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253 results on '"Landuzzi L"'

1. Re:Randomized trial of adjuvant human interferon gamma versus observation in high-risk cutaneous melanoma: a Southwest Oncology Group study.

Author

Lollini, PL, Nanni, P, de Giovanni, C, Nicoletti, G, and Landuzzi, L

Subjects
Killer Cells, Natural, Humans, Melanoma, Skin Neoplasms, Tumor Necrosis Factor-alpha, Membrane Glycoproteins, Neoplasm Proteins, Antineoplastic Agents, Chemotherapy, Adjuvant, Risk Factors, Genes, MHC Class I, Interferon-gamma, Killer Cells, Natural, Chemotherapy, Adjuvant, Genes, MHC Class I, Oncology & Carcinogenesis, Oncology and Carcinogenesis
Published
1996

9. Expression of an IGF-I receptor dominant negative mutant induces apoptosis, inhibits tumorigenesis and enhances chemosensitivity in Ewing's sarcoma cells

Author

Scotlandi K., Avnet S., Benini S., Manara M. C., Serra M., Cerisano V., Perdichizzi S., Lollini P. -L., De Giovanni C., Landuzzi L., Picci P., Scotlandi K., Avnet S., Benini S., Manara M.C., Serra M., Cerisano V., Perdichizzi S., Lollini P.-L., De Giovanni C., Landuzzi L., and Picci P.

Subjects
Time Factors, Time Factor, Cell Survival, Blotting, Western, Mice, Nude, Apoptosis, Sarcoma, Ewing, Transfection, Receptor, IGF Type 1, Mice, Tumor Cells, Cultured, Animals, Insulin-like growth factor-I, Chemosensitivity, Tumorigenesi, Animal, Apoptosi, Ewing's sarcoma, Gene Expression Regulation, Neoplastic, Survival Rate, Doxorubicin, Dominant negative mutant, Mutation, Nude mice, Cell Division, Neoplasm Transplantation
Abstract

IGF-IR plays an essential role in the establishment and maintenance of the transformed phenotype of ES cells and interference with the IGF-IR pathways causes reversal of the malignant potential of this neoplasm. In this report, we stably transfected a dominant negative IGF-IR expression plasmid in an ES cell line to determine the effectiveness of this strategy against the in vitro and in vivo growth of ES cells. DXR sensitivity of TC-71 cells expressing dominant negative mutants of IGF-IR was also examined. The mutated IGF-IR that we used carries a mutation in the ATP-binding domain of the intracellular β subunit, while the extracellular, ligand-binding α subunit remains unchanged. Cells carrying the dominant mutant IGF-IR had a marked decrease in proliferation, a significant increase in anoikis-induced apoptosis and a severely reduced ability to form colonies in soft agar. In vivo, when cells carrying dominant negative IGF-IR were injected into nude mice, the tumor formation and metastatic abilities of ES cells were reduced and survival increased. Furthermore, transfected clones showed significantly higher sensitivity to DXR, a major drug in the treatment of ES. These results indicate that the IGF/IGF-IR stimulation of ES cells may be inhibited by expression of mutated IGF-IR on their surfaces and that this strategy may be considered a possible alternative to impair this important target of ES cells, whose therapeutic potential was further confirmed. © 2002 Wiley-Liss, Inc.

Published
2002

12. Up-regulation of EphB and ephrin-B expression in rhabdomyosarcoma

Author

Anna C. Berardi, Marsilio, S., Rofani, C., Salvucci, O., Altavista, P., Perla, F. M., Diomedi-Camassei, F., Uccini, S., Kokai, G., Landuzzi, L., Mcdowell, H. P., Dominici, C., A.C. Berardi, S. Marsilio, C. Rofani, O. Salvucci, P. Altavista, F.M. Perla, F. Diomedi-Camassei, S. Uccini, G. Kokai, L. Landuzzi, H.P. McDowell, and C. Dominici.

