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Charrin, C and Magaud, JP and Sebban, C and Fiere, D and Dastugue, N and HuguetRigal, F and Attal, M and Sie, P and Lai, JL and Jouet, JP and Simon, M and Zandecki, M and Gregoire, MJ and Witz, F and Witz, B and Barin, C and Moraine, C and Mugneret, F and Favre, B and Raynaud, S and Baudoin, F and Gratecos, N and Thyss, A and Ayraud, N and Lafage, M and Arnoulet, C and Sainty, D and Mozziconacci, MJ and Stoppa, AM and Bernard, P and Reiffers, J and VandenAkker, J and Perrot, C and Bertheas, MF and Vasselon, C and Calmard, P and Guyotat, D and Talmant, P and Uettwiller, F and Maloisel, F and Ruch, JV and Oberling, F and Weh, HJ and VerellenDumoulin, C and Libouton, JM and Delannoy, A and Ferrant, A and Michaux, JL and Desangles, F and Riviere, D and PluchonRiviere, E and Berthou, C and Ped;
Cytogenetic abnormalities in adult acute lymphoblastic leukemia: Correlations with hematologic findings and outcome. A collaborative study of the Groupe Francais de Cytogenetique Hematologique
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Cytogenetic analyses performed at diagnosis on 443 adult patients with acute lymphoblastic leukemia (ALL) were reviewed by the Groupe Francais de Cytogenetique Hematologique, correlated with hematologic data, and compared with findings for childhood ALL. This study showed that the same recurrent abnormalities as those reported in childhood ALL are found in adults, and it determined their frequencies and distribution according to age. Hyperdiploidy greater than 50 chromosomes with a standard pattern of chromosome gains had a lower frequency (7\%) than in children, and was associated with the Philadelphia chromosome (Ph) in 11 of 30 cases. Tetraploidy (2\%) and triploidy (3\%) were more frequent than that in childhood ALL. Hypodiploidy 30-39 chromosomes (2\%), characterized by a specific pattern of chromosome losses, might be related to the triploid group that evoked a duplication of the 30-39 hypodiploidy. Both groups shared similar hematologic features. Ph(+) ALL (29\%) peaked in the 40- to 50-year-old age range (49\%) and showed a high frequency of myeloid antigens (24\%). ALL with t(1;19) (3\%) occurred in young adults (median age, 22 years). In T-cell ALL (T-ALL), frequencies of 14q11 breakpoints (26\%) and of t(10;14)(q24;q11) (14\%) were higher than those in childhood ALL. New recurrent changes were identified, ie, monosomies 7 present in Ph-ALL (17\%) and also in other ALL (8\%) and two new recurrent translocations, t(1;11)(p34;p11) in T-ALL and t(1;7)(q11-21;q35-36) in Ph(+) ALL. The ploidy groups with a favorable prognostic impact were hyperdiploidy greater than 50 without Ph chromosome (median event-free survival [EFS], 46 months) and tetraploidy (median EFS, 46 months). The recurrent abnormalities associated with better response to therapy were also significantly correlated to T-cell lineage. Among them, t(10;14)(q24;q11) (median EFS, 46 months) conferred the best prognostic impact (3-year EFS, 75\%). Hypodiploidy 30-39 chromosomes and the related triploidy were associated with poor outcome. All Ph-ALL had short EFS (median EFS, 5 months), and no additional change affected this prognostic impact. Most patients with t(1;19) failed therapy within 1 year. Patients with 11q23 changes not because of t(4;11) had a poor outcome, although they did not present the high-risk factors found in t(4;11). (C) 1996 by The American Society of Hematology.
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