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7. Adoptive Immunotherapy of Advanced Cancer with LAK Cells and Different Dosages of Interleukin-2:Analysis of Lymphocyte Subpopulations

Author

Samoggia, P., Ruggeri, E. M., Mariani, G., Carlini, P., Salvo, G., Giannella, G., Habetswallner, D., Montesoro, E., Arena, M. G., Masciulli, R., Bulgarini, D., Petrillo, G., Pollera, C. F., Marolla, P., Natali, S., Boccoli, G., Mastroberardino, G., Isacchi, G., Testa, U., Calabresi, F., Peschle, C., Freund, Mathias, editor, Link, Hartmut, editor, and Welte, Karl, editor

Published
1990
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30. Scientific Proceedings Second International Symposium on Cytostatic Drug Resistance

Author

Hill, Bridget T., Hosking, L. K., McClean, S., Shellard, S. A., Dempke, W. C. M., Whelan, R. D. H., Sehested, M., Friche, E., Demant, E. J. F., Jensen, P. B., Kopnin, B. P., Wolf, B., Seidel, A., Nickelsen, M., Brandt, I., Heinemann, G., Dietel, M., Bremer, S., Hoof, T., Tümmler, B., Broxterman, H. J., Versantvoort, C. H. M., Kuiper, C. M., Feller, N., Schuurhuis, G. J., Lankelma, J., Gupta, S., Tsuruo, T., Kim, C., Gollapudi, S., Bittl, A., Nap, M., Jäger, W., Lathan, B., Lang, N., Raikhlin, N. T., Perevozchikov, A. G., Volodina, J. L., Licht T., Fiebig H. H., Bross K. J., Herrmann F., Mertelsmann R., Bashir, I., Sikora, K., Foster, C. S., Castagna, M., Viacava, P., Cianfrigliao, M., Favati, A., Collecchi, P., Caligo, M. A., Cipollini, G., Bevilacqua, G., Schrenk, D., Gant, T. W., Silverman, J. A., Thorgeirsson, S. S., Harstrick, A., Zhang, Z. G., Schmoll, H. J., Rustum, Y., Mitze, M., Beck, T., Weikel, W., Brumm, C., Knapstein, P. G., McDonald, T., Gardner, P., Kang, N., van der Heyden, S. A. M., Elst, H. J., Stein, U., Jandrig, B., Krause, H., Schmidt-Peter, P., Frege, J., Wunderlich, V., Boven, E., van Kalken, C. K., Pinedo, H. M., Gebauer, W., Fallgren-Gebauer, E., Diete, M., Wagner, T., Müller, M. R., Lennartz, K., Nowrousian, H. R., Seeber, S., Shtil, A. A., Kazarov, A. R., Gudkov, A. V., Stavrovskaya, A. A., Djuraeva, F. H., Stromskaya, T. P., Noller, A., Frese, G., Neumann, M., Wilisch, A., Probst, H., Gekeler, V., Handgretinger, R., Schmidt, H., Muller, C. P., Dopfer, R., Klingebiel, T., Niethammer, D., Weger, S., Diddens, H., Daumiller, E., Bunge, A., Lilischkis, R., Salmassi, A., Kopun M., Scherthan H., Granzow C., Leuschner, I., Schmidt, D., Hoffmann, H., Harms, D., Scagliotli, G. V., Leonardo, E., Cappia, S., Esposito, G., Tombesi, M., Cianfriglia, M., Esposito, G. V., Merendino, N., Viora, M., Caserta, M., Tritarelli, E., Rocca, E., Boccoli, G., Samoggia, P., Fossati, C., Testa, U., Peschle, C., Darling, J. L., Ashmore, S. M., Peterson, D. C., Thomas, D. G. T., Kramer, R. A., Stanlunas, R., Summerhayes, T., Lion, T., Shoemaker, R. H., Wu, L., Smythe, A., Boyd, M. R., Beck, W. T., Danks, M. K., Wolverton, J. S., Chen, M., Bugg, B. Y., Suttle, D. P., Catapano, C. V., Fernandes, D. J., Gieseler, F., Boege, F., Erttmann, R., Arps, H., Zwelling, L., Wilms, K., Biersack, H., Kaspers, G. J. L., Pieters, R., Klumper, E., de Waal, F. C., van