Subjects
Cell Line, Tumor, Eph-B, Humans, Ephrin-B2, Ephrin-B1, RNA, Messenger, Ligands, Ephrins, RHABDOMYOSARCOMA, EPHRIN, Receptors, Eph Family, Up-Regulation
Abstract

BACKGROUND: Increased expression of Eph receptors and their ephrin ligands has been implicated in promoting angiogenesis and tumour progression in several malignancies. Here the expression of mRNA for ephrin-B and EphB receptors in rhabdomyosarcoma (RMS) cell lines and primary tumours was investigated. MATERIALS AND METHODS: Expression of mRNA for ephrin-B and EphB receptors in RMS cell lines and primary tumours was measured by real-time RT-PCR and compared with the expression in normal striated muscle. RESULTS: A dysregulation of both ligands and receptors was found in all cell lines. In embryonal tumours, overexpression of ephrin-B1 correlated with overexpression of EphB1 (r = 0.97, p < 0.01) and EphB3 (r = 0.94, p < 0.05); overexpression of ephrin-B2 correlated with overexpression of EphB1 (r = 0.94, p < 0.05), EphB2 (r = 0.88, p < 0.01) and EphB4 (r = 0.76, p < 0.01). In alveolar tumours, no similar correlations were found. A correlation between EphB2 and EphB4 receptors was demonstrated in both tumour types, being positive in embryonal cases (r = 0.81, p < 0.01) and negative in alveolar (r = -1.00, p < 0.01). CONCLUSION: A global up-regulation of ephrin-B and EphB receptors in RMS tumours was found. The correlation between EphB2 and EphB4 receptors suggests a possible role for ephrin-B and EphB receptors in RMS development

Published
2008

13. An aza-macrocycle containing maltolic side-arms (maltonis) as potential drug against human pediatric sarcomas

Author

Guerzoni, C, Amatori, S, Giorgi, L, Manara, Mc, Landuzzi, L, Lollini, P, Tassoni, A, Balducci, Mario, Manfrini, M, Pratelli, L, Serra, M, Picci, P, Magnani, M, Fusi, V, Fanelli, M, Scotlandi, K., Balducci, Mario (ORCID:0000-0003-0398-9726), Guerzoni, C, Amatori, S, Giorgi, L, Manara, Mc, Landuzzi, L, Lollini, P, Tassoni, A, Balducci, Mario, Manfrini, M, Pratelli, L, Serra, M, Picci, P, Magnani, M, Fusi, V, Fanelli, M, Scotlandi, K., and Balducci, Mario (ORCID:0000-0003-0398-9726)

Abstract

Identification of new drugs against paediatric sarcomas represents an urgent clinical need that mainly relies on public investments due to the rarity of these diseases. In this paper we evaluated the in vitro and in vivo efficacy of a new maltol derived molecule (maltonis), belonging to the family of molecules named hydroxypyrones.

Published
2014

14. Human responses against HER-2-positive cancer cells in human immune system-engrafted mice

Author

De Giovanni, C, primary, Nicoletti, G, additional, Landuzzi, L, additional, Romani, F, additional, Croci, S, additional, Palladini, A, additional, Murgo, A, additional, Antognoli, A, additional, Ianzano, M L, additional, Stivani, V, additional, Grosso, V, additional, Iezzi, M, additional, Stramucci, L, additional, Barbieri, E, additional, Lemoli, R M, additional, Nanni, P, additional, and Lollini, P-L, additional

Published
2012
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19. A Multi-DNA Preventive Vaccine for p53/Neu-Driven Cancer Syndrome

Author

De Giovanni, C., primary, Nicoletti, G., additional, Palladini, A., additional, Croci, S., additional, Landuzzi, L., additional, Antognoli, A., additional, Murgo, A., additional, Astolfi, A., additional, Ferrini, S., additional, Fabbi, M., additional, Orengo, A.M., additional, Amici, A., additional, Penichet, M.L., additional, Aurisicchio, L., additional, Iezzi, M., additional, Musiani, P., additional, Nanni, P., additional, and Lollini, P.-L., additional

