracellular vesicles that exhibit immunomodulatory properties. We studied the role of endometriotic tissue-secreted exosomes in the pathophysiology of endometriosis. Two exosome-mediated mechanisms known to impair the immune response were investigated: 1) downregulation of NKG2D-mediated cytotoxicity and 2) FasL- and TRAIL-induced apoptosis of activated immune cells. We showed that secreted endometriotic exosomes isolated from supernatants of short-term explant cultures carry the NKG2D ligands MICA/B and ULBP1-3 and the proapoptotic molecules FasL and TRAIL on their surface, i.e., signature molecules of exosome-mediated immune suppression. Acting as decoys, these exosomes downregulate the NKG2D receptor, impair NKG2D-mediated cytotoxicity, and induce apoptosis of activated PBMCs and Jurkat cells through the FasL- and TRAIL pathway. The secreted endometriotic exosomes create an immunosuppressive gradient at the ectopic site, forming a “protective shield” around the endometriotic lesions. This gradient guards the endometriotic lesions against clearance by a cytotoxic attack and creates immunologic privilege by induction of apoptosis in activated immune cells. Taken together, our results provide a plausible, exosome-based mechanistic explanation for the immune dysfunction and the compromised immune surveillance in endometriosis and contribute novel insights into the pathogenesis of this enigmatic disease.

Place, publisher, year, edition, pages
The American Association of Immunologists, 2024
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:umu:diva-229373 (URN)10.4049/jimmunol.2300781 (DOI)001338100000005 ()38984872 (PubMedID)2-s2.0-85201779379 (Scopus ID)
Funder
Swedish Research Council, 18-20-345240311Swedish Cancer Society, 2018/350Region VästernorrlandUmeå UniversityLions Cancerforskningsfond i Norr
Available from: 2024-09-13 Created: 2024-09-13 Last updated: 2025-04-24Bibliographically approved
Björk, E., Israelsson, P., Nagaev, I., Nagaeva, O., Lundin, E. & Ottander, U. (2024). Endometriotic tissue-derived exosomes downregulate NKG2D-mediated cytotoxicity and promote apoptosis: mechanisms for survival of endometriotic tissue at ectopic sites.
Open this publication in new window or tab >>Endometriotic tissue-derived exosomes downregulate NKG2D-mediated cytotoxicity and promote apoptosis: mechanisms for survival of endometriotic tissue at ectopic sites
Show others...
2024 (English)Manuscript (preprint) (Other academic)
Abstract [en]

Endometriosis, affecting 10% of women, is defined as implantation, survival, and growth of endometriumlike/endometriotic tissue outside the uterine cavity, causing inflammation, infertility, pain andsusceptibility to ovarian cancer. Despite extensive studies, its etiology and pathogenesis are poorlyunderstood and largely unknown. The prevailing view is that the immune system of endometriosispatients fails to clear ectopically disseminated endometrium from retrograde menstruation. Exosomes aresmall extracellular vesicles that exhibit immunomodulatory properties. We studied the role ofendometriotic tissue-secreted exosomes in the pathophysiology of endometriosis. Two exosome-mediatedmechanisms known to impair the immune response were investigated: 1) downregulation of NKG2Dmediatedcytotoxicity and 2) FasL- and TRAIL-induced apoptosis of activated immune cells. We showedthat secreted endometriotic exosomes isolated from supernatants of short-term explant cultures carry theNKG2D ligands MICA/B and ULBP1-3; and the proapoptotic molecules FasL and TRAIL on theirsurface, i.e. signature molecules of exosome-mediated immune suppression. Acting as decoys, theseexosomes downregulate the NKG2D receptor, impair NKG2D-mediated cytotoxicity and induce apoptosisof activated PBMC and Jurkat cells through the FasL- and TRAIL pathway. The secreted endometrioticexosomes create an immunosuppressive gradient at the ectopic site, forming a “protective shield” aroundthe endometriotic lesions. This gradient guards the endometriotic lesions against clearance by a cytotoxicattack and creates immunologic privilege by induction of apoptosis in activated immune cells. Takentogether, our results provide a plausible, exosome-based mechanistic explanation for the immunedysfunction and the compromised immune surveillance in endometriosis and contribute with novelinsights into the pathogenesis of this enigmatic disease.

