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1. Recurrent ETNK1 mutations in atypical chronic myeloid leukemia

Author

Gambacorti-Passerini, Carlo B., Donadoni, Carla, Parmiani, Andrea, Pirola, Alessandra, Redaelli, Sara, Signore, Giovanni, Piazza, Vincenzo, Malcovati, Luca, Fontana, Diletta, Spinelli, Roberta, Magistroni, Vera, Gaipa, Giuseppe, Peronaci, Marco, Morotti, Alessandro, Panuzzo, Cristina, Saglio, Giuseppe, Usala, Emilio, Kim, Dong-Wook, Rea, Delphine, Zervakis, Konstantinos, Viniou, Nora, Symeonidis, Argiris, Becker, Heiko, Boultwood, Jacqueline, Campiotti, Leonardo, Carrabba, Matteo, Elli, Elena, Bignell, Graham R., Papaemmanuil, Elli, Campbell, Peter J., Cazzola, Mario, and Piazza, Rocco

Published
2015
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5. Μελέτη έκφρασης και προγνωστικής αξίας της Poly (ADP-ribose) Polymerase 1 mRNA στα μυελοδυσπλαστικά σύνδρομα

Author

Zervakis Konstantinos

Subjects
Health Sciences, Επιστήμες Υγείας
Abstract

Η πολυμεράση της πολυ (ADP-ριβόζης) 1 (PARP-1) αποτελεί βασικό μέλος οικογένειας πυρηνικών ενζύμων που συμμετέχουν στην επιδιόρθωση του DNA και ήδη είναι θεραπευτικός στόχος σε συμπαγείς όγκους. Στην παρούσα μελέτη ποσοτικοποιήθηκαν τα επίπεδα έκφρασης του mRNA της PARP1 με ποσοτική PCR ( qpcr) και τη μέθοδο SYBR στον μυελό των οστών 74 ασθενών με διάγνωση μυελοδυσπλαστικού συνδρόμου (MDS). Τα επίπεδα έκφρασης του mRNA της PARP1 αποτυπώθηκαν με τη μορφή του λόγου των μεταγράφων parp1/actin και συσχετίστηκαν με τα δημογραφικά, αιματολογικά και προγνωστικά χαρακτηριστικά των ασθενών. Τα αποτελέσματα εκφράστηκαν ως διάμεσος ± απόκλιση λάθους (median± SEM). Τα επίπεδα έκφρασης του mRNA της PARP1 συσχετίστηκαν στη συνέχεια με τον τύπο MDS (ταξινόμηση WHO 2008/2016, p = 0.005) και με το IPSS score (p = 0.002). Επίσης, διαπιστώθηκε συσχέτιση με το IPSS-R (p = 0,011) και την προγνωστική σημασία των κυτταρογενετικών ευρημάτων (p = 0,008). Σε όλες τις περιπτώσεις, υψηλότερα επίπεδα PARP1 συσχετίστηκαν με υψηλότερη κατηγορία κινδύνου. Επιπλέον, διαπιστώθηκε ένα στατιστικά σημαντικό μειονέκτημα επιβίωσης για τους ασθενείς με υψηλά επίπεδα PARP1 ( η διάμεση επιβίωση ασθενών ήταν 37,4 μήνες, ενώ η διάμεση επιβίωση ασθενών με χαμηλά επίπεδα PARP1 δεν επιτεύχθηκε, p = 0,0001). Η επιβίωση στα 5 χρόνια ήταν 29,8% έναντι 88,9% αντίστοιχα. Τα επίπεδα mRNA της PARP1 βρέθηκαν να είναι ο ισχυρότερος προγνωστικός παράγοντας της επιβίωσης σε ανάλυση πολλαπλών μεταβλητών. Αυτές οι συσχετίσεις δεν έχουν αναφερθεί ποτέ στο παρελθόν και μπορεί να καταστήσουν την PARP1 έναν προγνωστικό παράγοντα που μπορεί να ενσωματωθεί στα τρέχοντα προγνωστικά συστήματα για το MDS, θέτοντας επίσης τη βάση για τις κλινικές δοκιμές που αξιολογούν τους αναστολείς PARP1 σε MDS υψηλού κινδύνου. Poly (ADP-ribose) polymerase 1 (PARP-1) has a central role in the repair of DNA breaks and is a promising treatment target in malignancy. We measured PARP1 mRNA levels by a SYBR-green-based PCR in the bone marrow of 74 patients with myelodysplastic syndrome (MDS) and correlated them to their demographic, hematologic and prognostic characteristics. The median PARP1 mRNA levels were correlated to the type of MDS (2008/2016 WHO classification, P = 0.005) and to the IPSS score (P = 0.002). A correlation was also found with the IPSS-R score (P = 0.011) and the cytogenetic risk (P = 0.008). In all cases, higher PARP1 levels were correlated with a higher risk category. Moreover, we found a significant survival disadvantage for patients with high PARP1 levels (median survival of 37.4 months versus ‘not reached’ for low PARP1 levels, P = 0.0001, and a 5-year survival rate of 29.8 versus 88.9%, respectively). PARP1 mRNA levels were found to be the stronger predictor of survival in multivariate analysis. These correlations have never been reported in the past and may render PARP1 a prognostic factor to be incorporated in the current prognostic systems for MDS, also laying the basis for clinical trials evaluating PARP1 inhibitors in higher-risk MDS.

