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149 results on '"Giugliano, E"'

1. miR-15a targets the HSP90 co-chaperone Morgana in chronic myeloid leukemia

Author

Poggio, P, Rocca, S, Fusella, F, Ferretti, R, Ala, U, D'Anna, F, Giugliano, E, Panuzzo, C, Fontana, D, Palumbo, V, Carrà, G, Taverna, D, Gambacorti-Passerini, C, Saglio, G, Fava, C, Piazza, R, Morotti, A, Orso, F, Brancaccio, M, Poggio, Pietro, Rocca, Stefania, Fusella, Federica, Ferretti, Roberta, Ala, Ugo, D'Anna, Flora, Giugliano, Emilia, Panuzzo, Cristina, Fontana, Diletta, Palumbo, Valeria, Carrà, Giovanna, Taverna, Daniela, Gambacorti-Passerini, Carlo, Saglio, Giuseppe, Fava, Carmen, Piazza, Rocco, Morotti, Alessandro, Orso, Francesca, Brancaccio, Mara, Poggio, P, Rocca, S, Fusella, F, Ferretti, R, Ala, U, D'Anna, F, Giugliano, E, Panuzzo, C, Fontana, D, Palumbo, V, Carrà, G, Taverna, D, Gambacorti-Passerini, C, Saglio, G, Fava, C, Piazza, R, Morotti, A, Orso, F, Brancaccio, M, Poggio, Pietro, Rocca, Stefania, Fusella, Federica, Ferretti, Roberta, Ala, Ugo, D'Anna, Flora, Giugliano, Emilia, Panuzzo, Cristina, Fontana, Diletta, Palumbo, Valeria, Carrà, Giovanna, Taverna, Daniela, Gambacorti-Passerini, Carlo, Saglio, Giuseppe, Fava, Carmen, Piazza, Rocco, Morotti, Alessandro, Orso, Francesca, and Brancaccio, Mara

Abstract

Morgana is a ubiquitous HSP90 co-chaperone protein coded by the CHORDC1 gene. Morgana heterozygous mice develop with age a myeloid malignancy resembling human atypical myeloid leukemia (aCML), now renamed MDS/MPN with neutrophilia. Patients affected by this pathology exhibit low Morgana levels in the bone marrow (BM), suggesting that Morgana downregulation plays a causative role in the human malignancy. A decrease in Morgana expression levels is also evident in the BM of a subgroup of Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) patients showing resistance or an incomplete response to imatinib. Despite the relevance of these data, the mechanism through which Morgana expression is downregulated in patients’ bone marrow remains unclear. In this study, we investigated the possibility that Morgana expression is regulated by miRNAs and we demonstrated that Morgana is under the control of four miRNAs (miR-15a/b and miR-26a/b) and that miR-15a may account for Morgana downregulation in CML patients.

Published
2024

2. Clonal hematopoiesis by DNMT3A mutations as a common finding in idiopathic splanchnic vein thrombosis

Author

Carrà, G, Giugliano, E, Camerlo, S, Rosati, G, Branca, E, Maffeo, B, Russo, I, Piazza, R, Cilloni, D, Morotti, A, Carrà, Giovanna, Giugliano, Emilia, Camerlo, Sofia, Rosati, Giorgio, Branca, Enrica, Maffeo, Beatrice, Russo, Isabella, Piazza, Rocco, Cilloni, Daniela, Morotti, Alessandro, Carrà, G, Giugliano, E, Camerlo, S, Rosati, G, Branca, E, Maffeo, B, Russo, I, Piazza, R, Cilloni, D, Morotti, A, Carrà, Giovanna, Giugliano, Emilia, Camerlo, Sofia, Rosati, Giorgio, Branca, Enrica, Maffeo, Beatrice, Russo, Isabella, Piazza, Rocco, Cilloni, Daniela, and Morotti, Alessandro

Published
2023

9. An Italian Multicentre Study Using Different Digital PCR Instruments on BCR-ABL1 Positive Patients at Different Levels of CML Disease

