Publications by authors named "B Vanova"

Article Synopsis
  • PARP inhibitors work by blocking the repair of single-strand DNA breaks caused by tumor growth, leading to cell death when the homologous recombination repair system is dysfunctional, especially relevant for patients with serous ovarian epithelial tumors.
  • Studies show that women with BRCA mutations exhibit the highest progression-free survival rates, although PARP inhibitors are also beneficial for those with a disrupted homologous recombination deficiency system, regardless of BRCA status.
  • The research analyzed a group of women with high-grade serous ovarian cancer who had undergone at least two chemotherapy treatments, using the SOPHIA DDM™ tool to identify pathogenic variants in BRCA genes, confirming mutations in 50% of the participants in order to enhance patient management and treatment
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Colorectal cancer (CRC) is the third-most common cancer type in males and the second-most common cancer type in females, and has the second-highest overall mortality rate worldwide. Approximately 50% of patients in stage I-III develop metastases, mostly localized to the liver. All physiological conditions occurring in the organism are also reflected in the levels of circulating microRNAs (miRNAs/miRs) in patients.

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Ovarian cancer is the leading cause of mortality among all gynecological cancers in developed countries and its most common and most lethal type is the high-grade serous ovarian carcinoma (HGSC). At the molecular level, nearly half of all HGSCs exhibit ineffective homologous DNA recombination and disruption of DNA damage/repair pathway inactivation caused often by BRCA1 and BRCA2 gene mutation. Recently, the detection of BRCA1/2 mutations became important for personalized treatment of HGSC patients with the PARP-inhibitors in the defined clinical setting of relapse after positive adjuvant platinum-based chemotherapeutic response.

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Background: Nowadays, modern treatment methods for cancer patients are based on targeting specific molecules involved in cellular signaling system associated with tumor initiation and progression. The success of such approach depends on a correctly chosen dia-gnostic test with high sensitivity that identifies the occurrence and level of bio-markers in patients to select those who will respond and benefit from the treatment. The development of new technologies and the upgrades of the known ones contribute to the innovations in molecular characterization of cancer, which allows the detection of patients mutational status with high sensitivity and specificity.

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BRAF V600E mutations in GISTs are considered to be one of the mutational events in KIT/PDGFRA negative or positive GISTs, respectively. BRAF mutated GISTs usually do not respond to imatinib treatment, even more GISTs with imatinib sensitive KIT mutation. However, they are almost phenotypically and morphologically identical with KIT/PDGFRA positive GISTs.

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