TP53BP1 (Tumor Protein P53 Binding Protein 1)

These findings suggest that while ERCC6 safeguards transcriptional continuity during RS, its activity is associated with a biased retention of stress-induced mutations within coding regions in the surviving cell population. These findings reveal a previously unrecognized link between transcription-coupled repair and mutation distribution in human cells, linking TC-NER to context-dependent somatic evolution and tumor heterogeneity.

These findings highlight a central role for CXCR2-mediated signaling in the development of radioresistance in HPV-negative HNSCC cells.

This study confirmed that RHPN1-AS1 expression inhibits the radiosensitivity of NPC cells. RHPN1-AS1 may affect NPC radiotherapy sensitivity by targeting CELF2 to regulate the MAPK pathway.

Our findings further revealed previously uncharacterized somatic copy number alterations, extrachromosomal DNA landscape, and human-HPV fusion peptides, with implications for genetic heterogeneity and therapeutic targets. This study enhances the understanding of cervical cancer through deeper proteogenomic insights, and facilitates the development of personalized therapeutic strategies to improve patient outcomes.

Cytogenetic analysis revealed inhibition of chromosome break repair and visible chromatin decondensation, suggesting that condensins function to maintain an appropriate chromatin state for efficient DSB repair in G2-phase. These results identify for the first time condensins as G2 phase-specific regulators of genome stability by fine-tuning HR and other resection-dependent DSB repair pathways.

The WTAP/TP53BP1 axis impairs periodontal tissue regeneration by promoting P-PDLSC senescence and suppressing osteogenic differentiation in an m6A-dependent manner, revealing a new cellular-level target for treating periodontitis.

These alterations correlate with topologically more variable DSB sites, slower (more challenging) repair focus formation but faster repair once foci are established, compared to NHDF cells. More disorganized repair and persistent topological alterations likely contribute to genetic instability of cancer cells after irradiation and the development of radioresistant clones, posing challenges for effective radiotherapy.

PARP inhibition with olaparib increased residual γH2AX/53BP1 foci post-irradiation in ERG+ cells, indicating enhanced radiosensitization...These findings suggest that ERG expression promotes dependency on PARP1-EJ, rendering ERG+ PCa more susceptible to PARP inhibition. Combining PARP inhibitors with RT may offer a tumor-selective radiosensitization for ERG+ PCa patients.

Our findings reveal differential toxicological and chemical profiles for nicotine and 6-MN aerosols; however, flavorings may confer similar cytotoxicity, as measured by LDH and metabolic activity, in 6-MN formulations as they do in those with nicotine. Thus, 6-MN is not a "safer" nicotine alternative.

Moreover, H3.3-specific post translational modifications, particularly K36 tri-methylation, play a key role in these processes. Altogether, these findings indicate that DAXX and H3.3 mutations may contribute to tumorigenesis-enhancing genome instability.

Clinical studies have linked levothyroxine therapy with higher Oncotype DX Recurrence Scores in breast cancer (BC), suggesting a potential effect of thyroid hormone signaling on genomic risk...T3 also enhanced proliferation at 10 μM but inhibited growth at higher concentrations. Our findings indicate that acute exposure to T3 induces transient genomic stress, providing a potential mechanistic basis for the observed association between thyroid hormone therapy and increased BC recurrence risk.

In contrast to typical results obtained through photon irradiation, where γH2AX and H3K9me3 markers were well separated, the results obtained here also showed a close spatial proximity ("co-localization") in many cases (minimum distance of markers = marker size), even with the strictest co-localization distance threshold (20 nm) for γH2AX and H3K9me3. The data support the results from the literature where only one DSB induced by low-dose low LET irradiation (<100 mGy) can remain without heterochromatin relaxation for subsequent repair.