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Featured researches published by Renato Gagliardi.


International Journal of Cancer | 1996

Down-regulation of tumour gelatinase/inhibitor balance and preservation of tumour endothelium by an anti-metastatic ruthenium complex

Gianni Sava; Ilaria Capozzi; Alberta Bergamo; Renato Gagliardi; Moreno Cocchietto; Laura Masiero; Maurizio Onisto; Enzo Alessio; Giovanni Mestroni; Spiridione Garbisa

The anti‐metastatic ruthenium complex Na[trans‐RuCl4(DMSO)1m] was given i.p. at 22 and 44 mg/kg/day, on days 8–13 after tumour implantation, to mice carrying s.c. implants of MCa mammary carcinoma. The aim of the study was to compare the effects on lung metastasis formation with those on primary tumour cells. This investigation was based on flow cytometry analysis after propidium iodide and acridine orange staining, histology of tumour parenchyma and RT‐PCR analysis for the type‐IV collagenases MMP‐9 and MMP‐2 and their respective inhibitors TIMP‐1 and TIMP‐2 mRNAs. Na[trans‐RuCl4(DMSO)1m] is not cytotoxic for tumour cells but has the capacity of interacting with nucleic acids, giving a general reduction of nucleic acid content as shown by a marked reduction of acridine orange staining and a tendency to a reduction of DNA polyploidy with marked reduction of 8n and 4n cell populations. Na[trans‐RuCl4(DMSO)1m] also influences a proteolytic system which has the potential of degrading the basement membrane and has been related to metastatic aggressiveness: it markedly reduces, in a dose‐dependent manner, MMP‐2/TIMP‐2 balance, but not that of MMP‐9/TIMP‐1. The different enzyme/inhibitor mRNA levels between untreated and treated tumours seem to be unaffected by tumour‐infiltrating lymphocytes and are paralleled by the maintenance of connective tissue around blood vessels in the tumour mass. Correspondingly, lung metastasis formation is markedly reduced, to less than 10% of that seen in controls.


Clinical & Experimental Metastasis | 1994

Antimetastatic action and toxicity on healthy tissues of Na[trans-RuCl4(DMSO)Im] in the mouse

Renato Gagliardi; Gianni Sava; Sabrina Pacor; Giovanni Mestroni; Enzo Alessio

The ruthenium-dimethylsulfoxide complex Na(trans-RuCl4(DMSO)Im] was given i.v. to mice bearing MCa mammary carcinoma and its effects on tumor growth and on healthy host tissues were studied by macroscopic examination of primary tumor growth, by survival time, and by histological analysis using light microscopy and SEM. Either by means ofvivo-vivo bioassays or by microscopic examination it appeared that the growth of lung tumors was markedly reduced, whereas the growth of the i.m. primary tumor was much less affected. These effects account for the prolongation of survival time and for the cure rate observed. The favourable effect on survival time was also influenced by the lack of significant cytotoxicity for normal tissues such as lung and kidney epithelia, muscle and liver cells, splenocytes and bone marrow. It thus appears that the selective interaction with tumor cells in the lungs cannot simply be attributed to a selectively higher localization of the compound at this site, nor to a modification of the histological structure of primary tumor. These results highlight the pharmacologic properties of this compound for the control of solid tumor metastases, an effect that was shown to be similarly exerted on advanced tumor metastases.


Pathology & Oncology Research | 1998

Comparison of the effects of the antimetastatic compound ImH[trans-RuCl4(DMSO)Im] (NAMI-A) on the arthritic rat and on MCa mammary carcinoma in mice.

