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Abstract: Dysregulation of Maspin expression and constitutive activation of NF-κB subunits are important events in tumorigenesis of prostate cancer. Recent finding points that RelB, which contributes to the alternative NF-κB activity, interferes with carcinogenesis in the prostate. We report here, that both the classical and the alternative NF-κB activities are constitutively present in androgen-insensitive human prostate cancer cells. Maspin and RelB expression is correlated negatively in prostate cancer tissues at the later stage. TNF-α signaling triggers the nuclear accumulation of RelB and the concomitant reduction of Maspin expression in a time-dependent manner. In addition, the proteasome inhibitor-induced Maspin expression is accompanied by the reduction of RelB expression. A successful depletion of RelB expression, but not RelA expression, induces Maspin expression. RelB-deficiency abrogates the proteasome inhibitor-induced Maspin expression. Moreover, we demonstrate that the enforced expression of RelB protein in prostate cancer cells inhibits Maspin expression. We propose that RelB is an essential molecule controlling the endogenous and the proteasome inhibitor-induced Maspin expression. Developing a RelB-targeted therapeutic intervention, which might be coupled with the induction of a tumor suppressor Maspin, is valuable in treating advanced, metastatic prostate cancer. [Copyright &y& Elsevier]

This article discusses a case of pseudomyogenic hemangioendothelioma (PHE), a type of vascular tumor, with a specific gene fusion called EGFL7:FOSB. The first case of PHE with this fusion showed widespread metastasis, while the second case presented with a more typical clinical presentation without evidence of distant tumors or metastasis. The article explores the variations in PHE, including tumor size, location, and involvement of different tissues. The authors also discuss the potential role of the EGFL7:FOSB fusion and other genomic alterations in the clinical outcome of PHE, including distant metastasis. [Extracted from the article]

Background Recent studies have identified that exposure to particulate matter during pregnancy could result in adverse birth outcomes, but the effects of exposure at trimester-specific intervals are inconsistent. Objective Our primary goal was to investigate whether particulate matter exposure during pregnancy could affect birth weight and gestational age of neonates. Methods A retrospective cohort study was conducted to examine the relationship between maternal particulate matter exposure and neonatal birth weight. We collected 14,455 births records linked to hospital admission records (delivery and antenatal) from January 2013 to December 2015 in Suzhou Municipal Hospital. Air monitoring data in the same timeframe were also collected from Suzhou Environmental Protection Agency. The risk of low birth weight due to the exposure to PM 2.5 (with median aerodynamic diameter ≤ 2.5 μm) and PM 10 (with median aerodynamic diameter ≤ 10 μm) at each trimester and throughout the entire pregnancy were assessed. Linear regression models were applied and potential confounding factors were adjusted for data analysis. Gestational age, which was another important birth outcome, and its association with maternal particulate matter exposure were also studied. Results The final analysis included 10,915 singleton live births. Using multiple linear regression models, we found that gestational exposure to PM 2.5 and PM 10 at 10 μg/m 3 increments in the second trimester led to decreases in birth weight of 4.94 g (95% confidence interval: − 9.828, − 0.046) and 5.65 g (95% confidence interval: − 10.110, − 1.188), respectively. However, gestational age was not significantly associated with maternal particulate matter exposure in term neonates. Conclusion These findings indicate that pregnant women might be more susceptible to particulate matter during the second trimester which may lead to decreased neonatal birth weight. [ABSTRACT FROM AUTHOR]