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548 results on '"Giavazzi, R"'

102. Metabolism of tumour-derived urokinase receptor and receptor fragments in cancer patients and xenografted mice

Author

Sier, C, Nicoletti, I, Santovito, M, Frandsen, T, Aletti, G, Ferrari, A, Lissoni, A, Giavazzi, R, Blasi, F, Sidenius, N, Sier, CFM, Santovito, ML, Sidenius, N., LISSONI, ANDREA ALBERTO, Sier, C, Nicoletti, I, Santovito, M, Frandsen, T, Aletti, G, Ferrari, A, Lissoni, A, Giavazzi, R, Blasi, F, Sidenius, N, Sier, CFM, Santovito, ML, Sidenius, N., and LISSONI, ANDREA ALBERTO

Abstract

The urokinase-type plasminogen activator receptor (uPAR) is involved in cell migration and tissue remodelling, as a receptor for pro-uPA, as a cell adhesion component, and in a soluble form as a chemoattractant.We have analyzed the presence and the molecular forms of uPAR and uPAR-fragments in urine of ovarian cancer patients in comparison with tumour tissue, ascites, and serum. Carcinoma tissue contained high levels of uPAR, but more abundantly the D2D3-fragment. Ascitic fluid contained similar ratio's of suPAR fragments as corresponding tumour tissue, but serum only contained intact suPAR. Interestingly, urine contained predominantly the uPAR-fragments D1 and D2D3, and the pattern of these fragments was different in cancer patients as compared to healthy individuals. To confirm the hypothesis that circulating and urinary suPAR and suPAR-fragments originate from the tumour tissue, the presence of human suPAR (fragments) was analyzed in mice xenografted with human tumours. Indeed, high levels of urinary D1 fragment were found in mice carrying a tumour displaying cleaved uPAR on the cell surface, but little or no D1 was found in the urine from mice carrying a tumour with full-length uPAR. Mouse serum contained only intact suPAR. Our data demonstrate that the enhanced levels of suPAR fragments in the urine of cancer patients is likely to originate from uPAR expressed in the tumour tissue. Considering the biological activities that uPAR fragments display, the level and typing of uPAR fragments in urine might therefore be clinically more relevant than the plain serum uPAR content.

Published
2004

106. Expression of beta-tubulin isotypes in human ovarian carcinoma xenografts and in a sub-panel of human cancer cell lines from the NCI-Anticancer Drug Screen: correlation with sensitivity to microtubule active agents

Author

Nicoletti, M, Valoti, G, Giannakakou, P, Zhan, Z, Kim, J, Lucchini, V, Landoni, F, Mayo, J, Giavazzi, R, Fojo, T, Nicoletti, M I, Kim, J H, Mayo, J G, Nicoletti, M, Valoti, G, Giannakakou, P, Zhan, Z, Kim, J, Lucchini, V, Landoni, F, Mayo, J, Giavazzi, R, Fojo, T, Nicoletti, M I, Kim, J H, and Mayo, J G

Abstract

Paclitaxel resistance has been associated with overexpression of P-glycoprotein and alterations involving tubulin. To investigate the clinical relevance of these in vitro resistance mechanisms, we established 12 human ovarian carcinoma xenografts, using samples from patients before the start of therapy or after paclitaxel treatment. These xenografts showed a wide range of sensitivity to paclitaxel, and in 4 of them, very low levels of multidrug resistance-1 expression were detected. Using quantitative PCR and human specific primers, the expression of five beta-tubulin isotypes was determined. HM40 was the predominant, accounting for 84.7-98.7% of all tubulin; expression of the other four isotypes (Hbeta9, Hbeta4, H5beta, and Hbeta2) was also detected but at lower levels. No correlation could be demonstrated between isotype expression and paclitaxel sensitivity in these 12 xenografts. A similar pattern of beta-tubulin isotype expression was observed in a subset of cell lines from the National Cancer Institute-Anticancer Drug Screen. In these cell lines, however, a significant correlation between increased expression of Hbeta4 isotype and resistance to paclitaxel was found. Taken together, these results suggest that altered expression of specific beta-tubulin isotypes may not play a significant role in paclitaxel sensitivity in vivo and argue against a possible significance in a clinical setting

Published
2001

119. Inhibition of matrix metalloproteinases by over‐expression of tissue inhibitor of metalloproteinase‐2 inhibits the growth of experimental hemangiomas

Author

Vergani, V., primary, Garofalo, A., additional, Bani, M.R., additional, Borsotti, P., additional, Parker, M. Pelina, additional, Drudis, T., additional, Mazzarol, G., additional, Viale, G., additional, Giavazzi, R., additional, Stetler‐Stevenson, W.G., additional, and Taraboletti, G., additional

Published
2001
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120. Inhibition of matrix metalloproteinases by over-expression of tissue inhibitor of metalloproteinase-2 inhibits the growth of experimental hemangiomas

Author

Vergani, V., primary, Garofalo, A., additional, Bani, M.R., additional, Borsotti, P., additional, Parker, M. Pelina, additional, Drudis, T., additional, Mazzarol, G., additional, Viale, G., additional, Giavazzi, R., additional, Stetler-Stevenson, W.G., additional, and Taraboletti, G., additional

Published
2000
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143. Gemtuzumab ozogamicin (Mylotarg) has therapeutic activity against CD33+ acute lymphoblastic leukaemiasin vitroandin vivo.

Author

Golay, J., Di Gaetano, N., Amico, D., Cittera, E., Barbui, A. M., Giavazzi, R., Biondi, A., Rambaldi, A., and Introna, M.

