Z. Szallasi

The paper analyzes the ADP-ribosylome in breast cancer cell lines to identify site-specific ADP-ribosylation patterns and their relation to PARP inhibitor sensitivity.

The paper identifies DDR biomarkers and ploidy abnormalities in GEA that predict sensitivity to DDR inhibitors and premalignant progression.

This study analyzes prostate cancer clonal architecture and evolutionary dynamics in 845 tumors, finding that Black patients have more monoclonal tumors but higher recurrence rates, and identifies new mutational signatures linked to subclones.

This paper identifies NER deficiency as a targetable vulnerability in ccRCC, showing that 10% of patients may respond to irofulven based on mutational signatures and PTGR1 expression.

This study identifies HR and NER deficiencies in gastric and esophageal adenocarcinomas and shows their responsiveness to platinum chemotherapy and PARP inhibitors.

This study uses CRISPR screens to identify genetic factors affecting PARP inhibitor sensitivity and resistance in prostate cancer, revealing novel targets and mechanisms.

The paper shows that loss of RNASEH2B makes prostate cancer cells sensitive to PARP inhibitors, but co-deletion with RB1 reduces this sensitivity through BRCA2 upregulation, and ATR inhibition can restore sensitivity.

The paper identifies HRD-associated mutational signatures in lung cancer cases and links them to PARP inhibitor sensitivity and platinum response.

The paper identifies genomic aberration-based molecular signatures to detect homologous recombination deficiency in prostate cancer, finding that 5-8% of cases may benefit from PARP-inhibitor treatment.

This study examines how mutagenic and non-mutagenic pre-operative chemotherapy affects immune infiltration in breast cancer, finding that increased stromal tumor-infiltrating lymphocytes (StrTIL) correlates with better distant metastasis-free survival in HR-negative cases.

The paper compares HRD scores in primary breast cancer tumors and their brain metastases, finding higher HRD in metastases, suggesting potential changes in PARP inhibitor therapy strategies.