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Browse 1,019 clinical trials for pancreatic cancer. Find studies that match your criteria and connect with research centers.
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NCT05659914
Patients with metastatic pancreatic cancer and germline mutation in BRCA have benefit of therapy with PARP inhibitors. In addition, some studies have demonstrated that PDL-1 inhibitors synergize therapeutically with PARP inhibitors in tumours with homologous repair deficiency. Our hypothesis is that those patients with alterations in DNA damage repair genes (somatic and germline BRCA1, BRCA2, PALB2, RAD51C, RAD51D and other functional DDR genes) and who have benefit from platinum based therapy in first line might obtain an increased therapeutic effect with the combination of olaparib and durvalumab. This is an open-label, single-arm, multicentric phase II clinical trial of a combination of durvalumab and olaparib in patients with metastatic pancreatic cancer with alterations in DDR genes, who have had benefit with platinum-based chemotherapy in first line setting. The primary objective is to investigate the efficacy of this combination in terms of ORR. Patients will be eligible for the study based on alterations in a panel of specific DDR genes including BRCA1, BRCA2, PALB2, RAD51C, RAD51D and other DDR genes, as determined by a local assay according to local practice or by the central laboratory (if local assay is not available).
NCT06649474
Oesogastric and pancreatic adenocarcinomas are poor-prognosis cancers. Incidence of pancreatic cancer drastically increases to such an extent that it will become the second cause of cancer's mortality by 2030. A major challenge is to optimize the therapies for localized setting, when oxaliplatin-based chemotherapy is the standard, before and after surgical excision. Because in 50% of cases oxaliplatin triggers a grade 2-3 sinusoidal obstruction syndrome (SOS) which increases post-operative morbidity, decreases histological response to chemotherapy, increases tumor recurrence, and aggravates the risk of chemotherapy-induced peripheral neuropathy (CIPN). There is an urgent need to better understand the biological processes involved in SOS, in order to prevent and treat it without stopping or reducing oxaliplatin administration. The biological link between oxaliplatin and SOS has not been described, but recent murine experiments argue for HMGB1 to be the mediator released after exposure to oxaliplatin and inducing SOS, and thereafter CIPN. To date, no biomarker is established between murine and patient analyses, and the release of HMGB1 after oxaliplatin treatment and its effect on hepatic parenchyma is not described in patients. Investigators hypothesized is that HMGB1 would also been increased in patients after oxaliplatin treatment, and correlated to the development of SOS and CIPN. If confirmed, personalized treatment will be possible to target this pathway. Therefore, investigators propose to dynamically explore this hypothesis in localized oesogastric and pancreatic cancer patients who will be routinely managed by an initial laparoscopy and post-oxaliplatin surgical excision.