Publisher
p. 82 + 4 papers
Keywords
endometriosis, exosomes, NKG2D receptor, MICA/B, ULBP1-3, FasL, TRAIL
National Category
Gynaecology, Obstetrics and Reproductive Medicine Immunology in the medical area
Research subject
Obstetrics and Gynaecology; Immunology; Pathology
Identifiers
urn:nbn:se:umu:diva-224400 (URN)978-91-8070-409-0 (ISBN)978-91-8070-410-6 (ISBN)
Funder
Swedish Research CouncilSwedish Cancer SocietyRegion VästernorrlandUmeå UniversityLions Cancerforskningsfond i Norr
Available from: 2024-05-16 Created: 2024-05-16 Last updated: 2025-02-11
Jonsson, S., Jonsson, H., Lundin, E., Häggström, C. & Idahl, A. (2024). Pelvic inflammatory disease and risk of epithelial ovarian cancer: a national population-based case-control study in Sweden. American Journal of Obstetrics and Gynecology, 230(1), 75.e1-75.e15
Open this publication in new window or tab >>Pelvic inflammatory disease and risk of epithelial ovarian cancer: a national population-based case-control study in Sweden
Show others...
2024 (English)In: 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) Published
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.

Place, publisher, year, edition, pages
Elsevier, 2024
Keywords
epithelial ovarian cancer, high-grade serous carcinoma, ovarian cancer, pelvic inflammatory disease, population-based case-control study
National Category
Gynaecology, Obstetrics and Reproductive Medicine Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-216205 (URN)10.1016/j.ajog.2023.09.094 (DOI)001146343100001 ()37778677 (PubMedID)2-s2.0-85175294490 (Scopus ID)
Available from: 2023-11-06 Created: 2023-11-06 Last updated: 2025-02-11Bibliographically approved
Israelsson, P., Björk, E., Nagaev, I., Nagaeva, O., Lundin, E., Mincheva-Nilsson, L. & Ottander, U. (2023). NKG2D-mediated cytotoxicity improves after primary surgery for high-grade serous ovarian cancer. American Journal of Reproductive Immunology, 89(1), Article ID e13647.
Open this publication in new window or tab >>NKG2D-mediated cytotoxicity improves after primary surgery for high-grade serous ovarian cancer
Show others...
2023 (English)In: American Journal of Reproductive Immunology, ISSN 1046-7408, E-ISSN 1600-0897, Vol. 89, no 1, article id e13647Article in journal (Refereed) Published
Abstract [en]

Problem: Tumors compromise the patients’ immune system to promote their own survival. We have previously reported that HGSC exosomes play a central role, downregulating NKG2D cytotoxicity. Primary surgery's effect on tumor exosomes and NKG2D cytotoxicity in HGSC patients has not been studied before. The overall objective of this study was to explore the effect of surgery on the exosome-induced impairment of NKG2D cytotoxicity in HGSC.

Method of study: Paired pre- and post-operative blood samples were subjected to cell and exosome analyses regarding the NKG2D receptor and ligands, and NKG2D-mediated cytotoxicity. Lymphocytes were phenotyped by immunoflow cytometry. Exosomes, isolated by ultracentrifugation, and characterized by nanoparticle tracking analysis, transmission and immune electron microscopy and western blot were used in functional cytotoxic experiments. HGSC explant culture-derived exosomes, previously studied by us, were used for comparison.

Results: HGSC exosomes from patients’ sera downregulated NKG2D-mediated cytotoxicity in NK cells of healthy donors. In a subgroup of subjects, NKG2D expression on CTLs and NK cells was upregulated after surgery, correlating to a decrease in the concentration of exosomes in postoperative sera. An overall significantly improved NKG2D-mediated cytotoxic response of the HGSC patients’ own NK cells in postoperative compared to preoperative samples was noted.

Conclusions: Surgical removal of the primary tumor has a beneficial effect, relieving the exosome-mediated suppression of NKG2D cytotoxicity in HGSC patients, thus boostering their ability to combat cancer.

