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2. P434: MITOCONDRIAL MCL1 REGULATES LEUKEMIC CELLS METABOLISM VIA DIRECT INTERACTION WITH HEXOKINASE II. METABOLIC SIGNATURE AT ONSET PREDICTS OVERALL SURVIVAL IN AMLS’ PATIENTS

Author

Noguera, N. I., primary, Catalano, G., additional, Zaza, A., additional, Banella, C., additional, Ottone, T., additional, Pelosi, E., additional, Travaglini, S., additional, Divona, M., additional, Del Principe, M. I., additional, Buccisano, F., additional, Maurillo, L., additional, Amatuna, E., additional, Testa, U., additional, Venditti, A., additional, and Voso, M. T., additional

Published
2022
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6. 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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15. Targeting histone methyltransferase and demethylase in acute myeloid leukemia therapy

Author

Castelli G, Pelosi E, and Testa U

Subjects
Acute Myeloid Leukemia, hemic and lymphatic diseases, Demethylases, Epigenetic Modifications, Methyltransferases, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, lcsh:RC254-282
Abstract

Germana Castelli, Elvira Pelosi, Ugo Testa Department of Oncology, Istituto Superiore di Sanità, Rome, Italy Abstract: Acute myeloid leukemia (AML) is a clonal disorder of myeloid progenitors characterized by the acquisition of chromosomal abnormalities, somatic mutations, and epigenetic changes that determine a consistent degree of biological and clinical heterogeneity. Advances in genomic technologies have increasingly shown the complexity and heterogeneity of genetic and epigenetic alterations in AML. Among the genetic alterations occurring in AML, frequent are the genetic alterations at the level of various genes involved in the epigenetic control of the DNA methylome and histone methylome. In fact, genes involved in DNA demethylation (such as DNMT3A, TET2, IDH1, and IDH2) or histone methylation and demethylation (EZH2, MLL, DOT1L) are frequently mutated in primary and secondary AML. Furthermore, some histone demethylases, such as LSD1, are frequently overexpressed in AML. These observations have strongly supported a major role of dysregulated epigenetic regulatory processes in leukemia onset and development. This conclusion was further supported by the observation that mutations in genes encoding epigenetic modifiers, such as DMT3A, ASXL1, TET2, IDH1, and IDH2, are usually acquired early and are present in the founding leukemic clone. These observations have contributed to development of the idea that targeting epigenetic abnormalities could represent a potentially promising strategy for the development of innovative treatments of AML. In this review, we analyze those proteins and their inhibitors that have already reached the first stages of clinical trials in AML, namely the histone methyltransferase DOT1L, the demethylase LSD1, and the MLL-interacting protein menin. Keywords: acute myeloid leukemia, epigenetic modifications, methyltransferases, demethylases

Published
2017

26. Transcription factors implicated in late megakaryopoiesis as markers of outcome after azacitidine and allogeneic stem cell transplantation in myelodysplastic syndrome

Author

Falconi, G., Fabiani, Emiliano, Criscuolo, Marianna, Fianchi, Luana, Finelli, C., Cerqui, E., Pelosi, E., Screnci, M., Gurnari, C., Zangrilli, I., Postorino, M., Laurenti, Luca, Piciocchi, A., Testa, U., Lo-Coco, F., Voso, Maria Teresa, Fabiani E. (ORCID:0000-0002-6209-8934), Criscuolo M., Fianchi L., Laurenti L. (ORCID:0000-0002-8327-1396), Voso M. T., Falconi, G., Fabiani, Emiliano, Criscuolo, Marianna, Fianchi, Luana, Finelli, C., Cerqui, E., Pelosi, E., Screnci, M., Gurnari, C., Zangrilli, I., Postorino, M., Laurenti, Luca, Piciocchi, A., Testa, U., Lo-Coco, F., Voso, Maria Teresa, Fabiani E. (ORCID:0000-0002-6209-8934), Criscuolo M., Fianchi L., Laurenti L. (ORCID:0000-0002-8327-1396), and Voso M. T.

Abstract

The hypomethylating agent azacitidine (AZA) is used to treat higher-risk myelodysplastic syndromes (HR-MDS) and elderly patients with low-blast count acute myeloid leukemia (LBC-AML). Platelet recovery is an early predictor of AZA response. We prospectively studied the expression profile of transcription factors, critical for late megakaryopoiesis and changes in their expression after AZA treatment in patients with HR-MDS and LBC-AML enrolled in the BMT-AZA trial (EudraCT number 2010-019673-15). Twenty-five additional patients with low-risk (LR)-MDS were also studied. At the time of diagnosis, GATA2 mRNA levels were significantly higher in MDS as compared to controls, with increasing levels from LR- to HR-MDS/AML. RUNX1 expression was also significantly higher in MDS, as compared to controls, but no differences were found between LR- and HR-MDS. Looking at biomarkers of response, we found that patients AZA responsive had higher basal GATA1 and lower FLI1 expression, compared to those with stable or progressive disease after treatment. Univariate analysis showed that increased GATA2 mRNA expression was associated with a worse overall survival. Our findings suggest that high GATA2 expression is a poor prognostic marker for survival in patients with HR-MDS and LBC-AML treated with azacitidine. Moreover, GATA1 and FLI1 mRNA expression may predict response to AZA treatment.