Author

Daraio, F, Giugliano, E, Fava, C, Lorenzatti, R, Varotto, M, Barberio, D, Bernardi, S, Izzo, B, Errichiello, S, Bochicchio, Mt, Venturi, C, Albano, F, Saglio, G, Pane, F, Martinelli, G, Specchia, G, Russo, D, Gottardi, Em, and Filomena Daraio, Emilia Giugliano, Carmen Fava, Roberta Lorenzatti, Marta Varotto, Davide Barberio, Simona Bernardi, Barbara Izzo, Santa Errichiello, Maria Teresa Bochicchio, Claudia Venturi, Francesco Albano, Giuseppe Saglio, Fabrizio Pane, Giovanni Martinelli, Giorgina Specchia, Domenico Russo, Enrico Marco Gottardi

Subjects
bcr-abl1, ddpcr
Published
2017

11. Chromosome abnormalities additional to the Philadelphia chromosome at the diagnosis of chronic myelogenous leukemia: pathogenetic and prognostic implications

Author

Zaccaria, A, Testoni, N, Valenti, Am, Luatti, S, Tonelli, M, Marzocchi, G, Cipriani, R, Baldazzi, C, Giannini, B, Stacchini, M, Gamberini, C, Castagnetti, F, Rosti, G, Azzena, A, Cavazzini, Francesco, Cianciulli, Am, Dalsass, A, Donti, E, Giugliano, E, Gozzetti, A, Grimoldi, Mg, Ronconi, S, Santoro, A, Spedicato, F, Zanatta, L, Baccarani, M, GIMEMA Working Party on, C. M. L., Zaccaria A, Testoni N, Valenti AM, Luatti S, Tonelli M, Marzocchi G, Cipriani R, Baldazzi C, Giannini B, Stacchini M, Gamberini C, Castagnetti F, Rosti G, Azzena A, Cavazzini F, Cianciulli AM, Dalsass A, Donti E, Giugliano E, Gozzetti A, Grimoldi MG, Ronconi S, Santoro A, Spedicato F, Zanatta L, and Baccarani M

Subjects
Adult, Male, Cancer Research, medicine.medical_specialty, Antineoplastic Agents, Biology, Philadelphia chromosome, Gastroenterology, Piperazines, NO, Myelogenous, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, hemic and lymphatic diseases, Internal medicine, Aged, Aged, 80 and over, Benzamides, Female, Humans, Imatinib Mesylate, Karyotyping, Middle Aged, Protein-Tyrosine Kinases, Pyrimidines, Remission Induction, Treatment Outcome, Chromosome Aberrations, Philadelphia Chromosome, Molecular Biology, Genetics, 80 and over, medicine, Chronic, Leukemia, Karyotype, Imatinib, medicine.disease, Imatinib mesylate, Immunology, BCR-ABL Positive, Sokal Score, Chronic myelogenous leukemia, medicine.drug
Abstract

Additional chromosome abnormalities (ACAs) occur in less than 10% of cases at diagnosis of Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML). In some cases, on the basis of the persistence of the ACAs in Ph-negative cells after response to imatinib, a secondary origin of the Ph chromosome has been demonstrated. In this study, the possible prognostic value of this phenomenon was evaluated. Thirty-six Ph-positive CML patients were included in the study. In six patients, ACAs persisted after the disappearance of the Ph. A complete cytogenetic response (CCR) was obtained in five of these six patients, and five of six also had a high Sokal score. In all the other cases, ACAs disappeared together (in cases of response to therapy with imatinib) or persisted with the Ph (in cases of no response to imatinib). In the former cases, the primary origin of the Ph was demonstrated. CCR was obtained in 22 cases (17 with low to intermediate Sokal scores), while no response was observed in 8 patients (5 with a high Sokal score). Sokal score seems to maintain its prognostic value for patients in whom the Ph occurs as a primary event, but not in those in whom it occurs as a secondary one.

Published
2010

13. MORGANA/CHP1 ACTS AS AN ONCOSUPPRESSOR IN CHRONIC MYELOID LEUKEMIA

Author

DI SAVINO, Augusta, Panuzzo, Cristina, Rocca, S, Familiari, U, Piazza, R, Crivellaro, Sabrina, Carrà, G, Ferretti, R, Fusella, F, Giugliano, E, Camporeale, A, Franco, I, Miniscalco, Barbara, Cutrin, Juan Carlos, Turco, Emilia, Silengo, L, Hirsch, Emilio, Gambacorti Passerini, C, Pandolfi, Pp, Papotti, Mauro Giulio, Saglio, Giuseppe, Tarone, G, Morotti, Alessandro, and Brancaccio, Mara

