Adenomyosis is a commonly diagnosed benign condition characterized by the presence of ectopic endometrial glands within the underlying myometrium. The most common presenting signs and symptoms are abnormal uterine bleeding, chronic pelvic pain, and infertility. The clinical relevance of this condition is evident in both medical and surgical care. Histopathology and imaging studies are used for the diagnosis and classification of adenomyosis, which are hallmarks of the advancement of our ability to diagnose adenomyosis. Importantly, the diagnosis and classification of adenomyosis lacks standardization due to the nature of imaging techniques, features of adenomyosis, and the clinical spectrum of adenomyosis. We reviewed the literature to summarize the available classification systems for adenomyosis and highlight the different imaging approaches and histologic criteria used in diagnosis. Despite the high prevalence of the disease, there is no clear consensus on one classification system. We provide a review of some of the classification systems available and discuss their strengths and limitations.

The portion of chromosome 2, including the gene codifying the receptor of FSH (FSHR gene), can display point mutations that cause variations in the amino acid sequence of the receptor protein (FSHR protein). Some of these structural changes affect the receptor functional properties that may be enhanced (activating mutations) or impaired (inactivating mutations). Activating mutations confer to FSHR a higher responsiveness to FSH, making it constitutively active even in the absence of the ligand, or render it able to nonspecifically respond to other tropic hormones (e.g., TSH). Inactivating mutations reduce the receptor's function up to a total block, altering either the formation of the receptor-ligand complex, or FSH signal transduction. FSHR inactivating mutations may cause primary or secondary amenorrhea, infertility, and premature ovarian failure (POF), whereas activating mutations can predispose to ovarian hyperstimulation syndrome (OHSS) as a consequence of exogenous FSH administration, or with a spontaneous onset. Beside point mutations, FSHR gene polymorphisms at specific sites (e.g., codons 307 and 680) may influence FSHR protein responsiveness to exogenous FSH, and finally affect the effectiveness of in vitro fertilization (IVF) treatment as well as the likelihood of developing a severe OHSS as a consequence of superovulation. This review summarizes the current knowledge about the FSHR gene mutations and polymorphisms, illustrating in the first part their clinical consequences for female reproductive function. In the second part, it describes the techniques to study the FSHR gene sequence, and gives more details about the molecular biology of FSHR protein, of FSHR gene and its mutations. Obstetricians & Gynecologists, Family Physicians. After reading this article, the reader should be able to list clinical disorders related to mutations in the follicle stimulating hormone receptor (FSHR) gene, explain the principles behind the study of FSHR mutations, and state possible future applications of knowledge of mutations in the FSHR gene in reproductive medicine.

This prospective study is a 3-year follow-up of patients included in the prospective longitudinal SENTICOL (Ganglion Sentinelle dans le Cancer du Col) study. Objectives The primary outcome was disease-free survival; the secondary outcome was the predictive value of the presence of micrometastasis and isolated tumor cells for recurrence. Methods The study included patients with cervical carcinoma FIGO (International Federation of Gynecology and Obstetrics) stage IA1 with lymphovascular space invasion, stage IA2 and IB1, who participated in the prospective SENTICOL study. A centralized histological analysis with re-reading and ultrastaging was performed 3 months after the interventions; discovery of micrometastasis or isolated tumor cells in the sentinel and non-sentinel lymph nodes did not change the treatment that was previously planned. Patients were followed up after 3 years. Results were compared according to prognostic factors. Results We found 13 recurrences during the 3-year follow-up: two recurrences in patients with positive sentinel lymph nodes (one macrometastasis and one micrometastasis) and 11 recurrences in patients with negative lymph nodes (sentinel lymph nodes and non-sentinel lymph nodes). There was no statistically significant difference in disease-free survival in terms of prognostic factors in our cohort, except patient age: we found a significant decrease in disease-free survival in patients >50 years old (p=0.01). Among patients with sentinel lymph nodes positive for micrometastasis, only one had a recurrence (negative predictive value 89%). Conclusions Unlike previous retrospective studies, this prospective study showed no impact of micrometastasis or isolated tumor cells in sentinel lymph nodes on disease-free survival. However, due to the relatively short follow-up, some late recurrences may have been missed.

Background: With the development of the sentinel node technique in early-stage cervical cancer, it is imperative to define the clinical significance of micrometastases (MICs) and isolated tumor cells (ITCs). Methods: We included all patients who participated in the Senticol 1 and Senticol 2 studies. We analyzed the factors associated with the presence of low-volume metastasis, the oncological outcomes of patients with MIC and ITC and the correlation of recurrences and risk factors. Results: Twenty-four patients (7.5%) had low-volume metastasis. The risk factors associated with the presence of low-volume metastasis were a higher stage (p = 0.02) and major stromal invasion (p = 0.01) in the univariate analysis. The maximum specificity and sensitivity were found at a cutoff of 8 mm of stromal invasion. In multivariate analysis, the higher stage (p = 0.02) and the positive lymphovascular space invasion (p = 0.02) were significantly associated with the MIC and ITC. Patients with low-volume metastasis had similar disease-free survival (DFS) (92.7%) to node-negative patients (93.6%). The addition of adjuvant treatment in presence of low-volume metastasis did not modify the DFS. Conclusions: These results confirm our previous analysis of Senticol 1: the presence of low-volume metastasis did not decrease the DFS in early-stage cervical cancer patients.