2026-04-18T00:25:05Zhttps://recercat.cat/oai/request

oai:recercat.cat:2445/1202652025-12-05T09:24:09Zcom_2072_1057col_2072_478798col_2072_478799col_2072_478916col_2072_478917col_2072_478929

00925njm 22002777a 4500 dc Vives, Marta author Ginestà, Mireia M. author Gracova, Kristina author Graupera i Garcia-Milà, Mariona author Casanovas i Casanovas, Oriol author Capellá, G. (Gabriel) author Serrano Piñol, M. Teresa author Laquente, Berta author Viñals Canals, Francesc author 2018-02-26T14:32:54Z 2018-02-26T14:32:54Z 2013-11-15 2018-02-26T14:32:55Z In this article, the effectiveness of a multi-targeted chemo-switch (C-S) schedule that combines metronomic chemotherapy (MET) after treatment with the maximum tolerated dose (MTD) is reported. This schedule was tested with gemcitabine in two distinct human pancreatic adenocarcinoma orthotopic models and with cyclophosphamide in an orthotopic ovarian cancer model. In both models, the C-S schedule had the most favourable effect, achieving at least 80% tumour growth inhibition without increased toxicity. Moreover, in the pancreatic cancer model, although peritoneal metastases were observed in control and MTD groups, no dissemination was observed in the MET and C-S groups. C-S treatment caused a decrease in angiogenesis, and its effect on tumour growth was similar to that produced by the MTD followed by anti-angiogenic DC101 treatment. C-S treatment combined an increase in thrombospondin-1 expression with a decrease in the number of CD133+ cancer cells and triple-positive CD133+/CD44+/CD24+ cancer stem cells (CSCs). These findings confirm that the C-S schedule is a challenging clinical strategy with demonstrable inhibitory effects on tumour dissemination, angiogenesis and CSCs. Quimioteràpia del càncer Medicaments antineoplàstics Angiogènesi Cèl·lules mare Cèl·lules canceroses Cancer chemotherapy Antineoplastic agents Neovascularization Stem cells Cancer cells Meetronomic chemotherapy following the maximum tolerated dose is an effective anti-tumour therapy affecting angiogenesis, tumour dissemination and cancer stem cells