Publications by authors named "G Lolli"

Article Synopsis
  • The acetylpyrrole scaffold, a lysine mimic, has been researched for developing bromodomain inhibitors and was tested on cancer cell lines Huh7 and MDA-MB-231, showing cell death at higher concentrations.
  • While assessing various human bromodomains, the acetylpyrrole compounds notably inhibited both BRPF1 and BET bromodomains, leading to distinct cellular effects.
  • The study involved structural analysis of BRD4 and BRPF1 bromodomains engaged with acetylpyrrole-thiazole compounds, revealing similar binding interactions but different orientations in their acetyl-lysine pockets.
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Epitranscriptomic mRNA modifications affect gene expression, with their altered balance detected in various cancers. YTHDF proteins contain the YTH reader domain recognizing the mA mark on mRNA and represent valuable drug targets. Crystallographic structures have been determined for all three family members; however, discrepancies are present in the organization of the mA-binding pocket.

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Article Synopsis
  • The COVID-19 pandemic significantly affected cancer care and management of diffuse large B-cell lymphoma (DLBCL), prompting a study comparing patient outcomes during the pandemic to the previous year.
  • Data showed an increase in DLBCL diagnoses during the pandemic (60 vs. 29 in Italy and 54 vs. 39 in Israel), with trends indicating older patient ages and longer diagnosis times.
  • Despite consistent treatment intensity, progression-free survival was slightly worse during the pandemic (64.9% vs. 70.6%), mainly linked to patient characteristics rather than changes in treatment protocol.
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53BP1 acts at the crossroads between DNA repair and p53-mediated stress response. With its interactors p53 and USP28, it is part of the mitotic surveillance (or mitotic stopwatch) pathway (MSP), a sensor that monitors the duration of cell division, promoting p53-dependent cell cycle arrest when a critical time threshold is surpassed. Here, we show that Polo-like kinase 1 (PLK1) activity is essential for the time-dependent release of 53BP1 from kinetochores.

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BAZ2A promotes migration and invasion in prostate cancer. Two chemical probes, the specific BAZ2-ICR, and the BAZ2/BRD9 cross-reactive GSK2801, interfere with the recognition of acetylated lysines in histones by the bromodomains of BAZ2A and of its BAZ2B paralog. The two chemical probes were tested in prostate cancer cell lines with opposite androgen susceptibility.

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