Gianni Sava; Renato Gagliardi; Moreno Cocchietto; Katiuscia Clerici; Ilaria Capozzi; M. Marrella; Enzo Alessio; Giovanni Mestroni; R. Milanino

The effects of the new molecule ImH[trans-RuCl4(DMSO)Im] (NAMI-A), administered orally or intraperitoneally to adjuvant-arthritic rats or orally to mice bearing s.c. or i.m. implants of MCa mammary carcinoma, were studied. NAMI-A was not able to modify the progression of chronic inflammation in the complete Freund-adjuvant injected animals. Histology indicated a significant worsening of the inflammatory process, characterised by an increased infiltration of inflammatory cells, as well as by a remarkable deposition of connective tissue fibres around the blood vessels and alveolar walls. NAMI-A had no effect on primary i.m. implanted MCa mammary carcinoma growth and its lung metastasis formation, but significantly interfered with the cell cycle of primary tumor cells following bolus oral administration. On the contrary, NAMI-A caused a significant inhibition of lung metastasis accompanied by a dramatic deposition of connective tissue fibres around the primary tumor mass, when given as medicated food to mice implanted s.c. with MCa tumor. These data indicated that NAMI-A is well absorbed after oral administration although there is no connection between lung concentration and the antimetastatic activity. Conversely, the marked deposition of connective tissues in NAMI-A treated animals is in agreement with the reported effects of the compund on extracellular matrix and tumor blood vessels.


Pathology & Oncology Research | 1999

Paracrine Effects of IL-4 Transfection on TS/A Adenocarcinoma Cells Mediate Reduced In Vivo Growth

Sabrina Pacor; Renato Gagliardi; Paola Spessotto; Giuliano Zabucchi; Gianni Sava

Thein vitro/in vivo growth capacity and phenotype of TS/A and the IL4-transfected TS/A-IL4 cell lines were studied by cell cycle analysis, expression of ICAM-1/CD54, transferrin receptor/CD71 and E-cadherin and by histology of the primary tumors. TS/A-IL4, unlike the TS/A line, showsin vitro a marked increase in the fibroblastoid cell type and a decreased E-cadherin expression. Administration of conditioned medium containing IL4 obtained from the TS/A-IL4 cell line, stimulates CD54 expression in the TS/A cell line. TS/A-IL4 tumors grow more slowlyin vivo and are ultimately rejected. These processes are accompanied by a marked increase in collagen and extracellular matrix proteins and increased recruitment and degranulation of mast cells. The paracrine effect of IL4, released by the transfected tumor cells, might be responsible for the reducedin vivo growth of the TS/A cell line in the presence of TS/A-IL4 cells.


Journal of Pharmacology and Experimental Therapeutics | 1999

In Vitro Cell Cycle Arrest, In Vivo Action on Solid Metastasizing Tumors, and Host Toxicity of the Antimetastatic Drug NAMI-A and Cisplatin

Alberta Bergamo; Renato Gagliardi; Vito Scarcia; Ariella Furlani; Enzo Alessio; Giovanni Mestroni; Gianni Sava


Anticancer Research | 1999

Treatment of metastases of solid mouse tumours by NAMI-A: comparison with cisplatin, cyclophosphamide and dacarbazine.

Gianni Sava; Renato Gagliardi; Alberta Bergamo; Enzo Alessio; Giovanni Mestroni


International Journal of Molecular Medicine | 1999

In vitro down regulation of ICAM-1 and E-cadherin and in vivo reduction of lung metastases of TS/A adenocarcinoma by a lysozyme derivative.

Sabrina Pacor; Renato Gagliardi; E. Di Daniel; Marta Vadori; Gianni Sava


Anticancer Research | 1996

Cytofluorimetric analysis of gut-intraepithelial and mesenteric lymph node lymphocytes of tumour bearing mice fed with egg-white lysozyme

Sabrina Pacor; Giacomello E; Alberta Bergamo; Renato Gagliardi; Moreno Cocchietto; Gianni Sava


Journal of Experimental Therapeutics and Oncology | 1996

Stimulation of GALT and activation of mesenteric lymph node lymphocytes by a modified lysozyme in CBA mice with MCa mammary carcinoma.

Gianni Sava; Alberta Bergamo; Ilaria Capozzi; Katiuscia Clerici; Sabrina Pacor; Renato Gagliardi; Emiliana Giacomello; Marina Zacchigna; G. Di Luca; E. Boccù


Pharmacological Research | 1995

Modification of lymphocytes of peyer's patches - mesenteric lymph nodes - spleen by egg-white lysozyme

Sabrina Pacor; Gianni Sava; A. Bergamo; E. Giacomello; Renato Gagliardi; E. Boccù; M. Zacchigna

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