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1. The proportion of different BCR-ABL1 transcript types in chronic myeloid leukemia. An international overview

Author

Baccarani, M, Castagnetti, F, Gugliotta, G, Rosti, G, Soverini, S, Albeer, A, Pfirrmann, M, Bekadja, Ma, Entasoltan, B, Nachi, M, Elghandour, A, El Sorady, M, Abdelfattah, R, El Nahass, Y, Samra, M, Azzazi, M, Elsobki, E, Moussa, M, Fahmy, O, Mattar, M, Shehata, Azmy, Se, (Azmy, E, 9 ), Emad), Bolarinwa, (Bolarinwa, Ra, ( 10 ), Rahman A., Eid, (Eid, S, Samir)( 11, ), Khelif, (Khelif, A, Abderrhaim)( 11, ), Hached, (Hached, F, Farhat)( 11, ), Menif, (Menif, S, Samia)( 12, ), Rahman, (Rahman, H, Hafizur)( 13, ), Huang, (Huang, Xj, Xiaojun)(, 14, 15, ), Jiang, (Jiang, Q, Qian)(, 14, (Ye, Yx, Yuanxin)( 16, ), Zhu, (Zhu, Hl, Huanling)( 16, ), Chen, (Chen, Sn, Suning)( 17, ), Varma, (Varma, N, Neelam)( 18, ), Ganesan, (Ganesan, P, Prasanth)( 19, ), Gundeti, (Gundeti, S, Sadashivudu)( 20, ), Malhotra, (Malhotra, H, Hemant)( 21, ), Radhakrishnan, (Radhakrishnan, Vs, ( 22 ), Vivek S., Kumar, (Kumar, L, Lalit)( 23, ), Sharawat, (Sharawat, Sk, Surender Kumar)( 23, ), Seth, (Seth, T, Tulika)( 24, ), Ausekar, (Ausekar, Bv, ( 25 ), B. V., Balasubramanian, (Balasubramanian, P, Poonkuzhali)( 26, ), Poopak, (Poopak, B, Behzad)(, 27, 28, ), Inokuchi, (Inokuchi, K, Koiti)( 29, ), Kim, (Kim, Dw, Dong-Wook)( 30, ), Kindi, Al, S (Al Kindi, Salam)( 31, ), Mirasol, (Mirasol, A, Angelina)( 32, ), Qari, (Qari, M, Mohammed)( 33, ), Goh, (Goh, Yt, Yeow Tee)( 34, ), Shih, (Shih, Ly, Lee-Yung)(, 35, 36, ), Branford, (Branford, S, Susan)(, 37, 38, ), Lion, (Lion, T, Thomas)( 39, ), Valent, (Valent, P, Peter)( 40, ), Burgstaller, (Burgstaller, S, Sonja)( 41, ), Thaler, (Thaler, J, Joseph)( 41, ), Labar, (Labar, B, Boris)( 42, ), Zadro, (Zadro, R, Renata)( 42, ), Mayer, (Mayer, J, Jiri)(, 43, 44, ), Zackova, (Zackova, D, Daniela)(, 43, Faber, (Faber, E, Edgar)( 45, ), Pallisgaard, (Pallisgaard, N, Niels)( 46, ), Xavier-Mahon, (Xavier-Mahon, F, Francois)( 47, ), Lippert, (Lippert, E, Eric)( 48, ), Cayuela, (Cayuela, Jm, Jean Michel)( 49, ), Rea, (Rea, D, Delphine)( 49, ), Millot, (Millot, F, Frederic)( 50, ), Suttorp, (Suttorp, M, Meinolf)( 51, ), Hochhaus, (Hochhaus, A, Andreas)( 52, ), Niederwieser, (Niederwieser, D, Dietger)( 53, ), Saussele, (Saussele, S, Susanne)( 54, ), Haferlach, (Haferlach, T, Torsten)( 55, ), Jeromine, (Jeromine, S, Sabine)( 55, ), Panayiotidis, (Panayiotidis, P, Panayiotis)(, 56, 57, ), Conneally, (Conneally, E, Eibhlin)( 58, ), Langabeer, (Langabeer, S, Steve)( 58, ), Nagler, (Nagler, A, Arnon)(, 59, 60, ), Rupoli, (Rupoli, S, Serena)( 61, ), Santoro, (Santoro, N, Nicola)( 62, ), Albano, (Albano, F, Francesco)( 63, ), Castagnetti, (Castagnetti, F, Fausto), Ottaviani, (Ottaviani, E, Emanuela)(, 64, 65, ), Rambaldi, (Rambaldi, A, Alessandro)(, 66, 67, ), Stagno, (Stagno, F, Fabio)( 68, ), Molica, (Molica, S, Stefano)( 69, ), Biagiotti, (Biagiotti, C, Caterina)( 70, ), Scappini, (Scappini, B, Barbara)( 70, ), Lemoli, (Lemoli, R, Roberto)( 71, ), Iurlo, (Iurlo, A, Alessandra)(, 