Published
2019

6. Isolated skeletal muscle recurrence of an originally nodal diffuse large B cell lymphoma A case report and review of the literature

Author

Spetsieris, Nikolaos Giannakopoulou, Nefeli Variami, Eleni and Zervakis, Konstantinos Rougala, Niki Garefalakis, Georgios and Skarlatou, Vasiliki Viniou, Nora-Athina Diamantopoulos, Panagiotis

Subjects
hemic and lymphatic diseases
Abstract

Rationale: Diffuse large B cell lymphoma (DLBCL) is a malignancy of the B cells with extranodal primary involvement being estimated at 30% to 40% of cases. Primary skeletal muscle presentation of DLBCL is extremely rare, with an estimated incidence of about 0.5% of extranodal lymphomas, presenting mostly in the lower extremities. The possible mechanisms of muscle involvement of DLBCL include primary extranodal disease, extension from adjacent organs (such as lymph nodes) or disseminated disease. Patient concerns: We report a case of a 70-year-old woman with an advanced initially nodal DLBCL, treated with R-CHOP, that presented with an enlargement of her left thigh and restricted mobility 3 months after completion of chemotherapy. Imaging studies were performed, which showed possible infiltration of the muscles of the left thigh, without any nodal disease present. Diagnoses: Muscle biopsy documented the recurrence of the lymphoma at the left thigh. Interventions: The patient started second-line treatment with gemcitabine and vinorelbine. Outcomes: A partial response was achieved after the first cycle. Lessons: The remarkable element lies in the reappearance of the lymphoma at the left thigh muscles, with no radiographic or clinical evidence of involvement of lymph nodes, despite the extensive lymph node disease at initial presentation. The further management of such recurrences remains to be clarified, as the odd biological behavior of the malignant cells dictates a special handling of the disease.

Published
2018

10. Evaluation of the performance of tuberculin skin test and Quantiferon-TB gold in tube test in patients with hematologic malignancies

Author

Diamantopoulos, Panagiotis T., primary, Tsilimidos, Gerasimos D., additional, Zervakis, Konstantinos, additional, Polonyfi, Katerina, additional, Sofotasiou, Maria, additional, Kyrtsonis, Marie-Christine, additional, Aessopos, Athanasios, additional, Kyriakakis, Georgios, additional, and Viniou, Nora A., additional

Published
2017
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11. Expression of Poly [ADP-Ribose] Polymerase 1 (PARP-1) and Uridine-Cytidine Kinase (UCK) 1 and 2 in Myelodysplastic Syndrome

