Increased translation driven by non-canonical EZH2 creates a synthetic vulnerability in enzalutamide-resistant prostate cancer.

Overcoming resistance to therapy is a major challenge in castration-resistant prostate cancer (CRPC). Lineage plasticity towards a neuroendocrine phenotype enables CRPC to adapt and survive targeted therapies. However, the molecular mechanisms of epigenetic reprogramming during this process are still poorly understood.

An in-vitro study on accuracy of modular templates used to fully guide implants in combination with bone reduction for complete arch restorations: Experts versus students.

Objectives: This in-vitro study evaluates the accuracy of modular surgical templates used to fully guide implants in combination with bone reduction, performed by expert and students, for complete arch restorations.

Methods: All the procedures were performed by dental students of the final year and an expert clinician, on twelve edentulous mandible models. A virtual implant planning, simulating a complete arch restoration on six implants were performed.

Biomonitoring of persistent pollutants in grey seal (Halichoerus seagrypus) pups from the Gulf of Riga, Baltic Sea.

We analyzed for the first time the concentration of potentially toxic trace elements Hg, As, Pb, Cr and Se and POPs (PCBs and OCPs) in tissues of 41 grey seal pups (Halichoerus grypus) stranded on the shores of the Gulf of Riga. Lanugo was the sample with the highest concentrations of all trace elements except Hg. The concentrations found in this biological matrix appeared as follows: Hg (2.

Opposing regulation of the STING pathway in hepatic stellate cells by NBR1 and p62 determines the progression of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) emerges from chronic inflammation, to which activation of hepatic stellate cells (HSCs) contributes by shaping a pro-tumorigenic microenvironment. Key to this process is p62, whose inactivation leads to enhanced hepatocarcinogenesis. Here, we show that p62 activates the interferon (IFN) cascade by promoting STING ubiquitination by tripartite motif protein 32 (TRIM32) in HSCs.

FBXO32-mediated degradation of PTEN promotes lung adenocarcinoma progression.

FBXO32, a member of the F-box protein family, is known to play both oncogenic and tumor-suppressive roles in different cancers. However, the functions and the molecular mechanisms regulated by FBXO32 in lung adenocarcinoma (LUAD) remain unclear. Here, we report that FBXO32 is overexpressed in LUAD compared with normal lung tissues, and high expression of FBXO32 correlates with poor prognosis in LUAD patients.