72, 73, ), Pungolino, (Pungolino, E, Ester)( 74, ), Menna, (Menna, G, Giuseppe), Pane, (Pane, F, Fabrizio)( 76, ), Gottardi, (Gottardi, E, Enrico)(, 77, 78, ), Rege-Cambrin, (Rege-Cambrin, G, Giovanna)(, 77, Binotto, (Binotto, G, Gianni)( 79, ), Putti, (Putti, Mc, Maria Caterina)( 80, ), Falzetti, (Falzetti, F, Franca)( 81, ), Visani, (Visani, G, Giuseppe)( 82, ), Galimberti, (Galimberti, S, Sara)( 83, ), Musto, (Musto, P, Pellegrino)( 84, ), Abruzzese, (Abruzzese, E, Elisabetta)( 85, ), Breccia, (Breccia, M, Massimo)( 86, ), Giona, (Giona, F, Fiorina)( 86, ), Chiusolo, (Chiusolo, P, Patrizia)( 87, ), Sica, (Sica, S, Simona)( 87, ), Fava, (Fava, C, Carmen)( 88, ), Ferrero, (Ferrero, D, Dario)( 88, ), Tiribelli, (Tiribelli, M, Mario)( 89, ), Bonifacio, (Bonifacio, M, Massimiliano)( 90, ), Griskevicius, (Griskevicius, L, Laimonas)( 91, ), Musteata, (Musteata, V, Vasile)( 92, ), Janssen, (Janssen, J, Jeroen)( 93, ), Prejzner, (Prejzner, W, Witold)( 94, ), Sacha, (Sacha, T, Tomasz)( 95, ), Waclaw, (Waclaw, J, Joanna)( 95, ), Almeida, (Almeida, Am, Antonio Medina)( 96, ), Kulikov, (Kulikov, S, Sergei)( 97, ), Turkina, (Turkina, A, Anna)( 97, ), Bogdanovic, (Bogdanovic, A, Andrija)( 98, ), Zupan, (Zupan, I, Irena)( 99, ), Marce, (Marce, S, Silvia)( 100, ), Cervantes, (Cervantes, F, Francisco)( 101, ), Steegmann, (Steegmann, Jl, Juan Luis)( 102, ), Kotlyarchuk, (Kotlyarchuk, K, Konstyantyn)( 103, ), Milner, (Milner, Bj, ( 104 ), Benedict J., Rose, (Rose, S, Susan)( 105, ), Clench, (Clench, T, Tim)( 106, ), Waits, (Waits, P, Paula)( 107, ), Austin, (Austin, S, Steve)( 108, ), Wickham, (Wickham, C, Caroline)( 109, ), Clark, (Clark, R, Richard)( 110, ), Apperley, (Apperley, J, Jane), Claudiani, (Claudiani, S, Simone)( 111, ), Foroni, (Foroni, L, Letizia)( 111, ), Szydlo, (Szydlo, R, Richard)( 111, ), Burt, (Burt, E, Emma)( 112, ), Bescoby, (Bescoby, R, Ruth)( 113, ), Cork, (Cork, L, Leanne)( 113, ), O'Brien, (O'Brien, S, Stephen)( 113, ), Green, (Green, B, Bethaney)( 114, ), Hawtree, (Hawtree, S, Sarah)( 114, ), Watson, (Watson, M, Mark)( 114, ), Bengio, (Bengio, Rm, Raquel Maria)( 115, ), Larripa, (Larripa, I, Irene)( 115, ), Pavlovsky, (Pavlovsky, C, Carolina)( 116, ), Moiraghi, (Moiraghi, B, Beatriz)( 117, ), Pinna, De, CAR (Requiao de Pinna, Cristiane Almeida)( 118, ), Magalhaes, GHR (Romani Magalhaes, Gustavo Henrique)( 119, ), Pagnano, (Pagnano, K, Katia)( 120, ), Funke, (Funke, V, Vaneuza)( 121, ), Tavares, (Tavares, Rs, Renato Sampaio)( 122, ), Prado, (Prado, A, Adriana)( 123, ), Azevedo, (Azevedo, Aa, Alita Andrade)( 124, ), Fogliatto, (Fogliatto, L, Laura)( 125, ), Bonecker, (Bonecker, S, Simone)( 126, ), Centrone, (Centrone, R, Renato)( 127, ), Moellman, (Moellman, A, Artur)( 128, ), Conchon, (Conchon, M, Monika)( 130, ), Centurion, (Centurion, Me, Maria Elida)( 131, ), (Prado, Ai, Ana-Ines)( 132, ), Lopez, (Lopez, Jl, ( 133 ), J. L., Petruzziello, (Petruzziello, F, Fara)( 75, ), Bendit, (Bendit, I, Israel), Baccarani M., Castagnetti F., Gugliotta G., Rosti G., Soverini S., Albeer A., and Pfirrmann M.

