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2. New data from the italian national register of congenital coagulopathies, 2016 annual survey

Author

Abbonizio F., Hassan H. J., Riccioni R., Santagostino E., Arcieri R., Giampaolo A., Contino L., Accorsi A., Caremani A., Ettorre P. C., Giordano P., Lassandro G., Valdre L., Notarangelo L., Aru A. B., Radossi P., Tagariello G., Cultrera D., Iannaccaro P., Santoro R., Biasoli C., Di Gregorio P., Daniele F., Testa S., Serino M. L., Castaman G., Linari S. S., Morfini M., Molinari A. C., Delios G., Cantori I., Franchini M., Caimi M. T., Mancuso M. E., Peyvandi F., Marietta M., Todisco A., Speciale V., Cerbone A. M., Di Minno G., Schiavulli M., Rocino A., Spiezia M. M., Zanon E., Gagliano F., Mansueto M. F., Siragusa S., Coppola A., Quintavalle G., Rivolta G. F., Tagliaferri A., Ambaglio C., Gamba G., Marchesini E., Oliovecchio E., Dragani A., Arbasi M. C., MacChi S., Vincenzi D., Sottilotta G., Pizzini A. M., Luciani M., De Cristofaro R., Baldacci E., Mazzucconi M. G., Santoro C., Mameli L. A., Coluccia A., Marino P., Borchiellini A., Schinco P. C., Messina M., Pollio B., Ricca I., Agostini P., Cristallo A. F., Barillari G., De Angelis V., Mosanghini M. E., Feola G., Bonetti E., Cesaro S., Gandini G., Giuffrida A., Tosetto A., Abbonizio, F., Hassan, H. J., Riccioni, R., Santagostino, E., Arcieri, R., Giampaolo, A., Contino, L., Accorsi, A., Caremani, A., Ettorre, P. C., Giordano, P., Lassandro, G., Valdre, L., Notarangelo, L., Aru, A. B., Radossi, P., Tagariello, G., Cultrera, D., Iannaccaro, P., Santoro, R., Biasoli, C., Di Gregorio, P., Daniele, F., Testa, S., Serino, M. L., Castaman, G., Linari, S. S., Morfini, M., Molinari, A. C., Delios, G., Cantori, I., Franchini, M., Caimi, M. T., Mancuso, M. E., Peyvandi, F., Marietta, M., Todisco, A., Speciale, V., Cerbone, A. M., Di Minno, G., Schiavulli, M., Rocino, A., Spiezia, M. M., Zanon, E., Gagliano, F., Mansueto, M. F., Siragusa, S., Coppola, A., Quintavalle, G., Rivolta, G. F., Tagliaferri, A., Ambaglio, C., Gamba, G., Marchesini, E., Oliovecchio, E., Dragani, A., Arbasi, M. C., Macchi, S., Vincenzi, D., Sottilotta, G., Pizzini, A. M., Luciani, M., De Cristofaro, R., Baldacci, E., Mazzucconi, M. G., Santoro, C., Mameli, L. A., Coluccia, A., Marino, P., Borchiellini, A., Schinco, P. C., Messina, M., Pollio, B., Ricca, I., Agostini, P., Cristallo, A. F., Barillari, G., De Angelis, V., Mosanghini, M. E., Feola, G., Bonetti, E., Cesaro, S., Gandini, G., Giuffrida, A., and Tosetto, A.

Subjects
Blood coagulation disorder, Haemophilia B, Haemophilia A, Von Willebrand's disease, Register
Abstract