Wering, E. R., Veerman, A. J. P., Schmidt, C. A., Lorenz, F., Schäfer, A., Kirsch, A., Siegert, W., Huhn, D., Simon, W. E., Siebert, G., Schneider, M., Oettling, M., Reymann, A., Entmann, R., Schmidt, S., Woermann, C., Windmeier, C., Herzig, I., Schaefer, B., Heidebrecht, H. J., Wacker, H. H., Künnemann, H., van Heijningen, Th. H. M., Slovak, M. L., Baak, J. P. A., Steidtmann, K., Fichtinger-Schepman, A. -M. J., Hill, B. I., Scanlon, K. J., Zeller, W. J., Chen, G., Gietema, J. A., de Vries, E. G. E, Sleijfer, D.Th, Willemse, P. H. B., Guchelaar, H. J., Uges, D. R. A., Aulenbacher, P., Voegeli, R., Mulder, N. H., Skrezek, C., Bertermann, H., Eichholtz-Wirth, H., Born, R., Bier, H., Koch, M., Bernhardt, G., Hählen, K., Reile, H., van Zantwijk, C. H., Wering, E. R. van, Görögh, T., Lippert, B., Werner, J. A., Eickbohm, J. E., Mickiseh, G. H., Gottesman, M. M., Pastan, I., Hofmann, J., Wolf, A., Spitaler, M., Bock, G., Grunicke, H., Ponstingl, H., Roth, I., Granzow, C., Dörner, C., Erttmann, R., Looft, G., Ossenkoppele, G. J., Scheffer, G. L., Atassi, G., Pierre, A., Kraus, L., Leonce, S., Regnier, G., Dhainaut, A., Ponstingl H., Stöhr M., Rohlff, C., Glazer, R. I., Cho-Chung, Y. S., Höllt, V., Kouba, M., Vogt, G., Allmeier, H., Nissen, N. I., Cros, S., Guilbaud, N., Dunn, T., Berlion, M., Atassi, G., Bizzari, J. P., Messing, A. M., Matuschek, A., Mutter, I., Kiwit, J. C. W., Bastian, L., Goretzki, P. E., Frilling, A., Simon, D., Röher, H. D., Reichle, A., Altmayr, F., Rastetter, J., Erbil, C., Jaques, G., Maasberg, M., Havemann, K., Häußermann, K., Heidebrecht, H. -J., Van de Vrie, W., Gheuens, E. E. O., Durante, N. M. C., De Bruijn, E. A., Marquet, R. L., Van Oosterom, A. T., Eggermont, A. M. M., Stow, M. W., Vickers, S. E., Warr, J. R., Roller, E., Eichelbaum, M., Klumpp, B., Krause, J., Schumacher, K., Hörner, S., Laßmann, A., Traugott, U., Schlick, E., Bürkle, D., Futscher BW, List AF, Dalton WS, Ladda, E., Bühl, K., Weimer, A., Eser, C., Hamprecht, K., Schalk, K. P., Jackisch, C., Brandt, B., Blum, M., Louwen, F., Schulz, K., Hanker, J. P., Rüther, U., Schmidt, A., Müller, H. A. G., Nunnensiek, C., Bader, H., Eisenberger, F., Jipp, P., Niethammer, B., Muller, C., Ling, V., Joncourt, F., Redmond, S., Stöhr, M., Buser, K., Fey, M., Tobler, A., Brunner, K., Gratwohl, A., Cerrry, T., Nuessler, V., Pelka-Fleischer, R., Nerl, C., Beckert, B., Wilmanns, W., Hegewisch-Becker, S., Fliegner, M., Zander, A., Hossfeld, D. K., Blanz, J., Mewes, K., Ehninger, G., Zeller, K. -P., Schuldes, H., Herrmann, G., Boeckmann, W., Schroeder, R., Jonas, D., Zurborn, K. -H., Bruhn, H. D., Uharek, L., Glass, B., Gassmann, W., Loeffler, H., Mueller-Ruohholtz, W., Gassmann W., Glass B., Uharek L., Loeffler H., Mueller-Ruchholtz W., Jaquet, K., Kreipe, H., Felgner, J., Radzun, H. J., Parwaresch, M. R., Kogan EA, Mazurenko NN, Sekamova SM, Wolf, H., Röhe, K., Wilkens, K., Clausen, M., Henze, E., van der Bosch, J., Rüller, S., Schlaak, M., Köhl, U., Schwabe, D., Rohrbach, E., Montag, E., Bauer, S., Cinatl, J., Cinatl, Jr, I., Mainke, M., Geiss, H., Kornhuber, B., Juhl, H., Stritzel, H., Kalhoff, H., Schniegel, W., Menke, T., Pröbsting, B., Schulze-Westhoff, P., Boos, J., Weidner, J., Wedemeyer, N., Wiedorn, K., Ueda, Y., Blasius, S., Wuisman, P., Böcker, W., Roessner, A., Dockhorn-Dworniczak, B., Ramm, D., Knebel, J., Sass, W., Aufderheide, M., and Seifert, J.