Subjects
Male, 0301 basic medicine, Cancer Research, bcr-abl, Fusion Proteins, bcr-abl, Global Health, 0302 clinical medicine, hemic and lymphatic diseases, 80 and over, Odds Ratio, Prevalence, Age Factor, Chronic, Young adult, Child, MOLECULAR RESPONSE, Leukemic, Aged, 80 and over, Leukemia, Hematology, Gene Expression Regulation, Leukemic, CHRONIC MYELOGENOUS LEUKEMIA, Age Factors, Myeloid leukemia, Middle Aged, Oncology, Child, Preschool, 030220 oncology & carcinogenesis, Female, Life Sciences & Biomedicine, Human, Adult, Transcriptional Activation, medicine.medical_specialty, Adolescent, Immunology, IMATINIB MESYLATE, DENDRITIC CELLS, CML PATIENTS, Young Adult, 03 medical and health sciences, Myelogenous, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Internal medicine, medicine, Humans, 1112 Oncology and Carcinogenesis, BCR/ABL TRANSCRIPT, Preschool, CYTOGENETIC RESPONSE, Aged, Science & Technology, CHRONIC-PHASE, business.industry, Infant, Newborn, Fusion Proteins, ABL FUSION PROTEINS, P190 BCR-ABL, Infant, 1103 Clinical Sciences, Odds ratio, Newborn, medicine.disease, International BCR-ABL Study Group, Settore MED/15 - MALATTIE DEL SANGUE, 030104 developmental biology, Imatinib mesylate, Gene Expression Regulation, BCR-ABL Positive, business, Chronic myelogenous leukemia
Abstract

There are different BCR-ABL1 fusion genes that are translated into proteins that are different from each other, yet all leukemogenic, causing chronic myeloid leukemia (CML) or acute lymphoblastic leukemia. Their frequency has never been systematically investigated. In a series of 45503 newly diagnosed CML patients reported from 45 countries, it was found that the proportion of e13a2 (also known as b2a2) and of e14a2 (also known as b3a2), including the cases co-expressing e14a2 and e13a2, was 37.9% and 62.1%, respectively. The proportion of these two transcripts was correlated with gender, e13a2 being more frequent in males (39.2%) than in females (36.2%), was correlated with age, decreasing from 39.6% in children and adolescents down to 31.6% in patients ≥ 80 years old, and was not constant worldwide. Other, rare transcripts were reported in 666/34561 patients (1.93%). The proportion of rare transcripts was associatedwith gender (2.27% in females and 1.69% in males) and with age (from 1.79% in children and adolescents up to 3.84% in patients ≥ 80 years old). These data show that the differences in proportion are not by chance. This is important, as the transcript type is a variable that is suspected to be of prognostic importance for response to treatment, outcome of treatment, and rate of treatment-free remission.