Place, publisher, year, edition, pages
John Wiley & Sons, 2023
Keywords
cytotoxicity, EOC/HGSC, epithelial ovarian cancer, exosomes, immune suppression, NKG2D, NKG2D ligands, surgery
National Category
Immunology in the medical area
Identifiers
urn:nbn:se:umu:diva-201334 (URN)10.1111/aji.13647 (DOI)000888859600001 ()36335434 (PubMedID)2-s2.0-85142285991 (Scopus ID)
Funder
Swedish Research Council, 18-20–345240311Swedish Cancer Society, CAN 2018/350, no. 18 07 17
Available from: 2022-12-15 Created: 2022-12-15 Last updated: 2024-11-18Bibliographically approved
Mukama, T., Fortner, R. T., Katzke, V., Hynes, L. C., Petrera, A., Hauck, S. M., . . . Kaaks, R. (2022). Prospective evaluation of 92 serum protein biomarkers for early detection of ovarian cancer. British Journal of Cancer, 126, 1301-1309
Open this publication in new window or tab >>Prospective evaluation of 92 serum protein biomarkers for early detection of ovarian cancer
Show others...
2022 (English)In: British Journal of Cancer, ISSN 0007-0920, E-ISSN 1532-1827, Vol. 126, p. 1301-1309Article in journal (Refereed) Published
Abstract [en]

Background: CA125 is the best available yet insufficiently sensitive biomarker for early detection of ovarian cancer. There is a need to identify novel biomarkers, which individually or in combination with CA125 can achieve adequate sensitivity and specificity for the detection of earlier-stage ovarian cancer.

Methods: In the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, we measured serum levels of 92 preselected proteins for 91 women who had blood sampled ≤18 months prior to ovarian cancer diagnosis, and 182 matched controls. We evaluated the discriminatory performance of the proteins as potential early diagnostic biomarkers of ovarian cancer.

Results: Nine of the 92 markers; CA125, HE4, FOLR1, KLK11, WISP1, MDK, CXCL13, MSLN and ADAM8 showed an area under the ROC curve (AUC) of ≥0.70 for discriminating between women diagnosed with ovarian cancer and women who remained cancer-free. All, except ADAM8, had shown at least equal discrimination in previous case-control comparisons. The discrimination of the biomarkers, however, was low for the lag-time of >9–18 months and paired combinations of CA125 with any of the 8 markers did not improve discrimination compared to CA125 alone.

Conclusion: Using pre-diagnostic serum samples, this study identified markers with good discrimination for the lag-time of 0–9 months. However, the discrimination was low in blood samples collected more than 9 months prior to diagnosis, and none of the markers showed major improvement in discrimination when added to CA125.

Place, publisher, year, edition, pages
Springer Nature, 2022
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-191667 (URN)10.1038/s41416-021-01697-z (DOI)000742583500001 ()35031764 (PubMedID)2-s2.0-85122722777 (Scopus ID)
Available from: 2022-01-21 Created: 2022-01-21 Last updated: 2022-07-15Bibliographically approved
Patthey, A., Boman, K., Tavelin, B., Lindquist, D., Lundin, E. & Hultdin, M. (2021). Combination of aneuploidy and high S-phase fraction indicates increased risk of relapse in stage I endometrioid endometrial carcinoma. Acta Oncologica, 60(9), 1218-1224
Open this publication in new window or tab >>Combination of aneuploidy and high S-phase fraction indicates increased risk of relapse in stage I endometrioid endometrial carcinoma
Show others...
2021 (English)In: Acta Oncologica, ISSN 0284-186X, E-ISSN 1651-226X, Vol. 60, no 9, p. 1218-1224Article in journal (Refereed) Published
Abstract [en]

INTRODUCTION: Endometrioid endometrial carcinoma is a cancer type with generally excellent prognosis when diagnosed at an early stage, but there is a subset of patients with relapsing disease in spite of early diagnosis and surgical treatment. There is a need to find prognostic markers to identify these patients with increased risk of relapse. Depth of myometrial invasion, histological grade, and presence of lymphovascular invasion are known risk factors. DNA content (ploidy) and proliferation measured as S-phase fraction (SPF) have been discussed as prognostic markers but need additional evaluation.