Published
1991
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39. Recent Advances in Erythropoietin Physiology

Author

Peschle, C., Magli, M. C., Cillo, C., Lettieri, F., Pizzella, F., Migliaccio, G., Soricelli, A., Scala, G., Mastroberardino, G., Sasso, G. F., Murphy, Martin J., Jr., editor, Peschle, Cesare, editor, Gordon, Albert S., editor, and Mirand, Edwin A., editor

Published
1978
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41. Ectopic expression of interferon regulatory factor-1 potentiates granulocytic differentiation

Author

Coccia, E M, Stellacci, E, Valtieri, M, Masella, B, Feccia, T, Marziali, G, Hiscott, J, Testa, U, Peschle, C, and Battistini, A

Subjects
Adult, Genetic Vectors, Down-Regulation, Transfection, Biochemistry, Cell Line, Interferon-gamma, Mice, Proto-Oncogene Proteins c-myb, Proto-Oncogene Proteins, Granulocyte Colony-Stimulating Factor, Animals, Humans, Growth Substances, Molecular Biology, Cell Differentiation, Cell Biology, Phosphoproteins, Growth Inhibitors, Hematopoiesis, DNA-Binding Proteins, Enzyme Activation, Repressor Proteins, Gene Expression Regulation, Culture Media, Conditioned, Trans-Activators, Muramidase, Biomarkers, Interferon Regulatory Factor-2, Research Article, Granulocytes, Interferon Regulatory Factor-1, Protein Binding, Transcription Factors
Abstract

Numerous transcription factors allow haematopoietic cells to respond to lineage- and stage-specific cytokines and to act as their effectors. It is increasingly evident that the interferon regulatory factor-1 (IRF-1) transcription factor can selectively regulate different sets of genes depending on the cell type and/or the nature of cellular stimuli, evoking distinct responses in each. In the present study, we investigated mechanisms underlying the differentiation-inducing properties of granulocytic colony-stimulating factor (G-CSF) and whether IRF transcription factors are functionally relevant in myeloid differentiation. Both normal human progenitors and murine 32Dcl3 myeloblasts induced to differentiate along the granulocytic pathway showed an up-regulation of IRF-1 expression. Ectopic expression of IRF-1 did not abrogate the growth factor requirement of 32Dcl3 cells, although a small percentage of cells that survived cytokine deprivation differentiated fully to neutrophils. Moreover, in the presence of G-CSF, granulocytic differentiation of IRF-1-expressing cells was accelerated, as assessed by morphology and expression of specific differentiation markers. Down-modulation of c-Myb protein and direct stimulation of lysozyme promoter activity by IRF-1 were also observed. Conversely, constitutive expression of IRF-2, a repressor of IRF-1 transcriptional activity, completely abrogated the G-CSF-induced neutrophilic maturation. We conclude that IRF-1 exerts a pivotal role in granulocytic differentiation and that its induction by G-CSF represents a limiting step in the early events of differentiation.

Published
2001
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42. Structural and functional characterization of FGF-2 sugar-induced modification

Author

FACCHIANO F, DARCANGELO D, RUSSO K, MENNELLA C, RAGONE R, ZAMBRUNO G, CARBONE V, RIBATTI D, PESCHLE C, CAPOGROSSI MC FACCHIANO A., FOGLIANO, VINCENZO, Facchiano, F, Darcangelo, D, Russo, K, Fogliano, Vincenzo, Mennella, C, Ragone, R, Zambruno, G, Carbone, V, Ribatti, D, Peschle, C, and CAPOGROSSI MC FACCHIANO, A.

