The aim of this review is to clarify the relative association between adenomyosis and infertility and the possible treatment for an infertile patient. Although adenomyosis is detected more often in women of late reproductive age, its influence on pregnancy rates is important, especially considering the tendency to delay pregnancy among women in developed countries. In this article, we present a critical analysis of the literature data concerning the impact of adenomyosis on fertility. The possible effects of treatment on the pregnancy rate will also be discussed. We conducted a literature search; publications from Pubmed, Embase and Cochrane databases published from 1982 to 2019 were retrieved using terms ’adenomyosis and infertility’ and ’adenomyosis and pregnancy outcomes’, extensively studied in the aspects of diagnosis, pathogenesis of infertility and possible treatment methods. Molecular studies have given deep insight into the pathogenesis of adenomyosis in the recent few years, but there is a huge discrepancy between in vitro studies and praxis. Oral contraceptive pills, anti-prostaglandins, oral or parenteral progestins, danazol and gonadotrophin-releasing hormone (GnRH) analogues have all been used to control menstrual pain and menorrhagia in women with adenomyosis, but they temporarily suppress the menstrual cycle. Additionally, endometrial ablation and hysterectomy used to alleviate pain caused by adenomyosis exclude pregnancy planning. The development of imaging techniques—ultrasound and MRI—enables the diagnosis of adenomyosis with very high accuracy nowadays, but the methods of treatment mentioned above have not given satisfactory results in women planning pregnancy. For these patients, the high-intensity-focused ultrasound method (HIFU) and combined treatment before assisted reproductive techniques can prove beneficial in adenomyosis patients.

Background and Objectives: Uterine fibroids develop in 25–40% of women of childbearing age; however, there are discrepancies resulting from population and socioeconomic differences. The pathogenesis of fibroids is not clear. The aim of the study was to assess the potential connection between the use of oral contraceptives and the occurrence of uterine fibroids in women of childbearing age. Materials and Methods: In this prospective, survey, case–control study, data were collected from Caucasian female patients (mean age = 30) using a questionnaire concerning the onset, duration and form of hormonal contraception, and medical and obstetrical history. The questionnaires were handed personally to hospitalized patients as well as distributed through Google forms on social media. Results: In a study group (n = 140) of patients using hormonal contraception, 37.8% of them were diagnosed with uterine fibroids, whereas among the patients not using hormonal contraception (n = 206), uterine fibroids were diagnosed in 59.6% of the patients. The most common hormonal contraception was two-component hormonal tablets used by 93.3% of the patients. Taking contraceptives was a uterine fibroids protective factor (OR = 0.4, p = 0.007). In the study group, 5.5% of the patients were pregnant and 60.42% were diagnosed with uterine fibroids (OR = 4.4, p < 0.000001). Conclusion: Contraception was found to be a protective factor for uterine fibroids among the women surveyed. The presented data confirm the theory about the hormonal dependence of uterine fibroids.

Adenomyosis is a common benign gynecological condition, defined as an extension of endometrial tissue into the myometrium. Some studies suggest that adenomyosis could be a favorable prediction factor associated with survival outcomes in endometrial cancer. The aim of our systematic review was to investigate the current knowledge regarding adenomyosis and a possible molecular mechanism of carcinogenesis in adenomyotic lesions. In addition, the long-term prognosis for patients with endometrial cancer and coexisting adenomyosis (and endometriosis) was a key point of the research. The current literature was reviewed by searching PubMed, using the following phrases: “adenomyosis and endometrial cancer” and “malignant transformation of adenomyosis”. According to the literature, genetic mutations, epigenetic changes, and inactivation of specific tumor suppressor genes in adenomyosis are still poorly understood. Data regarding the influence of adenomyosis on survival outcomes in endometrial cancer seem to be contradictory and require further clinical and molecular investigation.

Cancer antigen 125 (CA-125), known as a biomarker for women genital tract malignancies, could be also useful in detecting and monitoring endometriosis. The aim of this study was to evaluate CA-125 in serum and peritoneal fluid (PF) as an indicator of endometriosis. Fifty-six patients admitted to the First Department of Obstetrics and Gynaecology for diagnostic or therapeutic laparoscopy conducted for infertility, pelvic pain, suspected endometriosis or ovarian cysts entered the study. Those with laparoscopically confirmed endometriosis were assigned to group A, those without this condition to group B. Blood for CA-125 was taken prior to surgery, centrifuged and assayed in accordance with the manufacturer's instructions (VIDAS CA-125 II). Peritoneal fluid and an endometrial biopsy were taken during laparoscopy. Statistical comparisons were performed using Statistica 7.1. Group A consisted of 44 women with laparoscopically confirmed diagnosis; 15 patients served as a control group. The mean value of CA-125 concentration in the endometriosis group was 33.98 U/ml, vs. 9.3 U/ml in the control group. The mean value of CA-125 in peritoneal fluid was 1241.88 U/ml in the non-endometriosis group versus 2640.23 U/ml in the study group; both results were statistically significant (p < 0.05). There was a significant correlation between the stage of endometriosis and CA-125 plasma concentration (R = 0.5993, p < 0.001). Cancer antigen 125 concentration in serum was a moderate predictor to distinguish between patients with and without endometriosis (AUC 0.794; 95% CI 0.668-0.921; p = 0.001). Cancer antigen 125 is a well-known biomarker for endometriosis and helpful in daily clinical practice when endometriosis is suspected. The cut-off value in serum suggesting endometriosis with 68% sensitivity is 11 U/ml. This value is normal range for Ca-125 concentration.

Long noncoding RNAs (lncRNAs) are RNA molecules exceeding 200 nucleotides that do not encode proteins yet play critical roles in regulating gene expression at multiple levels, such as chromatin modification and transcription. These molecules are significantly engaged in cancer progression, development, metastasis, and chemoresistance. However, the function of lncRNAs in epithelial ovarian cancer (EOC) has not yet been thoroughly studied. EOC remains challenging due to its complex molecular pathogenesis, characterized by genetic and epigenetic alterations. Emerging evidence suggests that lncRNAs, such as XIST, H19, NEAT1, and MALAT1, are involved in EOC by modulating gene expression and signaling pathways, influencing processes like cell proliferation, invasion, migration, and chemoresistance. Despite extensive research, the precise mechanism of acting of lncRNAs in EOC pathogenesis and treatment resistance still needs to be fully understood, highlighting the need for further studies. This review aims to provide an updated overview of the current understanding of lncRNAs in EOC, emphasizing their potential as biomarkers and therapeutic targets. We point out the gaps in the knowledge regarding lncRNAs’ influence on epithelial ovarian cancer (EOC), deliberating on new possible research areas.

Endometriosis is a serious recurrent disease impairing the quality of life and fertility, and being a risk for some histologic types of ovarian cancer defined as endometriosis-associated ovarian cancers (EAOC). The presence of stem cells in the endometriotic foci could account for the proliferative, migrative and angiogenic activity of the lesions. Their phenotype and sources have been described. The similarly disturbed expression of several genes, miRNAs, galectins and chaperones has been observed both in endometriotic lesions and in ovarian or endometrial cancer. The importance of stem cells for nascence and sustain of malignant tumors is commonly appreciated. Although the proposed mechanisms promoting carcinogenesis leading from endometriosis into the EAOC are not completely known, they have been discussed in several articles. However, the role of endometriosis stem cells (ESCs) has not been discussed in this context. Here, we postulate that ESCs may be a main target for the carcinogenesis of EAOC and present the possible sequence of events resulting finally in the development of EAOC.