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For nearly a century, fundamental observations that prostate cancer (PCa) cells nearly always require AR stimulation for sustained proliferation have led to a unidirectional quest to abrogate such a pathway. Similarly focused have been efforts to understand AR-driven processes in the context of elevated expression of its target genes, and much less so on products that become overexpressed when AR signaling is suppressed. Treatment with ARSI results in an increased expression of the TLK1B splice variant via a 'translational' derepression driven by the compensatory mTOR activation and consequent activation of the TLK1 > NEK1 > ATR > Chk1 and NEK1 > YAP axes.

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Lung cancer continues to be the second most common cancer diagnosed and the main cause of cancer-related death globally, which requires novel and effective treatment strategies. When considering treatment options, non-small cell lung cancer (NSCLC) remained a challenge, seeking new therapeutic strategies High-power microwave (HPM) progressions have facilitated the advancement of new technologies as well as improvements to those already in use. The impact of HPM on NSCLC has not been investigated before.

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Cells evoke the DNA damage checkpoint (DDC) to inhibit mitosis in the presence of DNA double-strand breaks (DSBs) to allow more time for DNA repair. In budding yeast, a single irreparable DSB is sufficient to activate the DDC and induce cell cycle arrest prior to anaphase for about 12-15 hr, after which cells 'adapt' to the damage by extinguishing the DDC and resuming the cell cycle. While activation of the DNA damage-dependent cell cycle arrest is well understood, how it is maintained remains unclear.

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PrimPol-mediated repriming elicits gap-filling by template switching and promotes cellular tolerance to cidofovir.

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A nucleoside analog, Cidofovir (CDV), is used for the treatment of viral diseases such as cytomegalovirus retinitis and herpes virus infection. CDV converts to its active diphosphate metabolite (CDVpp) through cellular kinases and acts as a competitive inhibitor for viral polymerase thereby interfering with viral replication. However, the effect of this drug on the replication of healthy host cells and the mechanisms involved in the cellular tolerance to CDV are yet to be fully understood.

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