TP53BP1 (Tumor Protein P53 Binding Protein 1)

These co-regulated proteins highlight the integration of BRAF signaling with critical processes, such as cell cycle control, apoptosis, DNA damage response, and protein synthesis in melanoma. Our analysis suggests that targeting BRAF-interacting proteins may also modulate oncogenic signaling pathways and represent promising biomarkers for melanoma diagnosis and therapy.

By drug screening, Ibrutinib is identified as an effective inhibitor of HGSOC cells and patient-derived organoids with CBX2 condensates. Overall, CBX2 phase separation enhances DSB repair-mediated drug resistance in HGSOC cells, and Ibrutinib may offer a viable therapeutic option for CBX2-positive HGSOC patients.

Following treatment with temozolomide (TMZ), the level of m6A modification was increased, facilitating YTHDF3-mediated DNA damage repair...Mechanistically, YTHDF3 recognizes the m6A binding site of DNA damage response genes (BRCA1, RAD51, RIF1 and 53BP1) and promotes their translation through m6A methylation, thereby initiating homologous recombination (HR) and nonhomologous end joining (NHEJ) repair to resist endogenous and exogenous DNA damage. Consequently, our study elucidates the crucial role of YTHDF3 in GBM and provides valuable insights into its significance in the DNA damage response and chemoresistance.

Collectively, these findings underscore the potential of aptamer-functionalized exosomes in conjunction with DOX as a promising strategy for GBM treatment. This approach not only broadens the therapeutic applications of DOX but also provides a novel direction for targeted GBM therapies.

This study provides the first evidence of prolonged DSB repair kinetics in WAS patients, emphasising heightened radiosensitivity and genomic instability. These findings suggest tailored radiation strategies in WAS management, particularly for bone marrow transplantation or genotoxic therapies, to mitigate risks and optimize outcomes.

This review will discuss the cellular mechanisms governing the DDR with an emphasis on the multifaceted role of Rad9 in sensing and responding to DNA damage, and how phosphorylation events regulate its function within the DDR. As the cellular events governing the DDR are well conserved, discoveries in yeast can be extrapolated to humans and may lead to the identification of additional novel protein targets, with several DDR inhibitors currently in clinical use or showing promise in clinical trials.

Moreover, 11.1 MBq [177Lu]Lu-DOTA-latozinemab significantly suppressed tumor growth via induction of DNA damage, as evidenced by increased 53BP1 foci. These findings establish the first SORT1-directed theranostic radiopharmaceutical pair, exhibiting high specificity and therapeutic potency for managing SORT1-positive cancers.

Furthermore, we propose a "Minimum Reporting Standard" checklist to harmonize DRC quantification. By distinguishing established validation tools from experimental artifacts, this framework aligns assay selection with specific biological endpoints and clinical feasibility.

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.