Author

Diamantopoulos, Panagiotis Theodorou, primary, Zervakis, Panagiotis, additional, Sofotasiou, Maria, additional, Zervakis, Konstantinos, additional, Symeonidis, Argiris, additional, Elina, Kodandreopoulou, additional, Athanassios, Galanopoulos, additional, Vassiliki, Pappa, additional, Ioannis, Kotsianidis, additional, Georgia, Christopoulou, additional, Vasiliki, Papadopoulou, additional, Marina, Mantzourani, additional, and Viniou, Nora-Athina, additional

Published
2016
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12. An Adult Patient with Systemic Mastocytosis and B-Acute Lymphoblastic Leukemia

Author

Iliakis, Theodoros, Rougkala, Niki, Diamantopoulos, Panagiotis T., Papadopoulou, Vasiliki, Kalala, Fani, Zervakis, Konstantinos, Giannakopoulou, Nefeli, Chatzinikolaou, Polixeni, Levidou, Georgia, Lakiotaki, Eleftheria, Korkolopoulou, Penelope, Patsouris, Efstratios, Variami, Eleni, and Viniou, Nora-Athina

Subjects
Article Subject
Abstract

Mastocytosis is a myeloproliferative neoplasm characterized by clonal expansion of abnormal mast cells, ranging from the cutaneous forms of the disease to mast cell leukemia. In a significant proportion of patients, systemic mastocytosis (SM) coexists with another hematologic malignancy, termed systemic mastocytosis with an associated hematologic nonmast cell lineage disorder (SM-AHNMD). Despite the pronounced predominance of concomitant myeloid neoplasms, the much more unusual coexistence of lymphoproliferative diseases has also been reported. Imatinib mesylate (IM) has a role in the treatment of SM in the absence of the KITD816V mutation. In the setting of SM-AHNMD, eradicating the nonmast cell malignant clone greatly affects prognosis. We report a case of an adult patient with SM associated with B-lineage acute lymphoblastic leukemia (B-ALL). Three cases of concurrent adult ALL and mastocytosis have been reported in the literature, one concerning SM and two concerning cutaneous mastocytosis (CM), as well as six cases of concomitant CM and ALL in children.

Published
2014
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14. Bone Marrow Levels of PARP1 mRNA Predict Response to Treatment with 5-Azacytidine in Patients with Myelodysplastic Syndrome

Author

Diamantopoulos, Panagiotis Theodorou, Kodandreopoulou, Elina, Symeonidis, Argiris S., Kotsianidis, Ioannis, Pappa, Vassiliki, Galanopoulos, Athanasios, Dimou, Maria, Christopoulou, Georgia, Zervakis, Konstantinos, Solomou, Elena E., Kyrtsonis, Marie-Christine, Rougala, Niki, Siakantaris, Marina, Vassilakopoulos, Theodoros, Panayiotidis, Panayiotis, and Viniou, Nora-Athina

Published
2017
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15. Evidence of ETNK1 Somatic Variants in Atypical Chronic Myeloid Leukemia

Author

Donadoni, Carla, primary, Piazza, Rocco, additional, Fontana, Diletta, additional, Parmiani, Andrea, additional, Pirola, Alessandra, additional, Redaelli, Sara, additional, Signore, Giovanni, additional, Piazza, Vincenzo, additional, Malcovati, Luca, additional, Spinelli, Roberta, additional, Magistroni, Vera, additional, Gaipa, Giuseppe, additional, Peronaci, Marco, additional, Morotti, Alessandro, additional, Panuzzo, Cristina, additional, Saglio, Giuseppe, additional, Elli, Elena Maria, additional, Usala, Emilio, additional, Kim, Dong-Wook, additional, Rea, Delphine, additional, Zervakis, Konstantinos, additional, Viniou, Nora-Athina, additional, Symeonidis, Argiris, additional, Becker, Heiko, additional, Boultwood, Jacqueline, additional, Campiotti, Leonardo, additional, Carrabba, Matteo G, additional, Bignell, Graham R, additional, Papaemmanuil, Elli, additional, Campbell, Peter J, additional, Cazzola, Mario, additional, and Gambacorti-Passerini, Carlo, additional

