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AimTo investigate the safety and feasibility of extending the flushing interval for the totally implantable venous access port (TIVAP) during the non-treatment stage in patients with breast cancer (BC) by retrospectively analyzing the patients’ clinical data, including the incidence of TIVAP-related complications.MethodsThis single-center retrospective study included patients with BC who underwent TIVAP implantation at our hospital between January 2018 and March 2021 during their non-treatment phase and visited the hospital regularly for TIVAP flushing. Among the 1013 patients with BC who received TIVAP implantation, 617 patients were finally included on the basis of the inclusion and exclusion criteria and divided into three groups according to the length of the flushing interval: group 1 (≤30 days, n = 79), group 2 (31–90 days, n = 66), and group 3 (91–120 days, n = 472). The basic characteristics of patients in each group and the incidence of TIVAP-related complications (catheter obstruction, infection, and thrombosis) were analyzed.ResultsNo significant intergroup differences were observed in age, body mass index (BMI), tumor stage, pathological staging, implantation approach, chemotherapy regimen, duration of treatment, and TIVAP-related blood return rate (P > 0.05). Among patients from all three groups, 11 cases of catheter pump-back without blood and eight cases of TIVAP-related complications such as infection, thrombosis, and catheter obstruction were recorded. However, no significant differences in TIVAP-related complications were observed among the three groups (P > 0.05).ConclusionExtending the TIVAP flushing interval beyond three months during the non-treatment stage in BC patients is safe and feasible and did not increase the incidence of TIVAP-related complications.

Uveal melanoma (UM) is the most common primary intraocular carcinoma in adults. Cinobufagin, secreted by the Asiatic toad Bufo gargarizans, is a traditional Chinese medicine, widely used in tumor treatment. Here, we explored the potential antitumor function of cinobufagin and investigated its biochemical mechanisms in UM cells. The antitumor potential of cinobufagin was determined via cell viability, cell cycle, and apoptosis assays. Colony formation assays confirmed that cinobufagin exerted potent antitumor activity in a dose-dependent manner. We found that cinobufagin could induce cell apoptosis and upregulate the expression of cleaved caspase-3, cleaved poly(ADP-ribose) polymerase (PARP), and cleaved caspase-9 in vivo and in vitro. In addition, after treatment with increased concentrations of cinobufagin, the intrinsic mitochondrial apoptosis pathway was also activated, which was demonstrated by increased cell apoptosis with increased expression of Bad and Bax, decreased expression of Bcl-2 and Bcl-xl, and reduced mitochondrial membrane potential (MMP) in OCM1 cells. Taken together, the results of this preclinical study suggest that cinobufagin can both inhibit cell survival and induce cell apoptosis in a dose-dependent manner in UM cells, which provides new insights into the biochemical mechanism of cinobufagin and its potential as a future chemotherapeutic agent for UM.