Background - In Italy, the National Register of Congenital Coagulopathies (NRCC) collects epidemiological and therapeutic data from patients affected by haemophilia A (HA), haemophilia B (HB), von Willebrand's disease (vWD) and other rare coagulation disorders. Here we present data from the 2016 annual survey. Materials and methods - Data are provided by the Italian Haemophilia Centres, on a voluntary basis. Information flows from every Centre to a web-based platform of the Italian Association of Haemophilia Centres, shared with the Italian National Institute of Health, in accordance with current privacy laws. Patients are classified by diagnosis, disease severity, age, gender and treatment-related complications. Results - In 2016, the total number of patients with congenital coagulopathies in the NRCC was 10,360: 39.8% of these patients had HA, 31.5% had vWD, 8.5% had HB, and 20.2% had less common factor deficiencies. The overall prevalence of HA and HB was 13.9/100,000 males and 3.0/100,000 males, respectively. The overall prevalence of vWD was 5.4/100,000 inhabitants. During 2016, 126 patients had current alloantibodies to factor VIII (FVIII) or factor IX (FIX) and were under treatment with bypassing agents and/or immune tolerance induction. Overall, 388 patients with a history of alloantibodies were recorded in the NRCC of whom 337 with severe HA and 12 with severe HB. Coagulation factor use, evaluated from treatment plans, was approximately 451,000,000 IU of FVIII for HA patients (7.5 IU/inhabitant), and approximately 53,000,000 IU of FIX for HB patients (0.9 IU/inhabitant). Discussion - The prevalences of HA and HB fall within the ranges reported in more developed countries; the consumption of FVIII and FIX was in line with that of other European countries (France, United Kingdom) and Canada. The NRCC, with its bleeding disorder dataset, is a helpful tool for shaping public health policies, as well as planning clinical and epidemiological research projects.

Published
2020

13. 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

16. RELEASE OF HEMOPOIETIC AND ENDOTHELIAL PROGENITORS AFTER ENDURANCE AND MAXIMAL EXERCISE IN RUNNERS

Author

BONSIGNORE, Maria Rosaria, MORICI, Giuseppe, PATERNO', Alessandra, CHIMENTI, Laura, BELLIA, Vincenzo, TESTA, Alessandra, RICCIONI, R, RITI, V, PETRUCCI, E, PASQUINI, L, BONANNO, A, HUERTAS, A, VEGA, M, PALANGE, P, BONSIGNORE, MR, MORICI, G, RICCIONI, R, RITI, V, PETRUCCI, E, PASQUINI, L, BONANNO, A, PATERNO', A, HUERTAS, A, CHIMENTI, L, VEGA, M, BELLIA, V, PALANGE, P, and TESTA, U

Subjects
HEMOPOIETIC AND ENDOTHELIAL PROGENITORS, EXERCISE,RUNNERS
Published
2007

21. 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

23. High efficacy of Rituximab in indolent HCV-related lymphoproliferative disorders associated with systemic autoimmune diseases

Author

Cervetti, G, Mechelli, S, Riccioni, R, Galimberti, Sara, Caracciolo, F, and Petrini, Mario

Subjects
Adult, Male, Lymphoma, Non-Hodgkin, Antibodies, Monoclonal, Antineoplastic Agents, Hepatitis C, Chronic, Middle Aged, Autoimmune Diseases, Antibodies, Monoclonal, Murine-Derived, Treatment Outcome, Humans, Female, Rituximab, Aged
Abstract

The evidence of an increased frequency of B-non Hodgkin's lymphomas (NHL) in patients with HCV and systemic autoimmune diseases suggests a close relationship between infection, autoimmunity and cancer. Choosing the best therapy for patients affected either by HCV-related lymphoma or autoimmune disorders is not easy; in fact, some treatments may be accompanied by an excessive hepatic toxicity and may be followed by a reactivation of hepatitis. There is growing interest in the search for an ideal therapy for this kind of patient. Thanks to its mechanism of action and good toxicity profile, Rituximab could prove to be an attractive therapeutic option: it has been reported to be highly active in low-grade NHLs and has been proposed for the management of autoimmune diseases.In this paper we evaluate the role of anti-CD20 monoclonal antibody in mono-therapy in 10 patients with either indolent HCV-related lymphoma or autoimmune disease. A very high rate of response, of both NHL and of the associated autoimmune disease, was observed (100% of clinical response), with no significant hepatic and extra-hepatic toxicity.Thus, although the number of patients was small, our data strongly support the use of anti-CD20 in this patient setting.

Published
2006

27. A new complex rearrangement involving the ETV6, LOC115548, and MN1 in a of acute myeloid leukemia

Author

Belloni, E, Trubia, W, Mancini, M, Derme, V, Nanni, M, Lahortiga, I, Riccioni, R, Confalonieri, S, LO COCO, F, Di Fiore, P, and Pelicci, P