Published
2014

15. Morgana acts as an oncosuppressor in chronic myeloid leukemia

Author

Di Savino, A, Panuzzo, C, Rocca, S, Familiari, U, Piazza, R, Crivellaro, S, Carrà, G, Ferretti, R, Fusella, F, Giugliano, E, Camporeale, A, DE FRANCO, I, Miniscalco, B, Cutrin, J, Turco, E, Silengo, L, Hirsch, E, Rege Cambrin, G, GAMBACORTI PASSERINI, C, Pandolfi, P, Papotti, M, Saglio, G, Tarone, G, Morotti, A, Brancaccio, M, Brancaccio, M., PIAZZA, ROCCO GIOVANNI, DE FRANCO, IRENE, GAMBACORTI PASSERINI, CARLO, Di Savino, A, Panuzzo, C, Rocca, S, Familiari, U, Piazza, R, Crivellaro, S, Carrà, G, Ferretti, R, Fusella, F, Giugliano, E, Camporeale, A, DE FRANCO, I, Miniscalco, B, Cutrin, J, Turco, E, Silengo, L, Hirsch, E, Rege Cambrin, G, GAMBACORTI PASSERINI, C, Pandolfi, P, Papotti, M, Saglio, G, Tarone, G, Morotti, A, Brancaccio, M, Brancaccio, M., PIAZZA, ROCCO GIOVANNI, DE FRANCO, IRENE, and GAMBACORTI PASSERINI, CARLO

Abstract

We recently described morgana as an essential protein able to regulate centrosome duplication and genomic stability, by inhibiting ROCK. Here we show that morgana+/- mice spontaneously develop a lethal myeloproliferative disease resembling human atypical chronic myeloid leukemia (aCML), preceded by ROCK hyperactivation, centrosome amplification, and cytogenetic abnormalities in the bone marrow (BM). Moreover,we found that morgana is underexpressed in the BM of patients affected by atypical CML, a disorder of poorly understood molecular basis, characterized by nonrecurrent cytogenetic abnormalities. Morgana is also underexpressed in the BM of a portion of patients affected by Philadelphia-positive CML (Ph+ CML) caused by the BCR-ABL oncogene, and in this condition, morgana underexpression predicts a worse response to imatinib, the standard treatment for Ph+ CML. Thus,morgana acts as an oncosuppressor with different modalities: (1) Morgana underexpression induces centrosome amplification and cytogenetic abnormalities, and (2) in Ph+ CML, it synergizes with BCR-ABL signaling, reducing the efficacy of imatinib treatment. Importantly, ROCK inhibition in the BM of patients underexpressing morgana restored the efficacy of imatinib to induce apoptosis, suggesting that ROCK inhibitors, combined with imatinib treatment, can overcome suboptimal responses in patients in which morgana is underexpressed.

Published
2015

16. Pancreatic cancer with liver metastases in a pregnant patient: case report and review of the literature

Author

Roberto Marci, Pansini, G., Zavatta, C., Mossuto, E., Giugliano, E., Marzola, M., and Patella, A.

Subjects
Adult, Pancreatic Neoplasms, Pregnancy, Liver Neoplasms, Humans, Female, Adenocarcinoma, Pregnancy Complications, Neoplastic
Abstract

In this case report, the authors discuss clinical presentation, surgical procedure and early results of chemotherapy of pancreatic carcinoma with liver metastases diagnosed a few days after delivery. Pancreatic adenocarcinoma occurs infrequently in pregnant and childbearing women: only ten cases have been reported in the literature. The early diagnosis of pancreatic cancer is difficult because symptoms appear when cancer is about to reach an advanced stage. In pregnancy, it is even more difficult because symptoms like dyspepsia, vomiting and epigastric pain may result confusing. The authors outline the difficulties in diagnosis and treatment of this kind of disease during pregnancy.

Published
2012

19. CHROMOSOME ABNORMALITIES ADDITIONAL TO THE PHILADELPHIA CHROMOSOME AT THE DIAGNOSIS OF CHRONIC MYELOID LEUKEMIA. PATHOGENETIC AND PROGNOSTIC IMPLICATIONS

Author

Zaccaria, A., Testoni, N., Valenti, A. M., Luatti, S., Tonelli, M., Marzocchi, G., Cipriani, R., Baldazzi, C., Giannini, B., Stacchini, M., Gamberini, C., Castagnetti, F., Rosti, G., Azzena, A., Bernardi, F., Cavazzini, Francesco, Cianciulli, A., Dalsass, A., Donti, E., Giugliano, E., Gozzetti, A., Grimoldi, M. G., Manna, M., Modaferri, B., Piovani, G., Ronconi, S., Santoro, A., Santulli, B., Spedicato, F., Zanatta, L., and on behalf of the GIMEMA WP on CML, Baccarani M.