Published
2019
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2. Cytogenetic complexity in chronic lymphocytic leukemia: definitions, associations, and clinical impact

Author

Baliakas, P, Jeromin, S, Iskas, M, Puiggros, A, Plevova, K, Nguyen-Khac, F, Davis, Z, Rigolin, GM, Visentin, A, Xochelli, A, Delgado, J, Baran-Marszak, F, Stalika, E, Abrisqueta, P, Durechova, K, Papaioannou, G, Eclache, V, Dimou, M, Iliakis, T, Collado, R, Doubek, M, Calasanz, MJ, Ruiz-Xiville, N, Moreno, C, Jarosova, M, Leeksma, AC, Panayiotidis, P, Podgornik, H, Cymbalista, F, Anagnostopoulos, A, Trentin, L, Stavroyianni, N, Davi, F, Ghia, P, Kater, AP, Cuneo, A, Pospisilova, S, Espinet, B, Athanasiadou, A, Oscier, D, Haferlach, C, Stamatopoulos, K, and ERIC European Res Initiative CLL

Abstract

Recent evidence suggests that complex karyotype (CK) defined by the presence of >= 3 chromosomal aberrations (structural and/or numerical) identified by using chromosome-banding analysis (CBA) may be relevant for treatment decision-making in chronic lymphocytic leukemia (CLL). However, many challenges toward the routine clinical application of CBA remain. In a retrospective study of 5290 patients with available CBA data, we explored both clinicobiological associations and the clinical impact of CK in CLL. We found that patients with >= 5 abnormalities, defined as high-CK, exhibit uniformly dismal clinical outcomes, independently of clinical stage, TP53 aberrations (deletion of chromosome 17p and/or TP53 mutations [TP53abs]), and the expression of somatically hypermutated (M-CLL) or unmutated immunoglobulin heavy variable genes. Thus, they contrasted with CK cases with 3 or 4 aberrations (low-CK and intermediate-CK, respectively) who followed aggressive disease courses only in the presence of TP53abs. At the other end of the spectrum, patients with CK and 112,119 displayed an exceptionally indolent profile. Building upon CK, TP53abs, and immunoglobulin heavy variable gene somatic hyper-mutation status, we propose a novel hierarchical model in which patients with high-CK exhibit the worst prognosis, whereas those with mutated CLL lacking CK or TP53abs, as well as CK with 112,119, show the longest overall survival. Thus, CK should not be axiomatically considered unfavorable in CLL, representing a heterogeneous group with variable clinical behavior. High-CK with >= 5 chromosomal aberrations emerges as prognostically adverse, independent of other biomarkers. Prospective clinical validation is warranted before ultimately incorporating high-CK in risk stratification of CLL.

