We are analyzing https://link.springer.com/article/10.1007/s00262-012-1324-3.

Title:
Rosiglitazone and Gemcitabine in combination reduces immune suppression and modulates T cell populations in pancreatic cancer | Cancer Immunology, Immunotherapy
Description:
Pancreatic ductal adenocarcinoma is a leading cause of cancer mortality with a dismal 2–5 % 5-year survival rate. Monotherapy with Gemcitabine has limited success, highlighting the need for additional therapies that enhance the efficacy of current treatments. We evaluated the combination of Gemcitabine and Rosiglitazone, an FDA-approved drug for the treatment of type II diabetes, in an immunocompetent transplantable mouse model of pancreatic cancer. Tumor progression, survival, and metastases were evaluated in immunocompetent mice with subcutaneous or orthotopic pancreatic tumors treated with Pioglitazone, Rosiglitazone, Gemcitabine, or combinations of these. We characterized the impact of high-dose Rosiglitazone and Gemcitabine therapy on immune suppressive mediators, including MDSC and T regulatory cells, and on modulation of peripheral and intra-tumoral T cell populations. Combinations of Rosiglitazone and Gemcitabine significantly reduced tumor progression and metastases, enhanced apoptosis, and significantly extended overall survival compared to Gemcitabine alone. Rosiglitazone altered tumor-associated immune suppressive mediators by limiting early MDSC accumulation and intra-tumoral T regulatory cells. Combination therapy with Rosiglitazone and Gemcitabine modulated T cell populations by enhancing circulating CD8+ T cells and intra-tumoral CD4+ and CD8+ T cells while limiting T regulatory cells. The results suggest that Rosiglitazone, in combination with Gemcitabine, decreases immune suppressive mechanisms in immunocompetent animals and provides pre-clinical data in support of combining Rosiglitazone and Gemcitabine as a clinical therapy for pancreatic cancer.
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Keywords {🔍}

cancer, article, google, scholar, pubmed, cas, pancreatic, cells, rosiglitazone, gemcitabine, cell, peroxisome, proliferatoractivated, res, receptor, growth, tumor, gamma, bailey, hollingsworth, diabetes, regulatory, access, clin, combination, immune, progression, mice, mol, privacy, cookies, content, pioglitazone, therapy, immunol, chen, ppargamma, ligands, inhibit, data, publish, research, search, immunology, immunotherapy, reduces, suppression, populations, bunt, mohr,

Topics {✒️}

peroxisome proliferator-activated receptor-gamma 1-bis[3′-indolyl]-1-[p-substitutedphenyl]methanes peroxisome-proliferator-activated receptors month download article/chapter myeloid-derived suppressor cells nested case-control study ppargamma-independent signal pathways transforming growth factor-beta1 steroidal anti-inflammatory drugs nonsteroidal anti-inflammatory drugs prostate-specific antigen expression full article pdf related subjects article cancer immunology spontaneous pancreatic carcinoma cancer cell growth privacy choices/manage cookies rna interference suppression ppargamma independent mechanisms santos-gallego cg nci training grant pancreatic ductal adenocarcinoma tumor-bearing mice human pancreatic carcinomas bladder tumor growth pancreatic cancer cells human prostate cancer pancreatic tumour cells anti-cancer agent induce cell death cell activation induced resected pancreatic cancer pancreatic cancer development advanced pancreatic cancer unmc histology facility reactive tumor microenvironment facilitate tumor progression inflammatory mechanisms contributing nuclear factor-kappab unmc comparative medicine rosiglitazone altered tumor epithelial inflammatory response vivo glioma growth european economic area fda-approved drug immune suppressive mediators teff/treg ratio plasminogen activator system koeffler hp cd3/cd28 costimulation

Questions {❓}

Balkwill F, Mantovani A (2001) Inflammation and cancer: back to Virchow?

Schema {🗺️}

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         description:Pancreatic ductal adenocarcinoma is a leading cause of cancer mortality with a dismal 2–5 % 5-year survival rate. Monotherapy with Gemcitabine has limited success, highlighting the need for additional therapies that enhance the efficacy of current treatments. We evaluated the combination of Gemcitabine and Rosiglitazone, an FDA-approved drug for the treatment of type II diabetes, in an immunocompetent transplantable mouse model of pancreatic cancer. Tumor progression, survival, and metastases were evaluated in immunocompetent mice with subcutaneous or orthotopic pancreatic tumors treated with Pioglitazone, Rosiglitazone, Gemcitabine, or combinations of these. We characterized the impact of high-dose Rosiglitazone and Gemcitabine therapy on immune suppressive mediators, including MDSC and T regulatory cells, and on modulation of peripheral and intra-tumoral T cell populations. Combinations of Rosiglitazone and Gemcitabine significantly reduced tumor progression and metastases, enhanced apoptosis, and significantly extended overall survival compared to Gemcitabine alone. Rosiglitazone altered tumor-associated immune suppressive mediators by limiting early MDSC accumulation and intra-tumoral T regulatory cells. Combination therapy with Rosiglitazone and Gemcitabine modulated T cell populations by enhancing circulating CD8+ T cells and intra-tumoral CD4+ and CD8+ T cells while limiting T regulatory cells. The results suggest that Rosiglitazone, in combination with Gemcitabine, decreases immune suppressive mechanisms in immunocompetent animals and provides pre-clinical data in support of combining Rosiglitazone and Gemcitabine as a clinical therapy for pancreatic cancer.
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