Subjects
IMMUNOGLOBULINS, ANTINEOPLASTIC agents, ACUTE myeloid leukemia, ANTIBODY-toxin conjugates, IMMUNODEFICIENCY, CELL death
Abstract

Gemtuzumab ozogamicin (GO) is a humanized anti-CD33 antibody conjugated with the cytotoxic drug calicheamicin and approved for the treatment of relapsed acute myeloid leukaemia. As approximately 18% of acute lymphoblastic leukaemias (ALL) are also CD33 positive, we have investigated the cytotoxic activity of GO on CD33+ ALL cellsin vitroandin vivo. 10 ng/ml GO induced 30–95% inhibition of thymidine uptake and 30–70% cell death in four freshly isolated and onein vivopassaged CD33+ ALL-cell cultures. Furthermore, anin vivomodel of a CD33+ ALL carrying the Philadelphia chromosome [t(9;22)] was established. 5 × 106 ALL-2 cells inoculated in the tail vein of severe combined immunodeficient mice engrafted into haematopoietic organs, reaching a mean of 70%, 61% and 69% human CD45+ cells in bone marrow, spleen and liver, respectively, at 35 d. To test the therapeutic activity of GO, 50 or 100 μg immunotoxin was inoculated i.p. on days 7, 11 and 15 following tumour-cell inoculation. GO treatment dramatically inhibited expansion of ALL-2 cells in all tested organs and increased survival of tumour-injected animals by 28–41 d, relative to controls. These data demonstrated that GO is active bothin vitroandin vivoagainst CD33+ ALL cells. [ABSTRACT FROM AUTHOR]

Published
2005
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144. Intraperitoneal and subcutaneous xenografts of human ovarian carcinoma in nude mice and their potential in experimental therapy

Author

Massazza, G, Tomasoni, A, Lucchini, V, Allavena, P, Erba, E, Colombo, N, Mantovani, A, D'Incalci, M, Mangioni, C, Giavazzi, R, Giavazzi, R., COLOMBO, NICOLETTA, Massazza, G, Tomasoni, A, Lucchini, V, Allavena, P, Erba, E, Colombo, N, Mantovani, A, D'Incalci, M, Mangioni, C, Giavazzi, R, Giavazzi, R., and COLOMBO, NICOLETTA

Abstract

Human ovarian carcinomas (HOC) were established s.c. and i.p. in nude mice and the biological characteristics were investigated for 4 xenografts. HOC8 and HOC18, derived respectively from a primary tumor of the ovary and a pleural effusion (from 2 different patients) were established s.c. in nude mice. HOC10 and HOC22, derived from the ascites of 2 patients, were directly established as ascites after i.p. injection in nude mice. The s.c. and i.p. growth behavior of the 4 HOC lines was investigated. HOC18, HOC8 and HOC22 cells produced progressively growing tumor after s.c. injection but HOC10 ascites would not grow s.c. The cell suspension derived from HOC18 only produced carcinomatosis upon i.p. injection, while HOC8 cells produced both ascites and carcinomatosis. The 2 ascites HOC10 and HOC22 produced ascites in nude mice, but only HOC22 formed i.p. carcinomatosis. Histopathological characteristics of the patients' primary tumors persisted in nude mice, regardless of the site of tumor implantation. DNA histograms of the xenografts closely matched the patients' tumors and remained stable at different passages. Cisplatin, adriamycin and cyclophosphamide given i.v. were tested against HOC8 and HOC18 growing s.c. and HOC22 and HOC10 growing i.p. HOC8 showed a significant response to DDP and almost no sensitivity to ADR and CTX. HOC18 showed only moderate growth delay with all 3 drugs. Mice bearing HOC10 and HOC22 ascites had a prolonged survival time after DDP and ADR treatment.

Published
1989

148. Natural cytotoxic activity in human lungs.

Author

Bordignon, C., Villa, F., Vecchi, A., Giavazzi, R., Introna, M., Avallone, R., and Mantovani, A.

Subjects
CARDIOPULMONARY system, COMMUNICABLE diseases, PREVENTIVE medicine, LEUCOCYTES, ANTINEOPLASTIC agents, ANTIVIRAL agents
Abstract

Disease-free surgical lung specimens from 13 patients with neoplastic or infectious diseases and from three subjects with non-neoplastic, non-infectious pathology were mechanically disaggregated. Natural cytotoxicity was tested against 51Cr-labelled K562 larget cells. Unseparated lung cells had little cytotoxicity against K562 cells. Removal of plastic and nylon-wool-adherent cells resulted in cell preparations (morphologically 80% lymphoid) with increased cytolytic activity against K562 but cytotoxicity levels were considerably lower than those of blood lymphocytes tested in parallel. Similar results were obtained when phagocytic adherent cells were removed with carbonyl iron. The NK-resistant murine TU5 and human Raji lines were not affected by lung effector cells. In vitro exposure lo partially purified fibroblast interferon enhanced the cytotoxicity of unseparated or non-adherent lung cells. Thus, unlike in mouse pulmonary tissue, low levels of natural cytotoxic activity are associated with the human lung. [ABSTRACT FROM AUTHOR]

Published
1982

150. In vivo and in vitro models for the analysis of retroviral vector mediated expression of human ADA in ADA deficient cells from patients affected by severe combined immunodeficiency

Author

BORDIGNON , CLAUDIO, Hantzopoulos P., Fumagalli L., Rossini S., FERRARI, GIULIANA, Ungers G. E., Soldati M., Nobili N., Maggioni D., Giavazzi R., O’Reilly R. J., Mavilio F., E. Gilboa, Bordignon, Claudio, Hantzopoulos, P., Fumagalli, L., Rossini, S., Ferrari, Giuliana, Ungers, G. E., Soldati, M., Nobili, N., Maggioni, D., Giavazzi, R., O’Reilly, R. J., Mavilio, F., and E., Gilboa

Published
1989

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