Published
2019

3. The proportion of different BCR-ABL1 transcript types in chronic myeloid leukemia. An international overview

Author

Baccarani, M, Gugliotta, G, Rosti, G, Soverini, S, Albeer, A, Pfirrmann, M, Bekadja, MA, Entasoltan, B, Nachi, M, Elghandour, A, El Sorady, M, Abdelfattah, R, El Nahass, Y, Samra, M, Azzazi, M, Elsobki, E, Moussa, M, Fahmy, O, Mattar, M, Shehata, SE, Azmy, E, Bolarinwa, RA, Eid, S, Khelif, A, Hached, F, Menif, S, Rahman, H, Huang, XJ, Jiang, Q, Ye, YX, Zhu, HL, Chen, SN, Varma, N, Ganesan, P, Gundeti, S, Malhotra, H, Radhakrishnan, VS, Kumar, L, Sharawat, SK, Seth, T, Ausekar, BV, Balasubramanian, P, Poopak, B, Inokuchi, K, Kim, DW, Al Kindi, S, Mirasol, A, Qari, M, Goh, YT, Shih, LY, Branford, S, Lion, T, Valent, P, Burgstaller, S, Thaler, J, Labar, B, Zadro, R, Mayer, J, Zackova, D, Faber, E, Pallisgaard, N, Xavier-Mahon, F, Lippert, E, Cayuela, JM, Rea, D, Millot, F, Suttorp, M, Hochhaus, A, Niederwieser, D, Saussele, S, Haferlach, T, Jeromine, S, Panayiotidis, P, Conneally, E, Langabeer, S, Nagler, A, Rupoli, S, Santoro, N, Albano, F, Castagnetti, F, Ottaviani, E, Rambaldi, A, Stagno, F, Molica, S, Biagiotti, C, Scappini, B, Lemoli, R, Iurlo, A, Pungolino, E, Menna, G, Pane, F, Gottardi, E, Rege-Cambrin, G, Binotto, G, Putti, MC, Falzetti, F, Visani, G, Galimberti, S, Musto, P, Abruzzese, E, Breccia, M, Giona, F, Chiusolo, P, Sica, S, Fava, C, Ferrero, D, Tiribelli, M, Bonifacio, M, Griskevicius, L, Musteata, V, Janssen, J, Prejzner, W, Sacha, T, Waclaw, J, Almeida, AM, Kulikov, S, Turkina, A, Bogdanovic, A, Zupan, I, Marce, S, Cervantes, F, Steegmann, JL, Kotlyarchuk, K, Milner, BJ, Rose, S, Clench, T, Waits, P, Austin, S, Wickham, C, Clark, R, Apperley, J, Claudiani, S, Foroni, L, Szydlo, R, Burt, E, Bescoby, R, Cork, L, O'Brien, S, Green, B, Hawtree, S, Watson, M, Bengio, RM, Larripa, I, Pavlovsky, C, Moiraghi, B, de Pinna, CAR, Magalhaes, GHR, Pagnano, K, Funke, V, Tavares, RS, Prado, A, Azevedo, AA, Fogliatto, L, Bonecker, S, Centrone, R, Moellman, A, Conchon, M, Centurion, ME, Prado, AI, Lopez, JL, Petruzziello, F, and Bendit, I

Abstract

There are different BCR-ABL1 fusion genes that are translated into proteins that are different from each other, yet all leukemogenic, causing chronic myeloid leukemia (CML) or acute lymphoblastic leukemia. Their frequency has never been systematically investigated. In a series of 45503 newly diagnosed CML patients reported from 45 countries, it was found that the proportion of e13a2 (also known as b2a2) and of e14a2 (also known as b3a2), including the cases co-expressing e14a2 and el 3a2, was 37.9% and 62.1%, respectively. The proportion of these two transcripts was correlated with gender, e13a2 being more frequent in males (39.2%) than in females (36.2%), was correlated with age, decreasing from 39.6% in children and adolescents down to 31.6% in patients >= 80 years old, and was not constant worldwide. Other, rare transcripts were reported in 666/34561 patients (1.93%). The proportion of rare transcripts was associated with gender (2.27% in females and 1.69% in males) and with age (from 1.79% in children and adolescents up to 3.84% in patients >= 80 years old). These data show that the differences in proportion are not by chance. This is important, as the transcript type is a variable that is suspected to be of prognostic importance for response to treatment, outcome of treatment, and rate of treatment-free remission.

Published
2019

8. Pure infradiaphragmatic Hodgkin's lymphoma. Clinical features, prognostic factor and comparison with supradiaphragmatic disease

Author

Vassilakopoulos, T. P., Angelopoulou, M. K., Siakantaris, M. P., Konstantinou, N., Symeonidis, A., Karmiris, T., Repoussis, P., Roussou, P., Dimopoulos, A. M., Styliani Kokoris, Dimitriadou, E. M., Kyrtsonis, M. -C, Dimopoulou, M. N., Tsatalas, C., Kokkinis, G., Vrakidou, E., Grigoraki, V., Poziopoulos, C., Stamatellou, M., Liapis, D., Georgiou, G., Panayiotidis, P., and Pangalis, G. A.