Published
2019

27. 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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29. Pulmonary vascular endothelium: The orchestra conductor in respiratory diseases

Author

Huertas, A. Guignabert, C. Barberà, J.A. Bärtsch, P. Bhattacharya, J. Bhattacharya, S. Bonsignore, M.R. Dewachter, L. Dinh-Xuan, A.T. Dorfmüller, P. Gladwin, M.T. Humbert, M. Kotsimbos, T. Vassilakopoulos, T. Sanchez, O. Savale, L. Testa, U. Wilkins, M.R.

Abstract

The European Respiratory Society (ERS) Research Seminar entitled “Pulmonary vascular endothelium: orchestra conductor in respiratory diseases - highlights from basic research to therapy” brought together international experts in dysfunctional pulmonary endothelium, from basic science to translational medicine, to discuss several important aspects in acute and chronic lung diseases. This review will briefly sum up the different topics of discussion from this meeting which was held in Paris, France on October 27–28, 2016. It is important to consider that this paper does not address all aspects of endothelial dysfunction but focuses on specific themes such as: 1) the complex role of the pulmonary endothelium in orchestrating the host response in both health and disease (acute lung injury, chronic obstructive pulmonary disease, high-altitude pulmonary oedema and pulmonary hypertension); and 2) the potential value of dysfunctional pulmonary endothelium as a target for innovative therapies. Copyright © ERS 2018.

Published
2018

35. Techniques for Characterization of Leucocyte Antigens and Utilization of Antibodies in Therapy

Author

Avnstrøm, S., Bjerrum, O. J., Wilken, M., Plesner, T., Tinggaard, N., Boyd, A. W., Burns, G. F., Buican, T. N., Hoffmann, G. W., Chatenoud, L., Baudrihaye, M., Goldstein, G., Bach, J. F., Clark, E., Holly, R., Yokochi, T., Feller, A. C., Parwaresch, M. R., Wacker, H. H., Lennert, K., Hofman, F. M., Yanagihara, E., Byrne, B. A., Billing, R., Baird, S., Frisman, D., Taylor, C. R., Jansen, F. K., Blythman, H., Carrière, D., Casellas, P., Hellström, I., Hellström, K. E., Gros, O., Gros, P., Laurent, J. C., Poncelet, Ph., Richer, G., Royston, I., Vidal, H., Voisin, G., Kieda, C., Monsigny, M., Waxdal, M., Kurrle, R., Lang, W., Kanzy, E. J., Hofstaetter, Th., Seiler, F. R., Matejić, T., Terzić, G., Isaković, K., Janković, B. D., Radzun, H. J., Spring, F., Anstee, D., Stein, H., Gerdes, J., Schwab, U., Lemke, H., Tabilio, A., Vainchenker, W., Testa, U., Vinci, G., Guichard, J., Vernant, J. P., Mannoni, P., Breton-Gorius, J., Teodorescu, M., Ralapati, S., van Es, A., Tanke, H. J., Baldwin, W. M., III, Oljans, P. J., Ploem, J. S., van Es, L. A., Bernard, Alain, editor, Boumsell, Laurence, editor, Dausset, Jean, editor, Milstein, César, editor, and Schlossman, Stuart F., editor

Published
1984
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36. Lymphocyte Functions

Author

Bettens, F., Kristensen, F., Grove, S., Strong, D. M., Bonnard, G. D., Boylston, A. W., Burns, G. F., Boyd, A. W., Flomenberg, N., Duffy, E., Naito, K., Dupont, B., Gourdin, M. F., Vasconcelos, A. W., Tabilio, A., Mannoni, P., Jouault, H. H., Testa, U., Farcet, J. P., Reyes, F., Grillot-Courvalin, C., Labaume, S., Brouet, J. C., Guilherme, L., Kalil, J., Chouaib, S., Dastot, H., Reboul, M., Besluau, D., Dausset, J., Colombani, J., Izaguirre, C. A., Greaves, M. F., Mossalayi, M. D., Guilhot, F., Lemaire, M., Bernard, A., Tanzer, J., Goube de Laforest, P., Navarrete, C. V., Fainboim, L., Jaraquemada, D., Festenstein, H., Lister, A., Platsoucas, C. D., Quagliata, E., Beckerdite-Quagliata, S., Russo, C., Indiveri, F., Pellergino, F., Ferrone, S., Shi, L. G., Schneider, E. M., Ziegler, A., Wernet, P., Pawelec, G. P., Spits, H., Keizer, G., Ijssel, H., Terhorst, C., Borst, J., De Vries, J., Zagury, D., Morgan, D. A., Bernard, J., Gagne, I., Bernard, Alain, editor, Boumsell, Laurence, editor, Dausset, Jean, editor, Milstein, César, editor, and Schlossman, Stuart F., editor

Published
1984
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37. A miRNA signature in human cord blood stem and progenitor cells as potential biomarker of specific acute myeloid leukemia subtypes

