Publications by authors named "A Llop-Guevara"
Purpose: The randomized GeparOla trial reported comparable pathological complete response (pCR) rates with neoadjuvant containing olaparib vs. carboplatin treatment. Here, we evaluate the association between functional homologous repair deficiency (HRD) by RAD51 foci and pCR, and the potential of improving patient selection by combining RAD51 and stromal tumor infiltrating lymphocytes (sTILs).
View Article and Find Full Text PDFBackground: Poly (ADP-ribose) polymerase 1 and 2 (PARP1/2) inhibitors (PARPi) are targeted therapies approved for homologous recombination repair (HRR)-deficient breast, ovarian, pancreatic, and prostate cancers. Since inhibition of PARP1 is sufficient to cause synthetic lethality in tumors with homologous recombination deficiency (HRD), PARP1 selective inhibitors such as saruparib (AZD5305) are being developed. It is expected that selective PARP1 inhibition leads to a safer profile that facilitates its combination with other DNA damage repair inhibitors.
View Article and Find Full Text PDFArticle Synopsis
- RAD51C and RAD51D genes play a crucial role in DNA repair, and mutations in these genes significantly increase the risk of developing ovarian and breast cancer.
- This study analyzed the clinical characteristics of 91 patients and 90 relatives with pathogenic variants in RAD51C/D across multiple Spanish hospitals, focusing on their tumors' homologous recombination deficiency (HRD) status.
- Findings showed that a substantial portion of the carriers were women, with a high incidence of breast and ovarian cancer; the study also determined the prevalence of HRD in untreated tumors from these patients.
Article Synopsis
- Some breast cancer patients have mutations in genes PALB2 or RAD51C, which are linked to homologous recombination, a process important for DNA repair.
- Despite having these genetic variants, the patients still show proficiency in homologous recombination, meaning their DNA repair mechanisms are functioning effectively.
- This finding suggests that other pathways or mechanisms might compensate for the defective genes in these patients, potentially impacting treatment and prognosis.