Published
2006

43. Relation of various plasma growth factor levels in patients with stable angina pectoris and total occlusion of a coronary artery to the degree of coronary collaterals

Author

BRIGUORI C, TESTA U, COLOMBO A, PETRUCCI E, AIROLDI F, PESCHLE C, G. CONDORELLI, CONDORELLI, GEROLAMA, Briguori, C, Testa, U, Colombo, A, Petrucci, E, Condorelli, Gerolama, Airoldi, F, Peschle, C, and G., Condorelli

Abstract

We assessed (1) angiogenic factors in patients with stable angina and longstanding (> or =24 months) total occlusion of a single coronary artery and (2) the relation between plasma levels of angiogenic factors and the development of collateral vessels as evaluated by coronary angiography. Plasma concentrations of vascular endothelial growth factor (VEGF(165)), fibroblast growth factor, placenta-derived growth factors (PlGFs), and hepatocyte growth factor were assessed in 96 patients with stable angina and longstanding (> or =24 months) total occlusion of a single coronary artery. According to coronary angiographic results, 18 patients had no visible collaterals (group 0), 21 patients had visible collaterals but no filling of the recipient epicardial vessel (group 1), and 57 patients showed filling (partial or complete) of the recipient epicardial vessel by collaterals (group 2). Plasma VEGF(165) and PlGF concentrations were higher in group 1 than in groups 0 and 2 (VEGF(165) 75 pg/ml, range 24 to 105, vs 23 pg/ml, range 15 to 29, and 19 pg/ml, range 10 to 41, respectively, F = 5.53, p = 0.006; PlGF 35 pg/ml, range 3.5 to 105, vs 1 pg/ml, range 1 to 38, and 1 pg/ml, range 1 to 5, respectively, F = 7.09, p = 0.008). Plasma VEGF(165) and PlGF levels were similar in groups 0 and 2. There was no significant difference in plasma levels of fibroblast and hepatocyte growth factor concentrations across the 3 groups. In conclusion, plasma levels of angiogenic growth factors differ among patients with stable angina pectoris and longstanding total coronary occlusion.

Published
2006

44. Absence of caspase 8 and high expression of PED protect primitive neural cells from cell death

Author

Ricci Vitiani L, Pedini F, Mollinari C, Bonci D, Bez A, Colombo A, Parati E, Peschle C, De Maria R., CONDORELLI, GEROLAMA, Ricci Vitiani, L, Pedini, F, Mollinari, C, Condorelli, Gerolama, Bonci, D, Bez, A, Colombo, A, Parati, E, Peschle, C, and De Maria, R.

Subjects
apoptosis
Abstract

The mechanisms that control neural stem and progenitor cell survival are unknown. In several pathological conditions, death receptor (DR) ligands and inflammatory cytokines exert a deleterious effect on neurons, whereas primitive neural cells migrate and survive in the site of lesion. Here, we show that even in the presence of inflammatory cytokines, DRs are unable to generate death signals in primitive neural cells. Neural stem and progenitor cells did not express caspase 8, the presence of which is required for initiating the caspase cascade. However, exogenous or cytokine-mediated expression of caspase 8 was not sufficient to restore their DR sensitivity. Searching for molecules potentially able to block DR death-inducing signaling complex (DISC), we found that primitive neural cells expressed high levels of the death effector domain-containing protein PED (also known as PEA-15). PED localized in the DISC and prevented caspase 8 recruitment and activation. Moreover, lentiviral-mediated delivery of PED antisense DNA resulted in dramatic down-regulation of the endogenous gene expression and sensitization of primitive neural cells to apoptosis mediated by inflammatory cytokines and DRs. Thus, absence of caspase 8 and high expression of PED constitute two levels of protection from apoptosis induced by DRs and inflammatory cytokines in neural stem and progenitor cells.

Published
2004

45. Coordinate expression and proliferative role of HOXB genes in activated adult T lymphocytes

Author

Alessandra Carè, Testa, U., Bassani, A., Tritarelli, E., Montesoro, E., Samoggia, P., Cianetti, L., and Peschle, C.