Subjects
Treatment Outcome, Remission Induction, Humans, Prognosis, Hodgkin Disease, Survival Analysis
Abstract

Pure infradiaphragmatic Hodgkin's lymphoma (HL) is a rare disease. The prognostic impact of a purely infradiaphragmatic localization of this lymphoma is controversial. We aimed to evaluate the baseline clinicopathologic features, prognostic factors and outcome of a large series of consecutive patients with pure infradiaphragmatic HL.We analyzed 131 patients with clinical stage I/II infradiaphragmatic HL treated with ABVD or equivalent regimens with or without radiotherapy, and compared 54 of them with 444 patients with pure supradiaphragmatic disease, who were treated at the same center.Older age, clinical stage II (borderline), involvement ofor =3 sites, lymphocyte predominant histology, elevated serum beta2-microglobulin and higher International Prognostic Score were more frequent in patients with infradiaphragmatic disease than in those with supradiaphragmatic disease, while nodular sclerosis was less frequent. The complete remission rate was 100%, 97% and 82% for stages I, IIA and IIB, respectively. Only B-symptoms independently predicted for inferior failure-free survival, while inferior overall survival was independently associated with the involvement ofor =3 sites. At 10 years failure-free survival was 82+/-6% (vs. 85+/-2% for patients with supradiaphragmatic disease, p=0.45), overall survival was 74+/-8% (vs. 91+/-2%, p=0.0006), and disease-specific survival 87+/-5% (vs. 94+/-1%, p=0.04). In multivariate analysis the differences between infradiaphragmatic and supradiaphragmatic disease were obscured by older age and B-symptoms.Pure infradiaphragmatic HL presents with distinct clinicopathologic characteristics. The previously reported poorer outcome may be explained by the unfavorable profile of the patients rather than the infradiaphragmatic presentation per se. Patients with stage IIB disease should probably be classified as having advanced HL because of the unacceptable rate of primary refractory disease.

Published
2006

9. Influenza virus vaccine in B-cell chronic lymphocytic leukaemia patients

Author

Gribabis, D. A. Panayiotidis, P. Boussiotis, V. A. Hannoun, C. Pangalis, G. A.

Abstract

The clinical reaction and the immunological response to influenza virus vaccine were studied in 43 B-cell chronic lymphocytic leukaemia patients. The Vaxigrip vaccine was administered containing the antigens A/Ghizhou/54/89, A/Singapore/6/86, and B/Yamagata/16/88. The side-effects observed were minimal and well tolerated. Antibody production with titres > 1:20 on day 15 was observed at least for one antigen in 35 patients (81%). In 23 of them (63%) this response was retained on days 30 and 60. Patients with IgG levels (< 700 mg/dl) responded less well as compared to those having normal IgG levels (> 700 mg/dl).

Published
1994

14. ANALYSIS OF THE DEMOGRAPHIC, CLINICAL, LABORATORY AND TREATMENT-RELATED DATA OF ITP PATIENTS IN GREECE BASED ON THE NATIONAL ITP REGISTRY OF THE HELLENIC SOCIETY OF HAEMATOLOGY

Author

Stavroulaki, E., Tzikoulis, V., Kaparou, M., Kanellou, P., Panayiotidis, P., Tsaftaridis, P., Viniou, N., Bitsani, E., Bartzi, V., Iliakis, T., Galanopoulos, A., Kanavos, G., Hondropoulos, S., Michalis, E., Anagnostopoulos, N., Symeonidis, A., Kourakli, A., Lampropoulou, P., Megalakaki, A., Palla, A., Papaioannou, M., Kaiafa, G., Liapi, D., Vlachaki, E., Giannouli, S., Kotsianidis, I., Kyriakou, D., Protopappa, M., Eleftheria Hatzimichael, Zikos, P., Pontikoglou, C., Chalkiadakis, G., and Papadaki, H.

16. Efficacy and safety of copanlisib in patients with relapsed or refractory marginal zone lymphoma

Author

David Trevarthen, Panayiotis Panayiotidis, Barrett H. Childs, Don A. Stevens, Luigina Mollica, Florian Hiemeyer, Armando Santoro, Muhit Ozcan, George A Follows, Pier Luigi Zinzani, J. Garcia-Vargas, Arnon Nagler, Martin Dreyling, Panayiotidis P., Follows G.A., Mollica L., Nagler A., Ozcan M., Santoro A., Stevens D., Trevarthen D., Hiemeyer F., Garcia-Vargas J., Childs B.H., Zinzani P.L., and Dreyling M.