Published
2014
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16. Decrease in Transfusion Needs in Patients with Higher-Risk Myelodysplastic Syndrome and Acute Myeloid Leukemia Treated with 5-Azacytidine. a Retrospective Study

Author

Diamantopoulos, Panagiotis Theodorou, primary, Zervakis, Konstantinos, additional, Galanopoulos, Athanasios G., additional, Bakarakos, Panagiotis, additional, Papadopoulou, Vasiliki, additional, Iliakis, Theodoros, additional, Kalala, Fani, additional, Giannakopoulou, Nefeli, additional, Rougala, Niki, additional, Variami, Eleni, additional, Dimitrakopoulou, Aglaia, additional, and Viniou, Nora-Athina, additional

Published
2014
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17. Evidence for regulation of oxidative stress by latent membrane protein 1 oncoprotein in patients with low-grade leukemic B cell lymphoma with latent Epstein–Barr virus infection

Author

Papadopoulou, Vasiliki, primary, Diamantopoulos, Panagiotis T., additional, Kontandreopoulou, Elina, additional, Polonyfi, Katerina, additional, Variami, Eleni, additional, Kouzis, Panagiotis, additional, Galanopoulos, Athanasios, additional, Spanakis, Nikolaos, additional, Zervakis, Konstantinos, additional, Iliakis, Theodoros, additional, Perrea, Despoina, additional, Kollia, Panagoula, additional, Vassilakopoulos, Theodoros P., additional, Pangalis, Gerassimos A., additional, Kyrtsonis, Christine, additional, Vaiopoulos, George, additional, and Viniou, Nora-Athina, additional

Published
2014
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18. A Pilot Study Of Bone Marrow and Adipose Tissue – Derived Mesenchymal Stem Cells In Chronic Myeloid Leukemia (CML); Mesenchymal Stem Cells Of The Bone Marrow Harbor The Bcr-Abl Fusion Gene In a CML Patient

Author

Papadopoulou, Vasiliki, primary, Peste, Korina, additional, Koumpi, Dafni, additional, Stavropoulou, Vasiliki, additional, Diamantopoulos, Panagiotis Theodorou, additional, Dimitroulis, Dimitrios, additional, Zervakis, Konstantinos, additional, Kalala, Fani, additional, Giannakopoulou, Nefeli, additional, Rougkala, Niki, additional, Hatzinikolaou, Polyxeni, additional, Tsilimidos, Gerasimos, additional, Iliakis, Theodoros, additional, Variami, Eleni, additional, and Viniou, Nora-Athina, additional

Published
2013
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19. Poly [ADP-Ribose] Polymerase 1 (PARP-1) Expression Before and After Immunochemotherapy In Patients With B Chronic Lymphocytic Leukemia

Author

Diamantopoulos, Panagiotis Theodorou, primary, Sofotasiou, Maria, additional, Papadopoulou, Vasiliki, additional, Polonyfi, Katerina, additional, Iliakis, Theodoros, additional, Kalala, Fani, additional, Zervakis, Konstantinos, additional, Rougala, Niki, additional, Giannakopoulou, Nefeli, additional, Hatzinikolaou, Xenia, additional, Galanopoulos, Athanassios, additional, Variami, Eleni, additional, Pangalis, Gerassimos A, additional, and Viniou, Nora-Athina, additional

Published
2013
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20. A Study of the Expression of the LMP1 Oncoprotein in Low-Grade B Cell Lymphomas and Correlation with the Levels of Oxidative Stress

Author

Diamantopoulos, Panagiotis Theodorou, primary, Papadopoulou, Vasiliki, additional, Polonyfi, Aikaterini, additional, Galanopoulos, Athanasios G., additional, Kalala, Fani, additional, Zervakis, Konstantinos, additional, Iliakis, Theodoros, additional, Terpos, Evangelos, additional, Perrea, Despoina, additional, and Viniou, Nora-Athina, additional

Published
2012
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21. Recurrent ETNK1mutations in atypical chronic myeloid leukemia

