We are analyzing https://link.springer.com/article/10.1007/s10585-012-9506-0.

Title:
Dipyridamole prevents triple-negative breast-cancer progression | Clinical & Experimental Metastasis
Description:
Dipyridamole is a widely prescribed drug in ischemic disorders, and it is here investigated for potential clinical use as a new treatment for breast cancer. Xenograft mice bearing triple-negative breast cancer 4T1-Luc or MDA-MB-231T cells were generated. In these in vivo models, dipyridamole effects were investigated for primary tumor growth, metastasis formation, cell cycle, apoptosis, signaling pathways, immune cell infiltration, and serum inflammatory cytokines levels. Dipyridamole significantly reduced primary tumor growth and metastasis formation by intraperitoneal administration. Treatment with 15 mg/kg/day dipyridamole reduced mean primary tumor size by 67.5 % (p = 0.0433), while treatment with 30 mg/kg/day dipyridamole resulted in an almost a total reduction in primary tumors (p = 0.0182). Experimental metastasis assays show dipyridamole reduces metastasis formation by 47.5 % in the MDA-MB-231T xenograft model (p = 0.0122), and by 50.26 % in the 4T1-Luc xenograft model (p = 0.0292). In vivo dipyridamole decreased activated β-catenin by 38.64 % (p < 0.0001), phospho-ERK1/2 by 25.05 % (p = 0.0129), phospho-p65 by 67.82 % (p < 0.0001) and doubled the expression of IkBα (p = 0.0019), thus revealing significant effects on Wnt, ERK1/2-MAPK and NF-kB pathways in both animal models. Moreover dipyridamole significantly decreased the infiltration of tumor-associated macrophages and myeloid-derived suppressor cells in primary tumors (p < 0.005), and the inflammatory cytokines levels in the sera of the treated mice. We suggest that when used at appropriate doses and with the correct mode of administration, dipyridamole is a promising agent for breast-cancer treatment, thus also implying its potential use in other cancers that show those highly activated pathways.
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article, google, scholar, pubmed, cas, dipyridamole, cancer, metastasis, cells, cell, tumor, breast, res, tluc, vivo, naples, cytotoxicity, clinical, daniela, maria, treatment, primary, wnt, human, data, drug, mice, effects, formation, pathways, treated, vitro, clin, med, phase, supported, federico, university, moesmesmtif, figure, tiff, privacy, cookies, content, research, triplenegative, spano, massimo, zollo, mgkgday,

Topics {✒️}

beta-catenin/t-cell factor signaling anti-wnt/β-catenin signaling agents triple-negative breast cancer immune cell infiltration nf-kappab/akt-dependent induction mda-mb-231t xenograft model mda-mb-231t lung metastases multidrug-resistance-modulating agent dipyridamole 4t1-luc xenograft model month download article/chapter 15 mg/kg/day dipyridamole reduced transcription factor nf-kappab 30 mg/kg/day dipyridamole resulted myeloid-derived suppressor cells mda-mb-231t cells massimo zollo 4t1-luc cells treated intramural research program oxamide-hydrazone hybrid derivative adenosine a2a receptor-dependent 4t1-luc primary tumors extracellular signal-regulated kinase breast cancer metastasis nuclear factor-kappab erk1/2-mapk dipartimento di biochimica nf-kappab pathway 30 mg/kg/day dipyridamole structure-activity relationship study 4t1-luc cells interleukin-1α il-1β primary tumor growth nf-kappab functions nf-kb pathways human cancer cells full article pdf breast-cancer treatment author information authors dipyridamole significantly decreased inflammatory cytokines levels 15 mg/kg/day 30 mg/kg/day protein-protein interactions primary tumor size privacy choices/manage cookies cancer-related inflammation related subjects adenosine inhibits il-12 students’ t-test widely prescribed drug

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      headline:Dipyridamole prevents triple-negative breast-cancer progression
      description:Dipyridamole is a widely prescribed drug in ischemic disorders, and it is here investigated for potential clinical use as a new treatment for breast cancer. Xenograft mice bearing triple-negative breast cancer 4T1-Luc or MDA-MB-231T cells were generated. In these in vivo models, dipyridamole effects were investigated for primary tumor growth, metastasis formation, cell cycle, apoptosis, signaling pathways, immune cell infiltration, and serum inflammatory cytokines levels. Dipyridamole significantly reduced primary tumor growth and metastasis formation by intraperitoneal administration. Treatment with 15 mg/kg/day dipyridamole reduced mean primary tumor size by 67.5 % (p = 0.0433), while treatment with 30 mg/kg/day dipyridamole resulted in an almost a total reduction in primary tumors (p = 0.0182). Experimental metastasis assays show dipyridamole reduces metastasis formation by 47.5 % in the MDA-MB-231T xenograft model (p = 0.0122), and by 50.26 % in the 4T1-Luc xenograft model (p = 0.0292). In vivo dipyridamole decreased activated β-catenin by 38.64 % (p < 0.0001), phospho-ERK1/2 by 25.05 % (p = 0.0129), phospho-p65 by 67.82 % (p < 0.0001) and doubled the expression of IkBα (p = 0.0019), thus revealing significant effects on Wnt, ERK1/2-MAPK and NF-kB pathways in both animal models. Moreover dipyridamole significantly decreased the infiltration of tumor-associated macrophages and myeloid-derived suppressor cells in primary tumors (p < 0.005), and the inflammatory cytokines levels in the sera of the treated mice. We suggest that when used at appropriate doses and with the correct mode of administration, dipyridamole is a promising agent for breast-cancer treatment, thus also implying its potential use in other cancers that show those highly activated pathways.
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      pageEnd:68
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         Dipyridamole
         Metastasis
         ERK1/2-MAPK
         Wnt
         NF-kB
         Immune cell infiltration
         Tumor microenvironment
         Cancer Research
         Biomedicine
         general
         Oncology
         Hematology
         Surgical Oncology
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