Subjects
Myeloid, Male, Adolescent, Messenger, Translocation, Acute, Chromosomes, Fluorescence, Genetic, Models, Pair 12, Humans, Fusion, In Situ Hybridization, Oncogene Proteins, Chromosome Aberrations, Leukemia, Base Sequence, Proto-Oncogene Proteins c-ets, Reverse Transcriptase Polymerase Chain Reaction, Chromosome Mapping, Chromosomes, Human, Pair 12, Chromosomes, Human, Pair 22, Chromosomes, Human, Pair 3, Chromosomes, Human, Pair 5, DNA-Binding Proteins, In Situ Hybridization, Fluorescence, Leukemia, Myeloid, Acute, Models, Genetic, Oncogene Proteins, Fusion, RNA, Messenger, Repressor Proteins, Translocation, Genetic, Pair 3, RNA, Pair 22, Pair 5, Settore MED/15 - Malattie del Sangue, Human
Published
2004

29. Arsenic trioxide as an inducer of apoptosis and loss of PML/RAR alpha protein in acute promyelocytic leukemia cells

Author

Shao, W, Fanelli, M, Ferrara, F, Riccioni, R, Rosenauer, A, Davison, K, Lamph, W, Waxman, S, Pelicci, P, LO COCO, F, Avvisati, G, Testa, U, Peschle, C, Gambacorti Passerini, C, Nervi, C, and Miller, W

Subjects
Electrophoresis, Promyelocytic, Antineoplastic Combined Chemotherapy Protocols, Apoptosis, Arsenicals, Blotting, Northern, Blotting, Western, Down-Regulation, Electrophoresis, Polyacrylamide Gel, Flow Cytometry, Humans, Leukemia, Promyelocytic, Acute, Oxides, Receptors, Retinoic Acid, Transglutaminases, Tretinoin, Tumor Cells, Cultured, Polyacrylamide Gel, Leukemia, Cultured, Blotting, Retinoic Acid, Acute, Tumor Cells, Receptors, Northern, Western, Settore MED/15 - Malattie del Sangue
Published
1998

31. Improved rapid detection of the PML/RARalpha fusion gene in acute promyelocytic leukemia

Author

Diverio D, Riccioni R, Alessandra PISTILLI, Buffolino S, Avvisati G, Mandelli F, and Lo Coco F

Subjects
Base Sequence, Humans, Leukemia, Promyelocytic, Acute, Molecular Sequence Data, Neoplasm Proteins, Oncogene Proteins, Fusion, Polymerase Chain Reaction, Transcription, Genetic, Promyelocytic, Oncogene Proteins, Leukemia, Acute, Genetic, Fusion, Transcription, Settore MED/15 - Malattie del Sangue
Abstract

Acute promyelocytic leukemia (APL) is a medical emergency which requires rapid diagnosis and tailored treatment. Detection of the PML/RARalpha fusion gene in APL blasts is critical to start promptly the specific therapy with all-trans retinoic acid (ATRA). APL lacking this genetic lesion have been reported as being ATRA resistant. Reverse-transcription polymerase chain reaction (RT-PCR) has been extensively used to detect the PML/RARalpha cDNA. The reported PML/RARalpha amplification techniques are laborious and time consuming, and include conventional RNA extraction, cDNA synthesis and a two-round (nested) PCR. We hereby describe a few variations of the commonly adopted RNA extraction and PML/RARalpha RT-PCR protocols which allow a molecular diagnosis of APL to be carried out in less than 5 h. Processing of small volumes of leukemic cell lysate (0.5 ml) in a microfuge allows extraction of good quality RNA in 1 h. After reverse transcription to obtain cDNA, a 'hot start' PCR procedure was adopted which enabled us to amplify clearly visible and specific products after a single (not nested) amplification round. The PML/RARalpha fusion gene was detected in the blasts of six consecutive APL at diagnosis, and an APL-tailored protocol including ATRA was started in each case within 6 h of admission. On repeated experiments, the assay proved highly specific and sensitive for the rapid detection of all PML/RARalpha transcript types. Our data should encourage the use of this rapid procedure for the diagnosis of both typical APL and, particularly, less typical cases awaiting urgent therapeutic intervention.