Author

Gambacorti-Passerini, Carlo B., Donadoni, Carla, Parmiani, Andrea, Pirola, Alessandra, Redaelli, Sara, Signore, Giovanni, Piazza, Vincenzo, Malcovati, Luca, Fontana, Diletta, Spinelli, Roberta, Magistroni, Vera, Gaipa, Giuseppe, Peronaci, Marco, Morotti, Alessandro, Panuzzo, Cristina, Saglio, Giuseppe, Usala, Emilio, Kim, Dong-Wook, Rea, Delphine, Zervakis, Konstantinos, Viniou, Nora, Symeonidis, Argiris, Becker, Heiko, Boultwood, Jacqueline, Campiotti, Leonardo, Carrabba, Matteo, Elli, Elena, Bignell, Graham R., Papaemmanuil, Elli, Campbell, Peter J., Cazzola, Mario, and Piazza, Rocco

Abstract

Despite the recent identification of recurrent SETBP1mutations in atypical chronic myeloid leukemia (aCML), a complete description of the somatic lesions responsible for the onset of this disorder is still lacking. To find additional somatic abnormalities in aCML, we performed whole-exome sequencing on 15 aCML cases. In 2 cases (13.3%), we identified somatic missense mutations in the ETNK1gene. Targeted resequencing on 515 hematological clonal disorders revealed the presence of ETNK1variants in 6 (8.8%) of 68 aCML and 2 (2.6%) of 77 chronic myelomonocytic leukemia samples. These mutations clustered in a small region of the kinase domain, encoding for H243Y and N244S (1/8 H243Y; 7/8 N244S). They were all heterozygous and present in the dominant clone. The intracellular phosphoethanolamine/phosphocholine ratio was, on average, 5.2-fold lower in ETNK1-mutated samples (P< .05). Similar results were obtained using myeloid TF1 cells transduced with ETNK1 wild type, ETNK1-N244S, and ETNK1-H243Y, where the intracellular phosphoethanolamine/phosphocholine ratio was significantly lower in ETNK1-N244S (0.76 ± 0.07) and ETNK1-H243Y (0.37 ± 0.02) than in ETNK1-WT (1.37 ± 0.32; P= .01 and P= .0008, respectively), suggesting that ETNK1mutations may inhibit the catalytic activity of the enzyme. In summary, our study shows for the first time the evidence of recurrent somatic ETNK1mutations in the context of myeloproliferative/myelodysplastic disorders.

Published
2015
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22. Evidence of ETNK1Somatic Variants in Atypical Chronic Myeloid Leukemia

Author

Donadoni, Carla, Piazza, Rocco, Fontana, Diletta, Parmiani, Andrea, Pirola, Alessandra, Redaelli, Sara, Signore, Giovanni, Piazza, Vincenzo, Malcovati, Luca, Spinelli, Roberta, Magistroni, Vera, Gaipa, Giuseppe, Peronaci, Marco, Morotti, Alessandro, Panuzzo, Cristina, Saglio, Giuseppe, Elli, Elena Maria, Usala, Emilio, Kim, Dong-Wook, Rea, Delphine, Zervakis, Konstantinos, Viniou, Nora-Athina, Symeonidis, Argiris, Becker, Heiko, Boultwood, Jacqueline, Campiotti, Leonardo, Carrabba, Matteo G, Bignell, Graham R, Papaemmanuil, Elli, Campbell, Peter J, Cazzola, Mario, and Gambacorti-Passerini, Carlo

Abstract

Atypical Chronic Myeloid Leukemia (aCML) is a clonal disorder belonging to the Myeloproliferative/Myelodysplastic (MPN/MDS) group. The molecular lesions responsible for the onset of aCML remained unknown until 2013 when recurrent somatic mutations of SETBP1were identified. However, the frequency of SETBP1mutations in aCML does not exceed 25-30%, which suggests that other lesions may play a role in the remaining cases.

