Background: Long noncoding RNAs (lncRNAs) are potential biomarkers that are very important for the development of cancer. Studies show that lncRNAs are significantly correlated with the carcinogenesis and progression of bladder cancer (BLCA). In this research, we aimed at probing into the role of lncRNA MAFG-AS1 in the tumorigenesis of BLCA. Methods: RT-qPCR was employed to detect MAFG-AS1 expression in BLCA tissues and cells. MAFG-AS1 siRNA and overexpression plasmid were transfected into 5637 and T24 BLCA cell lines to inhibit or upregulate MAFG-AS1 expression, respectively, and then the regulatory functions of MAFG-AS1 on BLCA cell proliferation, migration, and invasion were assessed using cell counting kit-8 (CCK-8) assay, EdU method, and Transwell experiments, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation were conducted to validate the targeting relationships between MAFG-AS1 and miR-143-3p, and miR-143-3p and COX-2. In addition, miR-143-3p was repressed in MAFG-AS1-silenced 5637 and T24 cell lines, and the function of MAFG-AS1/miR-143-3p axis in BLCA cells was further evaluated. The regulatory effects of MAFG-AS1 and miR-143-3p on the expression of COX-2 protein were detected by Western blot. Results: MAFG-AS1 was remarkably upregulated in BLCA patient tissues and cell lines, and its high expression was closely related to histological grade, tumor size, and lymph node metastasis. Silencing of MAFG-AS1 inhibited BLCA cell proliferation, metastasis, and invasion, while overexpression of MAFG-AS1 in BLCA cells had opposite biological effects. MAFG-AS1 was proved to target miR-143-3p to repress its expression. Moreover, it was confirmed that MAFG-AS1 and miR-143-3p could modulate COX-2 expression. Conclusion: The MAFG-AS1/miR-143-3p/COX-2 axis contributes to BLCA progression.

Introduction: Calciphylaxis is a condition which involves ectopic deposition of calcium in arterioles of various organ systems. Here, we present a rare case of mammographic calcifications in a patient on long-standing renal dialysis. Case: This is a 57-year-old female who presented to breast clinic with unilateral severe pain and lumpiness of her breast. On mammography, calcifications were identified which were associated with focal lesions on ultrasound. An image-guided core biopsy showed numerous foci of histological calcification within a large area of fat necrosis. The location within arterioles was confirmed by CD31 immunohistochemistry. The diagnosis of fat necrosis with benign calcifications due to mammary calciphylaxis was made. Conclusion: The hallmark of calciphylaxis is the deposition of calcium within small- to medium-sized vessel walls. This leads to ischaemia and necrosis of tissue. In the breast, only a few cases were reported in which patients presented with a necrotic lesion resembling carcinoma. These are reviewed in this report.

Objective: To study the structural and immunohistochemical features of placentas in women after assisted reproductive technology (ART) with allogeneic eggs (oocyte donation and surrogate motherhood). Study Design: The study involved 89 women whose pregnancy occurred as a result of in vitro fertilization (IVF) with a donor egg in a surrogate motherhood program (IVF-SM, n = 47 patients) or oocyte donation (IVF-DO, n = 42). The comparison group consisted of 21 patients in whom pregnancy occurred as a result of IVF with their own egg (IVF-OE). A clinical and anamnestic analysis of the pregnant women was carried out. Morphological and immunohistochemical studies were performed on placental material. Immunohistochemical analysis of CD8, CD56, CD138, and CD25/CD4 markers indicating the processes of impaired tolerance in placenta was carried out. ­Results: We observed a predominance of women aged >40 (range 42.7–3.91) years with a burdened somatic and obstetric-gynecological history and a high incidence of hypertensive pregnancy complications, such as gestational arterial hypertension (27.4%) and preeclampsia (28.5%), in the IVF-DO group. The IVF-SM group included mainly somatically healthy women aged <30 (29.4–3.19) years with a high risk of termination of pregnancy in the third trimester (49.6%) and premature birth (21.6%). Placentas taken from women after allogeneic pregnancy had pronounced signs of immune alteration, such as chronic histiocytic intervillositis, lymphoplasmacytic deciduitis, chronic chorioamnionitis, chronic villitis, and perivillous fibrinoid with lymphocytes (p [F] < 0.05). Immunohistochemical study of the placentas showed accumulation of CD138+ plasma cells, CD8+ T lymphocytes, and uterine natural killer cells, and a decrease in the number of CD25/CD4+ regulatory T cells (Tregs) in the structures of the uteroplacental region (Kruskal-Wallis test, p < 0.05). Conclusion: Placentas after IVF with oocyte donation and surrogate motherhood programs are characterized by similar changes, associated with the development of chronic inflammation in the structures of the placenta and immunohistochemical signs of impaired immunological tolerance at the maternal-fetal interface. The data we obtained allow us to classify pregnancies under surrogate motherhood programs as a risk factor for the development of pregnancy complications with immune pathogenesis.

