O.N. Lipatov1,2, R.R. Rakhimov1, A.V. Sultanbaev1, R.R. Abdeev1, A.F. Bikmetov1, R.R. Saitov1, A.R. Akramov1, M.R. Zakareev1, V.A. Suravatkin2
1Republican Clinical Oncology Dispensary, Ufa
2Bashkir State Medical University, Ufa
Rakhimov Radmir R. ― Cand. of Sci. (Med.), oncologist of the Surgical Department №1 (stomach, esophagus) of the Republican Clinical Oncology Dispensary
73/1 Oktyabrya Ave., Ufa, 450054, Russian Federation, e-mail: firstname.lastname@example.org
Abstract. Pancreatic cancer is the seventh leading cause of cancer death worldwide. This is more than 20% of all deaths from malignant neoplasms of the abdominal cavity and approximately 5% of all deaths associated with malignant neoplasms. The most frequent deaths are histologically associated with ductal adenocarcinoma of the pancreas, accounting for approximately 85% of all cases of pancreatic cancer, often inoperable. Therefore, patients have limited treatment options and show high rates of morbidity and mortality. Poly (ADP-ribose) polymerase (PARP) inhibitors target tumor cells deficient in homologous recombination repair, based on the concept of synthetic lethality. The best known target gene is BRCA, whose mutations were first identified in breast and ovarian cancer. PARP inhibitors can trap the PARP-1 protein at single-strand breaks or DNA damage, and disrupt its catalytic cycle, which ultimately leads to the development of a replication fork and subsequent double-stranded DNA breaks. For tumor cells with a BRCA mutation, loss of homologous recombination recovery will result in cell death. It has also been reported that pancreatic cancer has a strong association with mutations in the BRCA gene, indicating that patients with pancreatic cancer may benefit from PARP inhibitor treatment.
Key words: olaparib, pancreatic cancer, targeted therapy, PARP inhibitor.