Published
2014
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23. 5-Azacytidine in the Treatment of Intermediate-2 and High-risk Myelodysplastic Syndromes and Acute Myeloid Leukemia. A Five-year Experience with 44 Consecutive Patients.

Author

Diamantopoulos P, Zervakis K, Papadopoulou V, Iliakis T, Kalala F, Giannakopoulou N, Rougala N, Galanopoulos A, Bakarakos P, Variami E, Dimitrakopoulou A, and Viniou NA

Subjects
Aged, Aged, 80 and over, Azacitidine adverse effects, Disease Progression, Female, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Retrospective Studies, Risk Factors, Treatment Outcome, Azacitidine therapeutic use, Leukemia, Myeloid, Acute drug therapy, Myelodysplastic Syndromes drug therapy
Abstract

Background/aim: The hypomethylating agent 5-azacytidine has been the standard-of-care for patients with higher-risk myelodysplastic syndrome (MDS) during the past few years. Its efficacy has been proven in large clinical trials, and its safety has been shown to be superior to that of conventional treatments., Patients and Methods: We conducted a retrospective study on the efficacy and safety of 5-azacytidine in 44 consecutive patients with MDS and acute myeloid leukemia treated with 5-azacytidine during a 63-month period. We recorded the clinical and laboratory characteristics of the patients and we analyzed the response to treatment, overall survival and adverse events during treatment., Results: The median overall survival was 13 months, while serious adverse events consisted mostly of neutropenic infections., Conclusion: We reached two possibly valuable conclusions: Younger patients (<73 years), as well as patients receiving treatment at longer than 28-day intervals had a significantly higher overall survival., (Copyright© 2015 International Institute of Anticancer Research (Dr. John G. Delinassios), All rights reserved.)

Published
2015

24. Cessation of tyrosine kinase inhibitors in patients with chronic-phase chronic myelogenous leukemia following durable complete molecular response: a single center facing the dilemma.

Author

Iliakis T, Papadopoulou V, Diamantopoulos PT, Panayiotidis P, Zervakis K, Giannakopoulou N, Tilimidos G, Angelopoulou M, Siakantaris MP, Pangalis G, Mantzourani M, Variami E, and Viniou NA

Subjects
Adult, Aged, Female, Fusion Proteins, bcr-abl genetics, Fusion Proteins, bcr-abl metabolism, Gene Expression Regulation, Leukemic, Humans, Male, Middle Aged, Treatment Outcome, Leukemia, Myeloid, Chronic-Phase drug therapy, Leukemia, Myeloid, Chronic-Phase genetics, Protein Kinase Inhibitors therapeutic use, Withholding Treatment
Abstract

Tyrosine kinase inhibitors (TKIs), namely imatinib mesylate (IM) and recently approved second-generation TKIs dasatinib and nilotinib, are currently considered the treatment of choice for newly-diagnosed chronic phase chronic myelogenous leukemia (CP-CML). Although treatment with TKIs has not yet been proven curative, it certainly accomplishes a sustained control of the disease in the vast majority of patients. More than a decade after the successful launching of IM in first-line treatment of CP-CML and the subsequent introduction of second-generation TKIs in this setting, the question of the possibility of TKI cessation in a specific subset of patients has emerged. Side-effects of TKIs, along with some patients' wish to abandon the drugs and the rising financial burden upon healthcare systems, have led to the dilemma whether IM can be safely withdrawn after achieving deep molecular remissions and which patients are suitable for this discontinuation. We examined the data of our patients with CML in search of potential canditates for cessation of TKI therapy and identified their characteristics. We also performed a thorough review of the relevant literature. Eight out of fifty patients were discriminated on grounds of sustained complete molecular response (CMR) exceeding 12 months, most of them with a low or intermediate Sokal score at diagnosis. The median interval from IM initiation to CMR was almost 2 years and the median duration of detected CMR reached 6.5 years. Based on the promising results of prospective clinical trials reporting successful cessation of treatment with TKIs on selected subgroups of patients, we decided to proceed to interruption of therapy in the specific subset of our patients and closely monitor their response.

Published
2013

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