BRCA2 (Breast cancer 2, early onset)

The survey results suggest that treatment selection of Japanese doctors may differ from those of the APCCC24. More extensive surveys are needed for further discussion on the treatment selection for patients with advanced prostate cancer in Japan.

In this retrospective cross-sectional study, cascade testing was underused, especially among specific demographic groups, with clinical and cultural factors appearing to play a larger role than financial barriers. These findings may guide efforts to address barriers preventing wider uptake of cascade testing and improve cancer prevention efforts, particularly among racial and ethnic minority groups.

Finally, we summarize current challenges-including limited accessibility, resistance mechanisms, and toxicities-and outline future directions, such as novel biomarkers, liquid biopsy for real-time resistance monitoring, and innovative adaptive trial designs. This review highlights the evolution of DDR-targeted therapy in pancreatic cancer toward personalized, combination-based precision medicine.

Our research suggests that this video message is a useful method for facilitating family sharing of BRCA1/2 results.

Our findings suggest that BRC8 overexpression stabilizes RAD51 by inhibiting ubiquitin-dependent degradation of RAD51, leading to increased persistence of RAD51 foci, indicating impaired timely removal of RAD51 from DNA damage sites and reduced HR efficiency. Moreover, altered cell cycle distribution may contribute to reduced non-homologous end-joining efficiency, further enhancing cellular sensitivity to DNA-damaging agents. Collectively, these findings provide a basis to further explore the potential of BRC8-based peptides as tools for modulating RAD51 stability and sensitizing cells to DNA damage.

We identified (likely) pathogenic variants in DNA repair genes in 18 patients, including several RECQ helicase and other DNA repair genes, an intragenic FANCM deletion, and six rare mobile element insertions (MEIs) in DNA repair genes. Incorporating PRS306 shifted estimated lifetime breast cancer risk by ≥5 percentage points in a subset of women (n = 75), including carriers of rare variants in DNA repair genes, resulting in both upward and downward risk estimation.

P=N/A, N=524, Active, not recruiting, Weill Medical College of Cornell University | Recruiting --> Active, not recruiting | N=820 --> 524 | Trial primary completion date: Mar 2026 --> Sep 2025

Furthermore, G73-mediated RAD51 degradation synergizes with the PARP inhibitor olaparib, inducing synthetic lethality and re-sensitizing olaparib-resistant cancers to PARP inhibition. This fully small-molecule-based strategy presents a compelling strategy to overcome resistance to PARP inhibitors, expanding their therapeutic potential beyond patients with HR-deficient tumors.

Although PARP inhibitor olaparib has been approved for metastatic CRPC patients bearing BRCA1/2 mutations, its application is confined to this specific patient subpopulation...Their synergistic effect was confirmed in ex vivo explants from human PCa specimens. Our findings demonstrated CDK9 as a master regulator of BRCAness and proposed targeting CDK9 as a potential strategy to sensitize CRPC patients without BRCA1/2 mutations to PARP inhibition.

Overall, integrating GGT into routine breast cancer care represents a key component of precision oncology and hereditary cancer prevention strategies worldwide, especially in early-onset disease populations. Implementation requires multidisciplinary coordination and equitable access to testing services.

These data demonstrate that targeting HRD yields promising outcomes in stage III, HER2-negative, HRD breast cancer and that intensified chemotherapy with autologous stem cell rescue does not provide any advantage over state-of-the-art chemotherapy plus olaparib.

These findings highlight recurrent alterations in TP53, RB1, and ATRX and suggest potential roles for IGF2 and AXIN1 in leiomyosrcoma metastatic disease that warrant further investigation.