Published
2009
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23. UNCOUPLING OF GROWTH-INHIBITION AND DIFFERENTIATION IN DEXAMETHASONE-TREATED HUMAN RHABDOMYOSARCOMA CELLS

Author

DEGIOVANNI, C, LOLLINI, PL, DOLCETTI, R, LANDUZZI, L, NICOLETTI, G, DANDREA, E, SCOTLAND, K, NANNI, P, DEGIOVANNI, C, LOLLINI, PL, DOLCETTI, R, LANDUZZI, L, NICOLETTI, G, DANDREA, E, SCOTLAND, K, and NANNI, P

Abstract

The effects of dexamethasone, a synthetic glucocorticoid, and of N,N-dimethylformamide on in vitro growth and differentiation and on proto-oncogene expression of human rhabdomyosarcoma cells were studied. RD/18 clone cells (derived from the embryonal rhabdomyosarcoma cell line RD) treated with 100 nM dexamethasone showed an almost complete block of differentiation: about 5% myosin-positive cells were observed after 2 weeks of culture in dexamethasone-supplemented differentiation medium, compared to 20% of untreated cultures. Dexamethasone also induced a 20-30% growth inhibition and a more flattened morphology. The treatment with N,N-dimethylformamide induced a significantly increased proportion of myosin-positive cells (reaching about 30%) and a 40% growth inhibition. Induction of differentiation inversely correlated with the levels of c-myc proto-oncogene expression: after a 2 week culture dexamethasone-treated cells showed the highest c-myc expression and N,N-dimethylformamide-treated cells the lowest. Culture conditions per se down-modulated c-erbB1 and up-regulated c-jun expression, with no relationship to the differentiation pattern. Other proto-oncogenes were not expressed (c-sis, N-myc, c-mos, c-myb) or were not modulated (c-fos, c-raf). Therefore dexamethasone and N,N-dimethylformamide, both causing a decreased growth rate, showed opposing actions on myogenic differentiation and on c-myc proto-oncogene expression of human rhabdomyosarcoma cells.

Published
1993

25. The Immune Response Elicited by Mammary Adenocarcinoma Cells Transduced with Interferon-γand Cytosine Deaminase Genes Cures Lung Metastases by Parental Cells

Author

Nanni, P., primary, de Giovanni, C., additional, Nicoletti, G., additional, Landuzzi, L., additional, Rossi, I., additional, Frabetti, F., additional, Giovarelli, M., additional, Forni, G., additional, Cavallo, F., additional, Di Carlo, E., additional, Musiani, P., additional, and Lollini, P.-L., additional

Published
1998
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29. Transduction of Genes Coding for a Histocompatibility (MHC) Antigen and for Its Physiological Inducer Interferon-γ in the Same Cell: Efficient MHC Expression and Inhibition of Tumor and Metastasis Growth

Author

Lollini, P.-L., primary, de Giovanni, C., additional, Landuzzi, L., additional, Nicoletti, G., additional, Frabetti, F., additional, Cavallo, F., additional, Giovarelli, M., additional, Forni, G., additional, Modica, A., additional, Modesti, A., additional, Musiani, P., additional, and Nanni, P., additional

Published
1995
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45. Decreased adhesion to endothelial cells and matrix proteins of H-2Kbgene transfected tumour cells

Author

Lauri, D, De Giovanni, C, Biondelli, T, Lalli, E, Landuzzi, L, Facchini, A, Nicoletti, G, Nanni, P, Dejana, E, and Lollini, P-L

