Soriano-Hernandez A.D.,University of Colima |
Soriano-Hernandez A.D.,Cancerology State Institute |
Madrigal-Perez D.,University of Colima |
Galvan-Salazar H.R.,University of Colima |
And 12 more authors.
Oncology Letters | Year: 2015
Uterine cervical cancer (UCC) is one of the main causes of cancer‑associated mortality in women. Inflammation has been identified as an important component of this neoplasia; in this context, anti‑inflammatory drugs represent possible prophylactic and/or therapeutic alternatives that require further investigation. Anti‑inflammatory drugs are common and each one may exhibit a different antineoplastic effect. As a result, the present study investigated different anti‑inflammatory models of UCC in vitro and in vivo. Celecoxib, sulindac, nimesulide, dexamethasone, meclofenamic acid, flufenamic acid and mefenamic acid were tested in UCC HeLa, VIPA, INBL and SiHa cell lines. The cytotoxicity of the drugs was evaluated in vitro. Celecoxib, sulindac, nimesulide, mefenamic acid and flufenamic acid presented with slight to moderate toxicity (10‑40% of cell death corresponding to 100 μM) in certain cell lines, while meclofenamic acid exhibited significant cytotoxicity in all essayed cell lines (50‑90% of cell death corresponding to 100 μM). The meclofenamic acid was tested in murine models (immunodeficient and immunocompetent) of UCC, which manifested a significant reduction in tumor growth and increased mouse survival. It was demonstrated that of the evaluated anti‑inflammatory drugs, meclofenamic acid was the most cytotoxic, with a significant antitumor effect in murine models. Subsequent studies are necessary to evaluate the clinical utility of this drug. © 2015, Spandidos Publications. All rights reserved. Source
Ramos-Flores C.,University of Colima |
Romero-Gutierrez T.,University of Colima |
Delgado-Enciso I.,University of Colima |
Delgado-Enciso I.,Cancerology State Institute |
And 9 more authors.
International Journal of Gynecological Cancer | Year: 2013
Introduction: The expression of plasminogen activator inhibitor type 1 (PAI-1), vascular endothelial growth factor (VEGF), and transforming growth factor A1 (TGF-β1) participates in the angiogenesis of several cancer types. The goal of this study was to investigate polymorphisms in genes related to angiogenesis (PAI-1-675 4G/5G, VEGF C936T, and TGF-β1 G-800A) to evaluate the risk for developing uterine cervical cancer (UCC). Methods: In a case-control study, 100 healthy subjects and 100 patients with UCC from Mexico were included. We determined the genetic profile of the polymorphic markers, which were evaluated by polymerase chain reaction using a sequence-specific primer. Results: There was no statistical difference in the allele distribution from the intergroup comparisons of PAI-1 675 4G/5G and VEGF C936T data; however, a significant difference was observed within TGF-β1 G-800A. The linkage disequilibrium analysis revealed that PAI-1 -675 4G and TGF-β1 -800A pair-haplotype was in strong linkage disequilibrium with a significantly increased risk (odds ratio, 3.44; 95%confidence interval, 1.66Y7.25) to UCC. Conclusions: The polymorphisms in the genes related to angiogenesis -675 4G/5G PAI-1 and G-800A TGF-β1, segregated solely or combined, might contribute to the increased susceptibility to UCC in a Mexican population. Copyright © 2013 by IGCS and ESGO. Source
Madrigal-Perez V.M.,University of Colima |
Garcia-Rivera A.,University of Colima |
Rodriguez-Hernandez A.,University of Colima |
Ceja-Espiritu G.,University of Colima |
And 14 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015
Nonalcoholic steatohepatitis (NASH) is currently one of the primary liver diseases. Recent studies have shown a clinical relation between NASH and atherosclerosis. There is much interest in these two diseases because they are both associated with great morbidity and mortality. Inflammation and the overexpression of COX-2 participate in the pathophysiology of the two diseases, and therefore simultaneous treatment is feasible. The role of the four NSAIDs, meclofenamate, mefenamate, flufenamate, and aspirin, was analyzed in a mouse model of NASH, as well as preclinical atherosclerosis induced by a high-fat diet (HFD). Six mouse groups were formed. Five of the groups were fed a high-fat diet for 6 months and one group was fed a standard diet, acting as the normality reference. Of the five groups fed a high-fat diet, four received a NSAID, each of them identified by the specific drug administered. One group received no treatment. Serum markers (cholesterol, triglycerides, ALT, and AST) and histologic changes in the aorta and liver were analyzed for the study. Aspirin significantly reduced the hepaticsteatosis. All the drugs significantly reduced the hepatic inflammatory infiltrate. In relation to atherosclerosis, there were significant reductions in all the study variables with the use of aspirin and flufenamate. The four medications were able to stop steatosis from progressing into steatohepatitis by reducing inflammation. However, aspirin was the most beneficial, simultaneously reducing steatosis, atherosclerosis, and serum cholesterol levels. © 2015, International Journal of Clinical and Experimental Medicine. All rights reserved. Source