Subjects
medicine.medical_specialty, Gastroenterology, Phosphatidylinositol 3-Kinases, chemistry.chemical_compound, Refractory, Internal medicine, medicine, Humans, In patient, Adverse effect, Copanlisib, Lymphoid Neoplasia, business.industry, Quinazoline, Lymphoma, B-Cell, Marginal Zone, Hematology, medicine.disease, Lymphoma, Diarrhea, Pyrimidines, Pyrimidine, chemistry, Quinazolines, Rituximab, Marginal zone B-cell lymphoma, Neoplasm Recurrence, Local, Phosphatidylinositol 3-Kinase, medicine.symptom, business, Human, medicine.drug
Abstract

Marginal zone lymphoma (MZL) is challenging to treat, with many patients relapsing following initial treatment. We report the long-term efficacy and safety of copanlisib, a pan-class I phosphoinositide 3-kinase (PI3K) inhibitor, in the subset of 23 patients with relapsed/refractory MZL treated in the phase 2 CHRONOS-1 study (#NCT01660451, Part B; www.clinicaltrials.gov). Patients had a median of 3 prior lines of therapy, including rituximab and alkylating agents, and received IV copanlisib 60 mg on days 1, 8, and 15 of 28-day cycles for a median of 23 weeks. The objective response rate was 78.3% (18/23; 3 complete responses and 15 partial responses). The median duration of response was 17.4 months (median follow-up, 9.4 months), and median time to response was 2.1 months. Median progression-free survival was 24.1 months (median follow-up, 10.3 months), and median overall survival was not reached (median follow-up, 28.4 months). The most common all-grade treatment-emergent adverse events (TEAEs) included fatigue (52.2%, 12/23), diarrhea, and transient, infusion-related hyperglycemia (each 47.8%, 11/23). Nineteen patients (82.6%) had grade 3/4 TEAEs, most commonly transient, infusion-related hyperglycemia and hypertension (each 39.1%, 9/23). TEAEs led to dose reduction or dose interruptions /delays in 9 patients (39.1%) and 18 patients (78.3%), respectively. Patients with activated PI3K/B-cell antigen receptor signaling had improved response rates. Overall, copanlisib demonstrated strong efficacy, with a short time to objective response, improved objective response rate with longer treatment duration, durable responses, and manageable safety, in line with previous reports. These data provide rationale for long-term treatment with copanlisib in patients with relapsed/refractory MZL.

Published
2021
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17. Cytogenetic complexity in chronic lymphocytic leukemia: definitions, associations and clinical impact

Author

Blanca Espinet, M. Jose Calasanz, Marie Jarošová, Carolina Moreno, Julio Delgado, Andrea Visentin, Niki Stavroyianni, Rosa Collado, Florence Cymbalista, Helena Podgornik, Kostas Stamatopoulos, Zadie Davis, Michael Doubek, Claudia Haferlach, Fred Davi, Achilles Anagnostopoulos, Arnon P. Kater, Šárka Pospíšilová, Panayiotis Panayiotidis, Sabine Jeromin, David Oscier, Florence Nguyen-Khac, Maria Dimou, Neus Ruiz-Xivillé, Antonio Cuneo, Anna Puiggros, Panagiotis Baliakas, Theodoros Iliakis, Aliki Xochelli, Anastasia Athanasiadou, Alexander C. Leeksma, Paolo Ghia, Pau Abrisqueta, Karla Plevová, Virginie Eclache, George Papaioannou, Livio Trentin, Gian Matteo Rigolin, Michalis Iskas, Kristina Durechova, Evangelia Stalika, Fanny Baran-Marszak, Graduate School, CCA - Cancer biology and immunology, Clinical Haematology, Experimental Immunology, Uppsala University, MLL Münchner Leukämielabor GmbH / MLL Munich Leukemia Laboratory [Munich, Germany], General Hospital of Thessaloniki George Papanikolaou, IMIM-Hospital del Mar, Generalitat de Catalunya, Central European Institute of Technology [Brno] (CEITEC MU), Brno University of Technology [Brno] (BUT), Masaryk University [Brno] (MUNI), University Hospital Brno, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Royal Bournemouth Hospital, Università degli Studi di Ferrara = University of Ferrara (UniFE), Università degli Studi di Padova = University of Padua (Unipd), Centre for Research and Technology Hellas (CERTH), Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Universitat de Barcelona (UB), Hôpital Avicenne [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Vall d'Hebron University Hospital [Barcelona], National and Kapodistrian University of Athens (NKUA), Consorcio Hospital General Universitario de Valencia, Universidad de Navarra [Pamplona] (UNAV), Universitat Autònoma de Barcelona (UAB), Hospital de la Santa Creu i Sant Pau, Academic Medical Center - Academisch Medisch Centrum [Amsterdam] (AMC), University of Amsterdam [Amsterdam] (UvA), Amsterdam institute for Infection and Immunity [Amsterdam, The Netherlands] (A3I), University Medical Centre Ljubljana [Ljubljana, Slovenia] (UMCL), Universita Vita Salute San Raffaele = Vita-Salute San Raffaele University [Milan, Italie] (UniSR), Lambert, Mélanie, Baliakas, P., Jeromin, S., Iskas, M., Puiggros, A., Plevova, K., Nguyen-Khac, F., Davis, Z., Matteo Rigolin, G., Visentin, A., Xochelli, A., Delgado, J., Baran-Marszak, F., Stalika, E., Abrisqueta, P., Durechova, K., Papaioannou, G., Eclache, V., Dimou, M., Iliakis, T., Collado, R., Doubek, M., Calasanz, M. J., Ruiz-Xiville, N., Moreno, C., Jarosova, M., Leeksma, A. C., Panayiotidis, P., Podgornik, H., Cymbalista, F., Anagnostopoulos, A., Trentin, L., Stavroyianni, N., Davi, F., Ghia, P., Kater, A. P., Cuneo, A., Pospisilova, S., Espinet, B., Athanasiadou, A., Oscier, D., Haferlach, C., and Stamatopoulos, K.