Abstract

Transfection of murine metastatic B78H1 cells (derived from B16 melanoma) with a syngeneic H-2Kb gene was used to study the effect of Major Histocompatibility Complex (MHC) gene products on tumour cell adhesion to endothelial cells and matrix proteins and the involvement in the metastatic process. H-2Kb-expressing transfectants showed a reduced adhesion to endothelial surfaces of different origin (four murine endotheliomas and human umbilical vein endothelial cells) when compared to parental B78H1 cells and to controls transfected with pSV2neo alone. On the average a 50-70% reduction in adhesion to endothelial cells was observed among H-2Kb transfectants. H-2Kb transfectants had a reduced expression of the alpha 4 integrin subunit, moreover the adhesion of Neo-transfected clones to endothelial cells was reduced to the levels of H-2Kb transfectants by antibodies directed against the beta 1 subunit and the endothelial VCAM-1 molecule, thus suggesting an impairment of the VLA-4/VCAM-1 interaction in H-2Kb transfectants. Adhesion to extracellular matrix components was also strongly decreased: in general the adhesion of H-2Kb cells showed a 50-75% inhibition with respect to Neo or parental controls. The highest difference was observed in adhesion to vitronectin and laminin, the lowest in adhesion to fibronectin. Reduction in adhesive properties of H-2Kb-expressing transfectants could be involved in the reduced metastatic ability, evaluated by means of intravenous injection of cells: H-2Kb transfectants yielded less than ten lung colonies, while all controls produced more than 100. Our data indicate that expression of a single class I MHC gene can significantly alter the metastatic phenotype of MHC-negative tumour cells and this could be related to a general alteration of tumour cell adhesive interactions.

Published
1993
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46. Transduction of Genes Coding for a Histocompatibility (MHC) Antigen and for Its Physiological Inducer Interferon- in the Same Cell: Efficient MHC Expression and Inhibition of Tumor and Metastasis Growth

Author

Lollini, P.-L., de Giovanni, C., Landuzzi, L., Nicoletti, G., Frabetti, F., Cavallo, F., Giovarelli, M., Forni, G., Modica, A., Modesti, A., Musiani, P., and Nanni, P.

Abstract

ABSTRACTThe mouse mammary carcinoma TS/A, of BALB/c (H-2d) origin, was transfected with the murine interferon- (IFN-) gene (Int. J. Cancer 55: 320, 1993). We used IFN- transfectants as recipients for a second round of transfections with murine allogeneic class I histocompatibility (H-2b) genes that are modulated by IFN. Transfectants with either gene alone, as well as parent TS/A cells (TS/A-pc), were used as controls. Only double transfectants expressed high levels of the allogeneic H-2bgenes, while in H-2bsingle transfectants the expression was very low (but was induced by treatment with exogenous IFN-). The tumorigenic potential of IFN- or H-2bsingle transfectants was reduced in comparison to TS/A-pc. IFN- H-2Kbdouble transfectants were almost nontumorigenic, while IFN- H-2Dbclones gave rise to tumors in about one-half of mice. The experimental metastatic ability of all IFN- H-2bdouble transfectants was very low. IFN- single transfectants were known to induce a strong macrophage response in the host. The expression of allogeneic H-2 antigens added a T-lymphocyte-mediated response that accounted for the lower tumorigenicity of double transfectants. These results show that it is possible to steer the immune response evoked by tumor cells for therapeutic purposes. Moreover, the high H-2 expression obtained in IFN- H-2bdouble transfectants suggests that single IFN- transfectants are ideal recipients for all IFN-sensitive genes. This approach can be used also for other general-purpose inducers of gene expression.

Published
1995
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47. The Immune Response Elicited by Mammary Adenocarcinoma Cells Transduced with Interferon-and Cytosine Deaminase Genes Cures Lung Metastases by Parental Cells

Author

Nanni, P., de Giovanni, C., Nicoletti, G., Landuzzi, L., Rossi, I., Frabetti, F., Giovarelli, M., Forni, G., Cavallo, F., Di Carlo, E., Musiani, P., and Lollini, P.-L.

