Mitochondria are semi-autonomous organelles of eukaryotic cells. They perform crucial functions such as generating most of the cellular energy through the oxidative phosphorylation (OXPHOS) system and some other metabolic processes. In addition, mitochondria are involved in regulation of cell death and reactive oxygen species (ROS) generation. Also, mitochondria play important roles in carcinogenesis via altering energy metabolism, resistance to apoptosis, increase of production of ROS and mtDNA (mitochondrial genome) changes. Studies have suggested that aerobic glycolysis is high in malignant tumors. Probably, it correlates with high glucose intake of cancerous tissues. This observation is contrary to Warburg's theory that the main way of energy generation in cancer cells is non-oxidative glycolysis. Further studies have suggested that in tumor cells both oxidative phosphorylation and glycolysis were active at various rates.An increase of intracellular oxidative stress induces damage of cellular structure and somatic mutations. Further studies confirmed that permanent activity of oxidative stress and the influence of chronic inflammation damage the healthy neighboring epithelium and may lead to carcinogenesis. For instance, chronic inflammatory bowel disease could be related to high risk of colon adenocarcinoma.The data have shown a role of ROS generation, mtDNA or nDNA alterations and abnormal apoptotic machinery in endometrial cancer progress. Recent studies suggest that mtDNA mutations might play a potential role in endometrial cancer progress and indicate an increase of mitochondrial biogenesis in this cancer. The investigators suggested that MtCOI and MtND6 alteration has an influence on assembly of respiratory complexes in endometrial cancer.In many human cancers, there is a deregulation of the balance between cell growth and death. The tumor cells can avoid apoptosis through a loss of balance between anti- and pro-apoptotic proteins, reduced caspase function and impaired death receptor signaling. Over-expression of the anti-apoptotic BCL-2 gene has also been identified in numerous cancers including colon, thyroid, breast and endometrial cancer. Most studies have found low BCL-2 family gene expression, which could be a sign of blocking apoptosis in breast and endometrial cancer. Moreover, BCL-2 gene expression is correlated with the degree of aggressiveness and differentiation in endometrial cancer. As a result, it could be a valuable predictor of disease progression.
Objective:To determine the long-term impact of laparoscopic cystectomy for endometriomas and benign cysts on ovarian reserve and selection of the most effective method of assessment. Methods:The present study was carried out between November 2013 and December 2016. Participants were assigned to laparoscopic cystectomy for diagnosed unilateral benign ovarian cysts and divided into groups: the endometrioma group (EG) (n=35) and the other benign ovarian tumor group (OG) (n=35). Before and at 3 and 12 months after the procedure, transvaginal ultrasonography was performed to assess antral follicle count (AFC) and ovarian volume (OvVol); laboratory tests were ordered for anti-Műllerian hormone (AMH) serum concentration assays. Pregnancy rates were counted in a 12-month follow-up. Statistica12 software was used for analysis. Results:The present study included 70 women aged 18-40 years. AMH serum concentration decreased significantly 3 months after laparoscopic cystectomy (4.89 ± 3.66 ng/mL to 3.45 ± 3.37 ng/mL; P<0.001). A greater decrease of AMH concentrations was observed in the EG (45.39% vs 14.87%; P=0.021). Twelve months of observation revealed a suppression in the drop of the AMH concentration, while AFC and OvVol remained unaffected. The likelihood of spontaneous pregnancy was three times higher in the OG (hazard ratio [HR] 3.57, 95% confidence interval [CI] 1.08-12.5). Conclusion:There was a significant decline in AMH levels in the EG 3 months after cystectomy. No further fall in AMH concentration was observed in the 12-month follow-up. The serum AMH concentration could be considered a valuable marker for ovarian reserve assessment after laparoscopic cystectomy. K E Y W O R D S
Leiomyomatosis peritonealis disseminata is a very rare, benign entity of unknown pathogenesis, characterized by the presence of multiple subperitoneal or peritoneal smooth muscle nodules throughout the peritoneal surface. Mostly the course is asymptomatic and it is found incidentally during laparotomy, laparoscopy or cesarean section. Non-specific symptoms such as abdominal pain, vaginal bleeding, abdominal mass or gastrointestinal signs are described. Rare cases of malignant transformation have been reported. We present a case of disseminated peritoneal leiomyomatosis with an unusual course and transformation to endometrial sarcoma in a 26-year-old previously healthy woman, where the appearance of peritoneal nodules was preceded by multiple incidents of fast fibroid growth and delivery of myomatous growth into the cervical canal.
Endometrial cancer is the most common malignancy within the female reproductive system (37.7%). The incidence increases with age. Frequently this type of cancer is diagnosed in peri- and post-menopausal women. 60-70% of cancers occur in women over 60 years of age, and less than 5% in women below 40 years of age.Angiogenesis is a process of formation of new microvessels from existing capillaries. There are four different mechanisms of new vessel growth: sprouting, intussusception, vessel elongation and incorporation of endothelial progenitor cells into new microvessels. Angiogenesis plays important roles in growth of endometrial cancers. This process is controlled by many angiogenic factors, for example vascular endothelial growth factor (VEGF). VEGF is the most powerful and most specific endothelial cell growth factor. It plays a crucial role in the initiation of physiological and pathological angiogenesis, lymphangiogenesis, and vasculogenesis. The VEGF family consists of VEGF-A, VEGF-B, VEGF-C, VEGF-D, VEGF-E, VEGF-F and PLGF (placental growth factor). The effects of VEGF are mediated through binding to the two specific and homologous receptors VEGFR-1 (FLT-1) and VEGFR-2 (KDR). Placental growth factor (PLGF) belongs to the VEGF family and it is also a very important growth factor. So far four isoforms of PLGF have been identified: PLGF-1 (PLGF131), PLGF-2 (PLGF152), PLGF-3 (PLGF203) and PLGF-4 (PLGF224).
Endometrial cancer is one of the most common cancers experienced by women throughout the world. It is also the most common malignancy within the female reproductive system, representing 37.7% of all disorders. The incidence increases with age, and is diagnosed most frequently in women between 45 and 65 years old. In the last few years, numerous studies have been performed to identify tumour biomarkers. Biomarkers include not only protein routinely used as tumour markers but also genes and chromosomes. The limiting factor in the use of markers in the diagnosis of endometrial cancer is their lack of specificity. However, specific markers for endometrial cancer are the subject of much research attention. Although moderately elevated levels of markers are present in a number of inflammatory or non-malignant diseases, significantly increased levels of markers indicate the development of cancer. Recently, research has been focused on the identification of molecular changes leading to different histological subtypes of endometrial cancer. In this paper the authors reviewed several currently investigated markers. Progress in these investigations is very important in the diagnostics and treatment of endometrial cancer. In particular, the identification of novel mutations and molecular profiles should enhance our ability to personalise adjuvant treatment with genome-guided targeted therapy.
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