Published
2009

22. Influence of additional chromosome abnormalities to PH on response to imatinib mesylate therapy in early chronic phase in chronic myeloid leukemia

Author

Luatti, S, 1 Marzocchi G, 1 Castagnetti F, 1 Gamberini C, 1 Baldazzi C, 1 Stacchini M, 1 Poerio A, 1 Zaccaria A, 2 Zanatta L, 3 Giugliano E, 4 Santulli B, 5 Grimoldi MG, 6 Gozzetti A, 7 Dalsass A, Piovani, Giovanna, 9 Manna M, 10 Modaferri, B, 11 Bernardi, F, 12 Bernasconi, P, 13 Kerim, S, 14 Abruzzese, E, 15 Palka, G, 16 Palandri, F, 1 Martinelli G, 1 Rosti G, 1 § Baccarani M, and 1 Testoni N1

Published
2008

35. From genes to therapy: the case of Philadelphia chromosome-positive leukemias

Author

Cilloni, Daniela, Guerrasio, Angelo, Giugliano, E, Scaravaglio, P, Volpe, G, Rege, Cambrin, G, and Saglio, Giuseppe

Subjects
ABL, Philadelphia Chromosome Positive, Molecular pathology, General Neuroscience, breakpoint cluster region, Chromosomal translocation, Biology, medicine.disease, Philadelphia chromosome, Minimal residual disease, General Biochemistry, Genetics and Molecular Biology, Translocation, Genetic, Cell Transformation, Neoplastic, History and Philosophy of Science, hemic and lymphatic diseases, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Immunology, Cancer research, medicine, Humans, Philadelphia Chromosome, Chronic myelogenous leukemia
Abstract

The Philadelphia chromosome (Ph-chromosome) has long represented the only cytogenetic abnormality known to be associated with a specific malignant disease in humans, being present in more than 95% of patients with chronic myelogenous leukemia. This abnormality is the result of a reciprocal translocation between the long arms of chromosome 9 and 22, t(9;22)(q34;q11), and its presence is not restricted to chronic myelogenous leukemia, but can also be found in 30% of cases of acute lymphoblastic leukemia in adults. In the 1980s, the molecular counterpart of the chromosomal rearrangement was identified to consist of the juxtaposition of parts of the BCR and ABL genes to form a BCR-ABL hybrid gene. The resulting chimeric proteins (P210 and P190), which retain constitutively activated tyrosine kinase activity, have demonstrated a causative role in the genesis of the leukemic process. Although many aspects of the BCR-ABL driven transformation remain unsolved, great advances in understanding the molecular pathology of Ph-positive leukemias resulted in meaningful improvement in the clinical setting. Molecular tools to diagnose disease (PCR, FISH, and southern blot) and to monitor minimal residual disease after potential curative treatment are now in current practice, and new powerful therapeutic tools have emerged that target the molecular oncogenic pathways activated in Ph-positive cells. Among them, specific ABL tyrosine kinase inhibitors recently obtained extraordinary results in many clinical protocols. This review summarizes the most recent advances in this field with special focus on the putative mechanisms of the transformation and progression of chronic myelogenous leukemia and on the major impact that understanding the molecular biology of these diseases is having in clinical practice.

Published
2002

41. The efficacy of imatinib mesylate in patients with FIP1L1-PDGFR -positive hypereosinophilic syndrome. Results of a multicenter prospective study

Author

Baccarani, M., primary, Cilloni, D., additional, Rondoni, M., additional, Ottaviani, E., additional, Messa, F., additional, Merante, S., additional, Tiribelli, M., additional, Buccisano, F., additional, Testoni, N., additional, Gottardi, E., additional, de Vivo, A., additional, Giugliano, E., additional, Iacobucci, I., additional, Paolini, S., additional, Soverini, S., additional, Rosti, G., additional, Rancati, F., additional, Astolfi, C., additional, Pane, F., additional, Saglio, G., additional, and Martinelli, G., additional

Published
2007
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42. A Prospective Study in Ph+ Chronic Myeloid Leukemia (CML) Patients Showing That Interphase Fluorescence in Situ Hybridization (FISH) Is Effective as Conventional Cytogenetics for Definition of Cytogenetic Response. Correlation with Molecular Response (by the GIMEMA CML WP).