Author

Cattaneo, M, Pelosi, E, Castelli, G, Cerio, A, D'Angio, A, Porretti, L, Rebulla, P, Pavesi, L, Russo, G, Giordano, A, Turri, J, Cicconi, L, LO COCO, F, Testa, U, and Biunno, I

Subjects
Myeloid, Biomarkers, Tumor, Cell Differentiation, Computational Biology, Fetal Blood, Hematopoietic Stem Cells, Humans, Leukemia, Myeloid, Acute, MicroRNAs, Oligonucleotide Array Sequence Analysis, Real-Time Polymerase Chain Reaction, Transcriptome, Clinical Biochemistry, Cell Biology, Physiology, Medicine (all), Tumor, Leukemia, Acute, Settore MED/15 - Malattie del Sangue, Biomarkers
Abstract

MicroRNAs (miRNAs) are important regulators of several cellular processes. During hematopoiesis, specific expression signatures have been reported in different blood cell lineages and stages of hematopoietic stem cell (HSC) differentiation. Here we explored the expression of miRNAs in umbilical cord blood stem (HSC) and progenitor cells (HPC) and compared it to unilineage granulocyte and granulo-monocyte differentiation as well as to primary blasts from patients with acute myeloid leukemia (AML). CD34 + CD38- ad CD34 + CD38 + cells were profiled using a global array consisting of about 2000 miRNAs. An approach combining bioinformatic prediction of miRNA targets with mRNA expression profiling was used to search for putative biologically enriched functions and networks. At least 15 miRNAs to be differentially expressed between HSC and HPC cell population, a cluster of 7 miRNAs are located in the q32 region of human chromosome 14 (miR-377-3p, -136-5p, 376a-3p, 495-3p, 654-3p, 376c-3p and 381-3p) whose expression decreased during the early stages of normal myelopoiesis but were markedly increased in a small set of AML. Interestingly, miR-4739 and -4516, two novel microRNA whose function and targets are presently unknown, showed specific and peculiar expression profile during the hematopoietic stem cells differentiation into unilineages and resulted strongly upregulated in almost all AML subsets. miR-181, -126-5p, -29b-3p and -22-3p resulted dis-regulated in specific leukemias phenotypes. This study provides the first evidence of a miRNA signature in human cord blood stem and progenitor cells with a potential role in hematopoietic stemness properties and possibly in leukemogenesis of specific AML subtypes.

Published
2015

38. 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

39. Haemopoietic and endothelial progenitor cells in PPH

Author

HUERTAS A, VIZZA CD, TESTA U, RICCIONI R, PETRUCCI E, RITI V, ANTONUCCI R, POSCIA R, BADAGLIACCA R, FEDELE F, PALANGE P., BONSIGNORE, Maria Rosaria, HUERTAS A, VIZZA CD, TESTA U, RICCIONI R, PETRUCCI E, RITI V, ANTONUCCI R, POSCIA R, BADAGLIACCA R, FEDELE F, BONSIGNORE MR, and PALANGE P

Published
2007

47. 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

48. Bone-marrow derived haematopoietic and endothelial progenitors and reticulocytes after aerobic and anaerobic exercise in athletes

Author

Huertas, A, Testa, U, Bonanno, A, Gioia, M, Mariani, G, Pasquini, L, Petrucci, E, Riccioni, R, ZANGLA, Daniele, MORICI, Giuseppe, BONSIGNORE, Maria Rosaria, Huertas, A, Testa, U, Bonanno, A, Gioia, M, Mariani, G, Pasquini, L, Petrucci, E, Riccioni, R, Zangla, D, Morici, G, and Bonsignore, M.R.

Subjects
muscle angiogenesis, muscle repair, marathon race, all-out test, Settore BIO/09 - Fisiologia
Published
2006

49. Low circulating CD34+ cells in chronic obstructive pulmonary disease (COPD)

Author

HUERTAS A, TESTA U, MARIANI G, ANTONUCCI R, PETRUCCI E, SERRA P, PALANGE P., MORICI, Giuseppe, VIGNOLA, Antonio Maurizio, BELLIA, Vincenzo, BONSIGNORE, Maria Rosaria, HUERTAS A, TESTA U, MARIANI G, ANTONUCCI R, PETRUCCI E, MORICI G, VIGNOLA M, BELLIA V, SERRA P, BONSIGNORE MR, and PALANGE P

Published
2005

50. Riduzione dei CD34+ circolanti nella broncopneumopatia cronica ostruttiva (BPCO)

Author

HUERTAS A, TESTA U, CALABRO' L, ANTONUCCI R, PETRUCCI E, SATTA A, BONSIGNORE G, SERRA P, PALANGE P., MORICI, Giuseppe, VIGNOLA, Antonio Maurizio, BONSIGNORE, Maria Rosaria, HUERTAS A, TESTA U, CALABRO' L, ANTONUCCI R, PETRUCCI E, SATTA A, MORICI G, VIGNOLA AM, BONSIGNORE G, SERRA P, BONSIGNORE MR, and PALANGE P

Published
2004

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