RBBP8 (RB Binding Protein 8, Endonuclease)

We moreover demonstrate the feasibility of employing FCCS for analysis of HNPCC-related factor MSH2 and MEN1 factor Menin variants in combination with DNA mismatch repair factor MSH6 and transcription factor JUND, respectively. We propose that FCCS may be an appealing complement to current clinical procedures for classifying variants for many monogenic diseases, given its generic nature and ease of use.

Prognostic models based on tumor microenvironment and immune score stratification and the construction of related genes have potential applications for prognostic analysis of GBM patients.

The miR-1284/EIF4A1 axis promotes the repair of DNA damage caused by RT, promotes the activation of the cGAS-STING pathway in GC, and has good biological safety. Our findings provide an important experimental basis for enhancing the anti-tumor immune effect of RT in the treatment of GC.

We further reveal that Brca1-deficient mammary tumour cells that have acquired PARP inhibitor (PARPi) resistance regain chemosensitivity after PIN1 or p38α inhibition. Collectively, our findings identify the PIN1-p38-CtIP signalling pathway as a critical regulator of replication fork integrity.

The HG and LG showed no significant difference in the number of TIICs; however, there was a difference in the number ratios of CD4+/CD8+ (P=0.012) and CD4+/CD3+ cells (P<0.001). Therefore, RBBP8 expression in patients with advanced gastric cancer is a prognostic marker that affects the proportion of CD4+ T-cell infiltration and may also be a biomarker for predicting ICI treatment response.

Mechanistically, we found that HDGF modulates DNA damage response and, by recruiting C-terminal binding protein-interacting protein (CtIP), it facilitates homologous recombination repair to influence CRC drug sensitivity. Furthermore, we propose that HDGF may serve as a recognition protein for H3K36me3, participating in the repair of damaged transcriptionally active genes, thus maintaining genomic stability in CRC.

Further analysis revealed that mutations in CDKN2B, PTEN, FGF6, and RBBP8 genes were significantly associated with an increased risk of death (P＜0.05). Albumin-bound paclitaxel as first-line treatment demonstrated feasible anti-tumor efficacy and manageable safety for patients with advanced pancreatic cancer in China.

Supplement with murine Ctip could efficiently restore (i.e. increase) HR repair and alleviate miscarriage in BaP-exposed mouse model. Collectively, this study not only reveals the association and causality among BaP/BPDE exposure, the defective HR repair, and miscarriage, but also discovers novel mechanism in lnc-HZ08-regulated BRCA1/CtIP-mediated HR repair, bridging epigenetic regulation and genetic instability and also providing an efficient approach for treatment against BaP/BPDE-induced unexplained miscarriage.

The findings recapitulated that UBAP2 promoted HCC progression and radioresistance via SLC27A5 stability mediated by the ubiquitin-proteasome pathway. It was also suggested that targeting the UBAP2/SLC27A5 axis could be a valuable radiosensitization strategy in HCC.

TMGsig can predict outcomes in patients with lung adenocarcinoma.

RBBP8(p.E281*) variant may promote tumor susceptibility and serve as a precision medicine biomarker in familial hereditary cancer syndrome. KEY MESSAGES: RBBP8(p.E281*) is a susceptibility gene in this familial hereditary cancer syndrome RBBP8(p.E281*) lost its ability to enter the nucleus and the BRCA1 binding motif A novel RBBP8(p.E281*) germline mutation promotes breast cancer tumorigenesis Patients with RBBP8(p.E281*) germline mutation may benefit from Olaparib, Cisplatin.

These findings implicate diverse glioma somatic mutations in cancer genes associated with peritumoral hyperexcitability. Tumor genetic profiling may facilitate glioma-related epilepsy prognostication and management.