MATERIAL AND METHODS: We evaluated relapse-free survival (RFS) with respect to ploidy and SPF, which was analyzed by flow cytometry on fresh tumor tissue, in a cohort of 1001 women treated for stage I endometrioid endometrial carcinoma in northern Sweden during the period of 1993-2010, with a median follow up time of 12.0 years. Data were obtained from historical records.

RESULTS: In simple analysis, both aneuploidy and high SPF were associated to increased risk of relapse with hazard ratios (HR) 2.37 (95% CI 1.52-3.70) and 1.94 (95% CI 1.24-3.02), respectively. Our data also confirmed stage, tumor grade, and ploidy as independent prognostic markers in an age adjusted cox regression multivariable analysis but we did not find SPF to contribute to prognosis. However, the combination of aneuploidy and high SPF identified a group of patients with increased risk of relapse, HR 2.02 (95% CI 1.19-3.44).

CONCLUSION: In this study, which is the largest study of ploidy and SPF in stage I endometrioid endometrial carcinoma using fresh frozen tissue, aneuploidy was shown to be an independent prognostic marker. Furthermore, the combination of aneuploidy and high SPF could be used to identify patients with increased risk of relapse.

Place, publisher, year, edition, pages
Taylor & Francis Group, 2021
Keywords
Endometrioid Endometrial Carcinoma, Ploidy, Prognosis, S-phase fraction
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-185073 (URN)10.1080/0284186X.2021.1939146 (DOI)000665673800001 ()34156893 (PubMedID)2-s2.0-85108629114 (Scopus ID)
Funder
Region Västerbotten
Available from: 2021-06-23 Created: 2021-06-23 Last updated: 2023-03-24Bibliographically approved
Hathaway, C. A., Rice, M. S., Townsend, M. K., Hankinson, S. E., Arslan, A. A., Buring, J. E., . . . Tworoger, S. S. (2021). Prolactin and risk of epithelial ovarian cancer. Cancer Epidemiology, Biomarkers and Prevention, 30(9), 1652-1659
Open this publication in new window or tab >>Prolactin and risk of epithelial ovarian cancer
Show others...
2021 (English)In: Cancer Epidemiology, Biomarkers and Prevention, ISSN 1055-9965, E-ISSN 1538-7755, Vol. 30, no 9, p. 1652-1659Article in journal (Refereed) Published
Abstract [en]

Background: Prolactin is synthesized in the ovaries and may play a role in ovarian cancer etiology. One prior prospective study observed a suggestive positive association between prolactin levels and risk of ovarian cancer.

Methods: Weconducted a pooled case-control study of 703 cases and 864 matched controls nested within five prospective cohorts. We used unconditional logistic regression to calculate adjusted odds ratios (OR) and 95% confidence intervals (CI) for the association between prolactin and ovarian cancer risk. We examined heterogeneity by menopausal status at blood collection, body mass index (BMI), age, and histotype.

Results: Among women with known menopausal status, we observed a positive trend in the association between prolactin and ovarian cancer risk (Ptrend = 0.045; OR, quartile 4 vs. 1 = 1.34; 95% CI = 0.97–1.85), but no significant association was observed for premenopausal or postmenopausal women individually (corresponding OR = 1.38; 95% CI = 0.74–2.58; Ptrend = 0.32 and OR = 1.41; 95% CI = 0.93–2.13; Ptrend = 0.08, respectively; Pheterogeneity = 0.91). In stratified analyses, we observed a positive association between prolactin and risk for women with BMI ≥ 25 kg/m2, but not BMI < 25 kg/m2 (corresponding OR = 2.68; 95% CI = 1.56–4.59; Ptrend < 0.01 and OR = 0.90; 95% CI = 0.58–1.40; Ptrend = 0.98, respectively; Pheterogeneity < 0.01). Associations did not vary by age, postmenopausal hormone therapy use, histotype, or time between blood draw and diagnosis.

Conclusions: We found a trend between higher prolactin levels and increased ovarian cancer risk, especially among women with a BMI ≥ 25 kg/m2.

Impact: This work supports a previous study linking higher prolactin with ovarian carcinogenesis in a high adiposity setting. Future work is needed to understand the mechanism underlying this association.