Author

Testoni, Nicoletta, primary, Luatti, S., primary, Marzocchi, G., primary, Amabile, M., primary, Gamberini, C., primary, Buontempo, F., primary, Baldazzi, C., primary, Iacobucci, I., primary, Mancini, M., primary, Cuneo, A., primary, Specchia, G., primary, Kerim, S., primary, Rege-Cambrin, G., primary, Giugliano, E., primary, Giussani, U., primary, Abruzzese, E., primary, Grimoldi, M.G., primary, Modaferri, B., primary, Castagnetti, F., primary, Palandri, F., primary, Mecucci, C., primary, Bernasconi, P., primary, Gozzetti, A., primary, Palka, G., primary, Zanatta, L., primary, Zaccaria, A., primary, Martinelli, G., primary, Rosti, G., primary, and Baccarani, Michele, primary

Published
2006
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43. The NF-κB pathway blockade by the IKK inhibitor PS1145 can overcome Imatinib resistance

Author

Cilloni, D, primary, Messa, F, additional, Arruga, F, additional, Defilippi, I, additional, Morotti, A, additional, Messa, E, additional, Carturan, S, additional, Giugliano, E, additional, Pautasso, M, additional, Bracco, E, additional, Rosso, V, additional, Sen, A, additional, Martinelli, G, additional, Baccarani, M, additional, and Saglio, G, additional

Published
2005
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44. Low dose of Betamethasone throughout the whole course of pregnancy and fetal growth: a clinical study.

Author

VESCE, F., GIUGLIANO, E., CAGNAZZO, E., MOSSUTO, E., and MARCI, R.

Abstract

AIM: To assess the eventual influence of low dose betamethasone throughout pregnancy on fetal growth. PATIENTS AND METHODS: 320 patients -- admitted to the Section of Obstetrics and Gynecology of Ferrara University from January 2005 to December 2010 -- were subdivided in two groups: 160 patients affected by recurrent spontaneous abortion (Group A), treated by low dose of betamethasone (0.5 mg/daily) throughout pregnancy for preventive purposes, 160 patients with physiological pregnancy as control group (Group B). Primary measured outcomes were neonatal biometric parameters such as birth weight, head circumference and neonatal length. Unpaired t-test was used to compare the neonatal biometric parameters. RESULTS: Birth weight, length and circumference head resulted significantly lower in groups treated by GCs. However, excluding bias as pregnancy complicated by diseases, which could affect fetal growth, biometric neonatal parameters were not different between two groups. Furthermore, analyzing the distribution of the value of birth weight we observed that in the group A there were 44 newborns with a weight even higher than fiftieth percentile. CONCLUSIONS: Betamethasone seems not to influence fetal growth. Our analysis demonstrates that fetal growth is influenced by several factors, therefore, homogeneous study population is essential to have convincing results. [ABSTRACT FROM AUTHOR]

Published
2014

48. Trisomy 11 in myeloid malignancies is associated with internal tandem duplication of both MLL and FLT3 genes

Author

Rege-Cambrin, G., Giugliano, E., Michaux, L., Stul, M., Scaravaglio, P., Serra, A., Giuseppe Saglio, and Hagemeijer, A.

Subjects
Adult, Aged, 80 and over, Time Factors, Chromosomes, Human, Pair 11, Trisomy, Histone-Lysine N-Methyltransferase, Middle Aged, Gene Expression Regulation, Neoplastic, fms-Like Tyrosine Kinase 3, Leukemia, Myeloid, Gene Duplication, Karyotyping, Humans, Myeloid-Lymphoid Leukemia Protein, Aged
Abstract

In 20 patients with myeloid malignancies and isolated trisomy 11 an internal tandem duplication of the MLL and FLT3 genes was observed in 41% and 31% of the cases, respectively; 80% of the FLT3+ cases showed MLL self-fusion. Concomitant presence of MLL and FLT3 anomalies could be relevant in determining the poor outcome of patients with acute myeloid leukemia with trisomy 11.