Published
1996

43. C-fms expression correlates with monocytic differentiation in PML-RARα+ acute promyelocytic leukemia.

Author

Riccioni, R, Saulle, E, Militi, S, Sposi, N M, Gualtiero, M, Mauro, N, Mancini, M, Diverio, D, Lo Coco, F, Peschle, C, and Testa, U

Subjects
*ACUTE leukemia, *GENE expression
Abstract

We have investigated the expression of the M-CSF receptor (c-fms) in 16 freshly isolated acute promyelocytic leukemias (APL) expressing the PML/RARα fusion protein. In parallel, we evaluated the capacity of these cells to differentiate along the granulocytic and monocytic pathways. c-fms was constitutively and constantly expressed in all cases sensitive in vivo to all-trans retinoic acid (ATRA) and its expression was further potentiated following in vitro induction with ATRA. Furthermore, gel-shift analysis of APL cells showed elevated levels of PU.1 binding activity to the M-CSF receptor promoter, particularly after ATRA stimulation. Interestingly, the rise of PU.1 binding activity as well as of PU.1 levels after ATRA treatment was significantly higher in APL patients exhibiting monocytic maturation, as compared to those that did not undergo monocytic differentiation. A variable proportion of ATRA-induced APL cells exhibited monocyte-like morphology and immunophenotype: the proportion of monocytic cells was consistently increased by combined treatment with ATRA and diverse hematopoietic growth factors cocktails, which always comprised M-CSF. Monocytic cells originating from in vitro ATRA-induced maturation of APL cells derive from the leukemic clone as suggested by two lines of evidence: (1) monocytic cells harbor the 15;17 translocation; (2) monocytic cells possess Auer bodies. The c-fms[SUPbright] leukemic blasts preferentially showed the capacity for monocytic differentiation as compared to the c-fms[SUPdim/-] subset: indeed, enforced expression of c-fms into NB4, a PML/RARα[SUB+] cell line, favored the onset of monocytic maturation. Finally, low c-fms expression was observed in an APL relapsing patient resistant to ATRA, as well as in an APL case with t(11;17), PLZF/RARα[SUP+]. These observations indicate that PML/RARα[SUP+] APL blasts are bipotent for differentiation through both neutrophilic and monocytic lineages, whereby... [ABSTRACT FROM AUTHOR]

Published
2003
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44. Arsenic trioxide as an inducer of apoptosis and loss of PML/RAR alpha protein in acute promyelocytic leukemia cells.

Author

Shao, Wenlin, Fanelli, Mirco, Ferrara, Fabiana F., Riccioni, Roberta, Rosenauer, Angelika, Davison, Kelly, Lamph, William W., Waxman, Samuel, Pelicci, Pier Giuseppe, Lo Coco, Francesco, Avvisati, Giuseppe, Testa, Ugo, Peschle, Cesare, Gambacorti-Passerini, Carlo, Nervi, Clara, Miller, Jr., Wilson H., Shao, W, Fanelli, M, Ferrara, F F, and Riccioni, R

Subjects
LEUKEMIA, LEUKEMIA inhibitory factor, BIOCHEMICAL mechanism of action, PATIENTS
Abstract

Background: Retinoids, which are derivatives of vitamin A, induce differentiation of acute promyelocytic leukemia (APL) cells in vitro and in patients. However, APL cells develop resistance to retinoic acid treatment. Arsenic trioxide (As2O3) can induce clinical remission in patients with APL, including those who have relapsed after retinoic acid treatment, by inducing apoptosis (programmed cell death) of the leukemia cells. In this study, we investigated the molecular mechanisms by which As2O3 induces apoptosis in retinoic acid-sensitive NB4 APL cells, in retinoic acid-resistant derivatives of these cells, and in fresh leukemia cells from patients.Methods: Apoptosis was assessed by means of DNA fragmentation analyses, TUNEL assays (i.e., deoxyuridine triphosphate labeling of DNA nicks with terminal deoxynucleotidyl transferase), and flow cytometry. Expression of the PML/RAR alpha fusion protein in leukemia cells was assessed by means of western blotting, ligand binding, and immunohistochemistry. Northern blotting and ribonuclease protection assays were used to evaluate changes in gene expression in response to retinoic acid and As2O3 treatment.Results and Conclusions: As2O3 induces apoptosis without differentiation in retinoic acid-sensitive and retinoic acid-resistant APL cells at concentrations that are achievable in patients. As2O3 induces loss of the PML/RAR alpha fusion protein in NB4 cells, in retinoic-acid resistant cells derived from them, in fresh APL cells from patients, and in non-APL cells transfected to express this protein. As2O3 and retinoic acid induce different patterns of gene regulation, and they inhibit the phenotypes induced by each other. Understanding the molecular basis of these differences in the effects of As2O3 and retinoic acid may guide the clinical use of arsenic compounds and provide insights into the management of leukemias that do not respond to retinoic acid. [ABSTRACT FROM AUTHOR]

Published
1998
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