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Interstitial cystitis and bladder pain syndrome are essentially interchangeable as there is no accepted definition that clearly delineates the interstitial cystitis syndrome from bladder pain syndrome. IC/BPS is generally agreed to be defined as chronic pelvic pain, pressure, or discomfort perceived to be related to the urinary bladder when accompanied by at least one other urinary symptom such as persistent urge to void or urinary frequency when in the absence of confusable diseases. The Consultation believes that patients who meet the definition and have a Hunner lesion should be considered to have a distinct confusable disease (Hunner lesion disease — HLD) and be managed accordingly. It follows that early cystoscopy is essential in establishing whether the diagnosis is HLD or IC/BPS. As no single treatment works well over time for a majority of patients, the treatment approach should be tailored to the specific symptoms of each patient and a multidisciplinary approach may be required. A reasonable diagnostic and treatment algorithm is offered by the Consultation. For methodology and the complete report of the committee with complete references, please refer to the 7th edition of the International Consultation on Urological Diseases Incontinence.

Regeneration of the endometrial stromal compartment in premenopausal women is likely maintained by the perivascular endometrial mesenchymal stem/stromal cells (eMSC) expressing sushi domain containing 2 (SUSD2). The fate of SUSD2+ eMSC during pregnancy and their role in decidualization is not fully known. The aim of our study was to determine the effect of progesterone on the stemness of the SUSD2+ eMSC isolated from non-pregnant uterine samples. Secondary objectives were to characterize the functional capacity including differentiation and clonogenicity assays of SUSD2+ eMSC isolated from decidua at full term and compare it to the capacity of those isolated from non-pregnant uterine samples. Progesterone treatment induced changes in the decidual gene expression profile in non-pregnant SUSD2+ eMSC. Data analysis of a publicly available single cell RNA-seq data set revealed differential expression of several mesenchymal and epithelial signature genes between the SUSD2+ eMSC and the decidual stromal cells, suggesting mesenchymal-to-epithelial transition occurs during decidualization. Histological analysis revealed a significantly lower abundance of SUSD2+ eMSC in 1st trimester and full term samples compared to non-pregnant samples, p = 0.0296 and 0.005, respectively. The differentiation and the colony forming capacity did not differ significantly between the cells isolated from non-pregnant and pregnant uterine samples. Our results suggest that SUSD2+ eMSC undergo decidualization in vitro, while maintaining MSC plasma membrane phenotype. Human eMSC seem to play an important role in the course of endometrial decidualization and embryo implantation. Pregnancy reduced the abundance of SUSD2+ eMSC, however eMSC function remains intact.

Placenta-specific trophoblast and tumor cells exhibit many common characteristics. Trophoblast cells invade maternal tissues while being tolerated by the maternal immune system. Similarly, tumor cells can invade surrounding tissues and escape the immune system. Importantly, both trophoblast and tumor cells are supported by an abetting microenvironment, which influences invasion, angiogenesis, and immune tolerance/evasion, among others. However, in contrast to tumor cells, the metabolic, proliferative, migrative, and invasive states of trophoblast cells are under tight regulatory control. In this review, we provide an overview of similarities and dissimilarities in regulatory processes that drive trophoblast and tumor cell fate, particularly focusing on the role of the abetting microenvironments.