Subjects
Male, Chronic lymphocytic leukemia, cytogenetics, complex karyotype, prognosis, Oncology, complex karyotype, medicine.medical_specialty, [SDV]Life Sciences [q-bio], Chronic lymphocytic leukemia, Immunology, Somatic hypermutation, Biochemistry, Somatic evolution in cancer, cytogenetics, NO, 03 medical and health sciences, 0302 clinical medicine, Internal medicine, Biomarkers, Tumor, Humans, Medicine, Survival rate, Aged, Retrospective Studies, Chromosome Aberrations, Hematology, business.industry, Cytogenetics, Cell Biology, Middle Aged, medicine.disease, Leukemia, Lymphocytic, Chronic, B-Cell, 3. Good health, Survival Rate, [SDV] Life Sciences [q-bio], Leukemia, 030220 oncology & carcinogenesis, Mutation, Chromosome abnormality, Female, Somatic Hypermutation, Immunoglobulin, prognosis, Tumor Suppressor Protein p53, business, Follow-Up Studies, 030215 immunology
Abstract

Recent evidence suggests that complex karyotype (CK) defined by the presence of =3 chromosomal aberrations (structural and/or numerical) identified by chromosome banding analysis (CBA) may be relevant for treatment decision-making in chronic lymphocytic leukemia (CLL). However, many challenges towards routine clinical application of CBA remain. In a retrospective study of 5290 patients with available CBA data, we explored both clinicobiological associations and the clinical impact of CK in CLL. We found that patients with =5 abnormalities, defined as high-CK, exhibit uniformly dismal clinical outcome, independently of clinical stage, TP53 aberrations (deletion of chromosome 17p and or TP53 mutations, TP53abs) and the expression of somatically hypermutated (M-CLL) or unmutated (U-CLL) immunoglobulin heavy variable genes (IGHV). Thus, they contrasted CK cases with 3 or 4 aberrations (low-CK and intermediate-CK, respectively) who followed aggressive disease courses only in the presence of TP53abs. At the other end of the spectrum, patients with CK and +12,+19 displayed an exceptionally indolent profile. Building upon CK, TP53abs and IGHV gene somatic hypermutation status, we propose a novel hierarchical model where patients with high-CK exhibit the worst prognosis, while M-CLL lacking CK or TP53abs as well as CK with +12,+19 show the longest overall survival. In conclusion, CK should not be axiomatically considered unfavorable in CLL, representing a heterogeneous group with variable clinical behavior. High-CK with =5 chromosomal aberrations emerges as prognostically adverse, independently of other biomarkers. Prospective clinical validation is warranted before finally incorporating high-CK in risk stratification of CLL.

Published
2019
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