Abstract

ABSTRACTThe parental cells of the TSA murine mammary adenocarcinoma (TSA-pc) were transfected with both the interferon-(IFN-) gene and the cytosine deaminase (CD) suicide gene to obtain a therapeutic vaccine active against TSA-pc lung metastases. Even in the absence of treatment with the prodrug 5-fluorocytosine (5-FC), the local growth of double transfectants (CD-clones) was inhibited by a marked recruitment of granulocytes and macrophages. In mice harboring TSA-pc micrometastases, therapeutic vaccination with either IFN-or CD single transfectants reduced the number of lung nodules, whereas CD-double transfectants abrogated metastasis growth in up to 80% of mice. Treatment of mice with 5-FC did not alter the curative efficacy of CD-double-transfectant cells. By contrast, in mice vaccinated with CD single-transfectant cells, 5-FC treatment caused a significant loss of their curative activity. Host T cells played an active role in the cure of lung metastases, because vaccination of nude mice with CD-cells was uneffective.

Published
1998
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48. Blockage of insulin-like growth factor-I receptor inhibits the growth of Ewing's sarcoma in athymic mice

Author

Scotlandi K, Benini S, Nanni P, Pier Luigi Lollini, Nicoletti G, Landuzzi L, Serra M, Mc, Manara, Picci P, and Baldini N

Subjects
Mice, Transplantation, Heterologous, Animals, Antibodies, Monoclonal, Mice, Nude, Antineoplastic Agents, Bone Neoplasms, Female, Receptors, Somatomedin, Sarcoma, Ewing, Suramin
Abstract

Innovative, more effective treatment modalities are needed for Ewing's sarcoma (ES), a neoplasm with a disappointingly low survival rate despite the use of aggressive multimodal therapeutic approaches. We have previously shown (K. Scotlandi et al, Cancer Res., 56: 4570-4574, 1996) the existence and the pathogenetic relevance of an autocrine loop that is mediated by the insulin-like growth factor-I receptor (IGF-IR) and is crucial for the survival and proliferation of ES cells in vitro. In this study, we report that the IGF-IR-blocking monoclonal antibody alphaIR3 may also significantly inhibit ES cell growth in vivo. In particular, in almost one-half of the animals tested, after s.c. inoculation with TC-71 ES cells, the blockage of IGF-IR by alphaIR3 induced a complete regression of tumors that developed, which suggests that IGF-IR is valuable as a specific target for novel therapeutic strategies. In addition, suramin, a drug that can interfere with growth factor binding with their receptors, inhibited the tumorigenic and the metastatic ability of TC-71 cells and, therefore, is a promising agent to be combined with conventional cytotoxic drugs for the design of more effective therapeutic regimens.

49. Metastatic ability and differentiative properties of a new cell line of human embryonal rhabdomyosarcoma (CCA)

Author

Giovanni, C., Patrizia Nanni, Nicoletti, G., Ceccarelli, C., Scotlandi, K., Landuzzi, L., and Lollini, P. -L

Subjects
Male, Transplantation, Heterologous, Teratoma, Mice, Nude, Cell Differentiation, Recombinant Proteins, Cell Line, Interferon-gamma, Mice, Culture Techniques, Rhabdomyosarcoma, Tumor Cells, Cultured, Animals, Humans, Neoplasm Metastasis, Child, Cyclophosphamide, Neoplasm Transplantation
Abstract

A new cell line (CCA) was established from a human embryonal rhabdomyosarcoma. It showed an "early" myogenic differentiation pattern: vimentin expression was found in 100% of cells, desmin in about 40% and myosin of the embryonic isoform in about 5%. Class I HLA expression on CCA cells was undeterctable but was greatly increased by in vitro treatment with human recombinant interferon-gamma and only marginally increased by human recombinant tumour necrosis factor-alfa. CCA cell line was tumorigenic in nude mice after either subcutaneous or intramuscular injection; macroscopic spontaneous metastases were not detected. The ability to induce metastatic nodules in the lungs was found when CCA cells were injected intravenously in cyclophosphamide-pretreated nude mice and, at low frequency, in untreated nude mice.

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