The fallopian tube is thought to be the site of origin of most high-grade serous carcinomas (HGSCs). However, how often the tube is abnormal in the setting of other ovarian tumors is unknown. The aim of this study is to define the frequency of tubal abnormalities in the tumoral (n = 245) and nontumoral (n = 184) setting. We found that in ovarian tumors, 52.2% of the tubes were normal, while 39.2% were affected by the tumor. Abnormal tubes were found in 80% of HGSCs, in 21% of mucinous carcinomas, in 83.3% of seromucinous carcinomas, in 33.3% of endometrioid carcinomas, in 20% of clear-cell carcinomas, and in 10.5% of borderline tumors. Among normal tubes, almost 70% were histologically normal; transitional metaplasia was present in 17.4%, endometriosis in 8.1%, and adenofibroma in 2.2%, and 1.1% had an incidental serous intraepithelial tubal carcinoma. To conclude, the fallopian tube is abnormal in most serous carcinomas, and in a smaller number of endometrioid, clear-cell and mucinous carcinomas as well as borderline tumors. It is often abnormal in seromucinous tumors, but larger series are needed to study this rare subtype.

Most cases of mastocytosis are indolent, usually cutaneous mastocytosis or indolent systemic mastocytosis (SM). Aggressive mast cell (MC) diseases are very rare and often fatal. They can develop de novo or due to progression of indolent forms and can present in different ways; either as MC sarcoma or as advanced SM which includes aggressive SM, MC leukemia, and SM with an associated hematological neoplasm. This review will describe these different aggressive forms of mastocytosis, illustrated by cases submitted to the workshop of the 18th Meeting of the European Association for Haematopathology, Basel 2016, organized by the European Bone Marrow Working Group. In addition, the diagnostic criteria for identifying myelomastocytic leukemia, an aggressive myeloid neoplasm with partial MC differentiation that falls short of the criteria for SM, and disease progression in patients with established mastocytosis are discussed.

Background: Effective antiretroviral therapy extends the survival of patients with human immunodeficiency virus (HIV)/acquired immune deficiency syndrome, but these patients remain at higher risk for heart diseases compared with the general population. Previous studies have suggested that HIV-1 glycoprotein 120 (gp120) may be associated with heart disease. However, the underlying mechanisms by which HIV-1 gp120-mediated myocardial injury occurs remain unknown. Objective: The current study aimed to uncover the mechanism of C-C chemokine receptor 5 (CCR5) coreceptor (R5) HIV-1 gp120-induced myocardial injury. Methods: Morphology analysis, determination of the percentage of cell apoptosis, as well as lactate dehydrogenase (LDH) and creatine kinase (CK) assays were used to analyze whether R5 HIV-1 gp120 induced myocardial cell injury. We analyzed the phosphorylation of p38 mitogen-activated protein kinase (MAPK) with the CCR5 antagonist D-Ala-peptide T-amide (DAPTA) and NMDA receptor antagonist MK801, detected LDH and CK assays with p38 MAPK antagonist SB203580 (SB), and detected the percentage of cell apoptosis and death with DAPTA to investigate the mechanism of R5 HIV-1 gp120-induced myocardial cell injury. Results: R5 HIV-1 gp120 damaged myocardial cells and induced p38 MAPK phosphorylation. SB blocked R5 HIV-1 gp120-induced myocardial cell injury. DAPTA blocked R5 HIV-1 gp120-mediated p38 MAPK phosphorylation, while MK801 did not. DAPTA inhibited R5 HIV-1 gp120-induced myocardial cell injury. Conclusion: Our data indicate that R5 HIV-1 gp120 activated p38 MAPK to trigger myocardial cell injury by the CCR5 coreceptor.