Subjects
Cell Biology, Molecular Biology
Abstract

We investigated the expression of HOXB cluster genes in purified phytohemagglutinin (PHA)-activated T lymphocytes from normal adult peripheral blood by reverse transcription PCR and RNase protection. These genes are not expressed in quiescent T cells, except for barely detectable B1 RNA. After the PHA stimulus, HOXB gene activation initiates coordinately as a rapid induction wave in the 3'-->5' cluster direction (i.e., from HOXB1 through B9 genes). Thus, (i) expression of the foremost 3'-located B1 and B2 genes peaks 10 min after PHA addition and then rapidly declines, (ii) activation of B3, B4, and B5 begins 10 min after PHA addition and peaks at later times (i.e., at 120 min for B5), (iii) B6, B7, and B9 are expressed at a low level starting at later times (45 to 60 min), and (iv) B8 remains silent. Treatment of PHA-activated T lymphocytes with antisense oligonucleotides to B2 or B4 mRNA causes a drastic inhibition of T-cell proliferation and a decreased expression of T-cell activation markers (i.e., interleukin 2 and transferrin receptors). Similarly, treatment of CEM-CCRF, Peer, and SEZ627 T acute lymphocytic leukemia cell lines with anti-B4 oligomer markedly inhibits cell proliferation. Finally, T cells stimulated by a low dosage of PHA in the presence of 1 microM retinoic acid show a marked increase of both HOXB expression, particularly B2, and cell proliferation. These studies provide novel evidence on the role of HOX genes in adult cell proliferation. (i) Coordinate, early activation of HOXB genes from the 3'-->5' cluster side apparently underlies T-cell activation. (ii) The expression pattern in adult PHA-activated T cells is strikingly similar to that observed in retinoic acid-induced teratocarcinoma cells (A. Simeone, D. Acampora, L. Arcioni, P. W. Andres, E. Boncinelli, and F. Mavilio, Nature (London) 346:763-766, 1990), thus suggesting that molecular mechanisms underlying HOX gene expression in the earliest stages of development may also operate in activated adult T lymphocytes.

Published
1994
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46. Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha

Author

Aloisi, F, Carè, A, Borsellino, G, Gallo, Paolo, Rosa, S, Bassani, A, Cabibbo, A, Testa, U, Levi, G, and Peschle, C.

Subjects
Immunology, Immunology and Allergy
Abstract

Astrocyte-enriched populations were established from human embryonic brain analyzed for their ability to synthesize cytokines potentially relevant for mechanisms of inflammation and immunity in the brain. Unstimulated astrocytes did not secrete significant IL-6, IL-8, macrophage CSF (M-CSF), granulocyte-macrophage CSF (GM-CSF), or granulocyte-CSF (G-CSF), as determined by specific ELISA and/or bioassay. With the exception of M-CSF mRNA, transcripts for the above factors were not detected in unstimulated astrocytes. On exposure of human astrocytes to IL-1 beta, high levels of IL-6, IL-8, M-CSF, G-CSF, and GM-CSF mRNAs were detected; moreover, active secretion of all the above cytokines was demonstrated. TNF-alpha was also able to stimulate IL-6, IL-8, M-CSF, GM-CSF, and G-CSF synthesis and secretion, but was generally less potent than IL-1 beta. No IL-3 mRNA or protein was detected in unstimulated or cytokine-treated astrocytes. IL-1 alpha and IL-1 beta mRNAs and proteins were not detected in unstimulated astrocytes, but were present in very small amounts after stimulation with TNF-alpha/IL-1 beta. No IL-6, M-CSF, GM-CSF, G-CSF, or IL-8 were induced by IL-1 beta or TNF-alpha in early primary cultures, which mainly contain undifferentiated neuronal/glial progenitor cells. These studies demonstrate for the first time the production of multiple cytokines by normal human astrocytes stimulated in culture by IL-1 beta and TNF-alpha. The capacity of human astrocytes to synthesize and release cytokines active on hemolymphopoietic cells supports the concept that these cells play an important role in the regulation of inflammatory and immune responses in a variety of brain pathologies.

Published
1992
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50. MicroRNA-133 controls cardiac myocyte hypertrophy

Author

Carè, A, Catalucci, D, Felicetti, F, Bonci, D., Addario, A, Gallo, P, Bang, Ml, Segnalini, P, Gu, Y, Dalton, Nd, Elia, L, Latronico, Mv, Høydal, M, Autore, Camillo, Russo, Matteo Antonio, DORN GW ND, Ellingsen, O, RUIZ LOZANO, P, Peterson, Kl, Croce, Cm, Peschle, C, and Condorelli, G.

Published
2007

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