Place, publisher, year, edition, pages
American Association for Cancer Research (AACR), 2021
National Category
Cancer and Oncology Public Health, Global Health and Social Medicine
Identifiers
urn:nbn:se:umu:diva-187455 (URN)10.1158/1055-9965.EPI-21-0139 (DOI)000696386200009 ()34244157 (PubMedID)2-s2.0-85114143616 (Scopus ID)
Funder
Region VästerbottenNIH (National Institute of Health), CA047988, CA182913, HL043851, HL080467, HL099355, P01 CA87969, P30 CA016087, P30 ES000260, R01 CA49449, R01 CA67262, U01 CA176726, U01 CA186107, UM1 CA182934, VR 2017–00650KSwedish Research Council
Available from: 2021-09-13 Created: 2021-09-13 Last updated: 2025-02-20Bibliographically approved
Razumova, Z., Oda, H., Govorov, I., Lundin, E., Östensson, E., Lindquist, D. & Mints, M. (2021). The prognostic role of lrig proteins in endometrial cancer. Cancers, 13(6), 1-12, Article ID 1361.
Open this publication in new window or tab >>The prognostic role of lrig proteins in endometrial cancer
Show others...
2021 (English)In: Cancers, ISSN 2072-6694, Vol. 13, no 6, p. 1-12, article id 1361Article in journal (Refereed) Published
Abstract [en]

Endometrial cancer (EC) is the most common gynecologic malignancy in Sweden and it has various prognostic factors. The LRIG family is a group of three integral surface proteins with a similar domain organization. The study aimed to explore LRIG family as prognostic factor proteins in EC. The initial study cohort included 100 women with EC who were treated at the Department of Women’s and Children’s Health, Karolinska University Hospital Solna, between 2007 and 2012. We assessed the associations between LRIG protein expression and type, grade, and stage of EC, as well as progression‐free and overall survival. Immunohistochemistry results revealed that most women in the analytical sample had >50% LRIG1‐, LRIG2‐ and LRIG3‐positive cells. A statistically significant association was observed between having a high number of LRIG3‐positive cells and superior overall survival (incidence rate ratio = 0.977; 95% confidence interval: 0.958–0.996, p = 0.019). Moreover, positive LRIG3 staining of the cell membrane was associated with reducing in the risk of death (hazard ratio = 0.23; 95% confidence interval: 0.09–0.57). Our results show that LRIG3 expression might be a prognostic factor in EC. The role of LRIG1 and LRIG2 expression remains to be further investigated.

Place, publisher, year, edition, pages
MDPI, 2021
Keywords
Endometrial cancer, LRIG1, LRIG2, LRIG3, Prognosis
National Category
Cancer and Oncology
Identifiers
urn:nbn:se:umu:diva-181783 (URN)10.3390/cancers13061361 (DOI)000634344300001 ()2-s2.0-85102558250 (Scopus ID)
Funder
Cancerforskningsfonden i Norrland
Available from: 2021-04-01 Created: 2021-04-01 Last updated: 2023-10-04Bibliographically approved
Jonsson, S., Lundin, E., Elgh, F., Ottander, U. & Idahl, A. (2020). Chlamydia trachomatis and Anti-MUC1 Serology and Subsequent Risk of High-Grade Serous Ovarian Cancer: A Population-Based Case-Control Study in Northern Sweden. Translational Oncology, 13(1), 86-91
Open this publication in new window or tab >>Chlamydia trachomatis and Anti-MUC1 Serology and Subsequent Risk of High-Grade Serous Ovarian Cancer: A Population-Based Case-Control Study in Northern Sweden
Show others...
2020 (English)In: Translational Oncology, ISSN 1944-7124, E-ISSN 1936-5233, Vol. 13, no 1, p. 86-91Article in journal (Refereed) Published
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.

Place, publisher, year, edition, pages
Elsevier, 2020
National Category
Gynaecology, Obstetrics and Reproductive Medicine
Identifiers
urn:nbn:se:umu:diva-174272 (URN)10.1016/j.tranon.2019.09.007 (DOI)000502822300010 ()31805519 (PubMedID)2-s2.0-85075720208 (Scopus ID)
Available from: 2020-08-19 Created: 2020-08-19 Last updated: 2025-02-11Bibliographically approved
Organisations

Search in DiVA

Show all publications