BACKGROUND: The stripping technique for endometriomas excision has been reported to be associated with follicular loss. The objective of this trial was to evaluate the presence and nature of ovarian tissue adjacent to the endometrioma cyst wall obtained by stripping with different techniques. METHODS: Forty-eight patients with ovarian endometrioma were enrolled in two consecutive independent randomized trials. Two different techniques were analysed at the initial adhesion site (circular excision and subsequent stripping versus immediate stripping). Two different techniques were analysed at the ovarian hilus (stripping versus coagulation and cutting). Histology analysis was performed in three portions of the cyst wall (initial adhesion site, intermediate part of the specimen, ovarian hilus). RESULTS: Recognizable ovarian tissue was inadvertently excised together with the endometrioma cyst wall in most cases. At initial adhesion sites more ovarian tissue was removed with the circular excision technique (<0.001). No significant difference in quality of ovarian tissue (number and type of follicles) was found between specimens obtained with different surgical techniques at the initial or at the final part of the procedure. At the initial adhesion site and at the intermediate part of the cyst wall, the ovarian tissue removed along with the endometrioma wall was mainly constituted by tissue with no follicles or only primordial follicles (60% and 48% of the specimens from the initial part with both techniques, and from the intermediate part, respectively, had no follicles or only primordial follicles). Close to the ovarian hilus the ovarian tissue removed along with the endometrioma wall mostly consisted of tissue which contained primary and secondary follicles (69% of the cases, combining the two groups). CONCLUSIONS: Ovarian tissue is inadvertently excised together with the endometrioma wall in most cases. The excised tissue is at normal functional development stages only near the ovarian hilus. The different techniques used do not influence significantly the quality of the resected tissue.

Dendritic cells (DCs) sense the microenvironment through several types of receptors recognizing pathogen‐associated molecular patterns. In particular, C‐type lectins, expressed by distinct subsets of DCs, recognize and internalize specific carbohydrate antigen in a Ca²⁺‐dependent manner. Targeting of these receptors is becoming an efficient strategy of delivering antigens in DC‐based anticancer immunotherapy. Here we investigated the role of the macrophage galactose type C‐lectin receptor (MGL), expressed by immature DCs (iDCs), as a molecular target for α‐N‐acetylgalactosamine (GalNAc or Tn)‐carrying tumor‐associated antigens to improve DC performance. MGL expressed by ex vivo‐generated iDCs from healthy donors was engaged by a 60‐mer MUC1_9Tn‐glycopeptide as a Tn‐carrying tumor‐associated antigen, and an anti‐MGL antibody, as a specific MGL binder. We demonstrated that MGL engagement induced homotrimers and homodimers, triggering the phosphorylation of extracellular signal‐regulated kinase 1,2 (ERK1,2) and nuclear factor‐κB activation. Analysis of DC phenotype and function demonstrated that MGL engagement improved DC performance as antigen‐presenting cells, promoting the upregulation of maturation markers, a decrease in phagocytosis, an enhancement of motility, and most importantly an increase in antigen‐specific CD8⁺ T‐cell activation. These results demonstrate that the targeting of MGL receptor on human DCs has an adjuvant effect and that this strategy can be used to design novel anticancer vaccines.

Background: Although exposure to endocrine disruptor compounds (EDCs) has been suggested as a contributing factor to a range of women’s health disorders including infertility, polycystic ovaries and the early onset of puberty, considerable challenges remain in attributing cause and effect on gynaecological cancer. Until recently, there were relatively few epidemiological studies examining the relationship between EDCs and endometrial cancer, however, in the last years the number of these studies has increased. Methods: A systematic MEDLINE (PubMed) search was performed and relevant articles published in the last 23 years (from 1992 to 2016) were selected. Results: Human studies and animal experiments are confirming a carcinogenic effect due to the EDC exposure and its carcinogenesis process result to be complex, multifactorial and long standing, thus, it is extremely difficult to obtain the epidemiological proof of a carcinogenic effect of EDCs for the high number of confusing factors. Conclusions: The carcinogenic effects of endocrine disruptors are plausible, although additional studies are needed to clarify their mechanisms and responsible entities. Neverthless, to reduce endocrine disruptors (ED) exposure is mandatory to implement necessary measures to limit exposure, particularly during those periods of life most vulnerable to the impact of oncogenic environmental causes, such as embryonic period and puberty.