50. The efficacy of imatinib mesylate in patients with FIP1L1-PDGFR -positive hypereosinophilic syndrome. Results of a multicenter prospective study

Author

Michele Baccarani, Enrico Gottardi, Michela Rondoni, Nicoletta Testoni, Emanuela Ottaviani, Cinzia Astolfi, Mario Tiribelli, Emilia Giugliano, Fabrizio Pane, Daniela Cilloni, Francesco Buccisano, Francesca Rancati, Serena Merante, Ilaria Iacobucci, Giovanni Martinelli, Gianantonio Rosti, Stefania Paolini, Francesca Messa, Giuseppe Saglio, Simona Soverini, Antonio De Vivo, Baccarani M, Cilloni D, Rondoni M, Ottaviani E, Messa F, Merante S, Tiribelli M, Buccisano F, Testoni N, Gottardi E, de Vivo A, Giugliano E, Iacobucci I, Paolini S, Soverini S, Rosti G, Rancati F, Astolfi C, Pane F, Saglio G, Martinelli G., Baccarani, M, Cilloni, D, Rondoni, M, Ottaviani, E, Messa, F, Merante, S, Tiribelli, M, Buccisano, F, Testoni, N, Gottardi, E, DE VIVO, A, Giugliano, E, Iacobucci, I, Paolini, S, Soverini, S, Rosti, G, Rancati, F, Astolfi, C, Pane, Fabrizio, Saglio, G, and Martinelli, G.

Subjects
Male, Receptor, Platelet-Derived Growth Factor alpha, Oncogene Proteins, Fusion, FIP1L1-PDGFRA FUSION, TYROSINE KINASE, THERAPY, Gastroenterology, Piperazines, Tyrosine-kinase inhibitor, Prospective Studies, FIP1L1-PDGFRALPHA, BCR-ABL, Aged, 80 and over, Gene Rearrangement, HYPEREOSINOPHILIC SYNDROME, Hematology, Hypereosinophilic syndrome, Middle Aged, Protein-Tyrosine Kinases, EOSINOPHILIC DISORDERS, Treatment Outcome, CHRONIC MYELOPROLIFERATIVE DISORDERS, Benzamides, Imatinib Mesylate, GROWTH, Female, Tyrosine kinase, medicine.drug, Adult, medicine.medical_specialty, Adolescent, medicine.drug_class, Antineoplastic Agents, CHRONIC MYELOID-LEUKEMIA, FACTOR RECEPTOR-BETA, MOLECULAR REMISSION, IMATINIB, TYROSINE, Internal medicine, medicine, Humans, Aged, mRNA Cleavage and Polyadenylation Factors, Chronic eosinophilic leukemia, business.industry, EOSINOPHILS, Imatinib, medicine.disease, Pyrimidines, Imatinib mesylate, Fusion transcript, Cancer research, business, Settore MED/15 - Malattie del Sangue
Abstract

BACKGROUND AND OBJECTIVES: The hypereosinophilic syndrome (HES) may be associated with the fusion of the platelet derived growth factor receptor a (PDGFRalpha) gene with the FIP1L1 gene in chromosome 4 coding for a constitutively activated PDGFRalpha tyrosine kinase. These cases with FIP1L1-PDGFRalpha rearrangement have been reported to be very sensitive to the tyrosine kinase inhibitor imatinib mesylate. DESIGN AND METHODS: A prospective multicenter study of idiopathic or primary HES was established in 2001 (Study Protocol Registration no. NCT 0027 6929). One hundred and ninety-six patients were screened, of whom 72 where identified as having idiopathic or primary HES and 63 were treated with imatinib 100 to 400 mg daily. RESULTS: Twenty-seven male patients carried the FIP1L1-PDGFRalpha rearrangement. All 27 achieved a complete hematologic remission (CHR) and became negative for the fusion transcripts according to reverse transcriptase polymerase chain reaction (RT-PCR) analysis. With a median follow-up of 25 months (15-60 months) all 27 patients remain in CHR and RT-PCR negative, and continue treatment at a dose of 100 to 400 mg daily. In three patients imatinib treatment was discontinued for few months, the fusion transcript became rapidly detectable, and then again undetectable upon treatment reassumption. Thirty-six patients did not carry the rearrangement; of these, five (14%) achieved a CHR, which was lost in all cases after 1 to 15 months. INTERPRETATION AND CONCLUSIONS: All patients meeting the criteria for idiopathic or primary HES should be screened for the FIP1L1-PDGFRalpha rearrangement. For all patients with this rearrangement, chronic imatinib treatment at doses as low as 100 mg daily ensures complete and durable responses.

Published
2007
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