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      New Complex Chromosomal Translocation in Chronic Myeloid Leukaemia: t(9;18;22)(q34;p11;q11)

      case-report

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          Abstract

          A Chronic myeloid leukaemia (CML) case with a new complex t(9;18;22)(q34;p11;q11) of a 29-year-old man is being reported. For the first time, this translocation has been characterized by karyotype complemented with fluorescence in situ hybridization (FISH). In CML, the complex and standard translocations have the same prognosis. The patient was treated with standard initial therapy based on hydroxyurea before he died due to heart failure four months later. Our finding indicates the importance of combined cytogenetic analysis for diagnosis and guidance of treatment in clinical diagnosis of CML.

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          Letter: A new consistent chromosomal abnormality in chronic myelogenous leukaemia identified by quinacrine fluorescence and Giemsa staining.

          J D Rowley (1973)
          Article 0 comments Cited 343 times – based on 0 reviews     Review now
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            On the genesis and prognosis of variant translocations in chronic myeloid leukemia.

            Peter Benn, Zihai Li, Shou-Min Fang … (2007)
            Variant translocations involving 9q, 22q, and at least one additional genomic locus occur in 5-10% of patients with chronic myeloid leukemia (CML). The mechanisms for the formation of these variant translocations are not fully characterized. Studies on the prognosis of these variant translocations revealed conflicting results. In addition, deletions in the derivative chromosome 9 are reportedly more frequent among variant translocation cases. We analyzed cytogenetic and FISH data from 22 CML patients with variant translocations tested at our laboratory. Deletions were observed in 6 of the 14 cases with FISH data available (43%), consistent with the literature and higher than in typical translocation cases (12-15%). Sequential changes of 9q deletions are possible and could be acquired as the disease progresses in addition to simultaneous formation of the Philadelphia chromosome with the deletion. Variant translocation CML patients with a deletion showed a worse cytogenetic response 1 year after therapy than those without a deletion (P < 0.05). Variant translocations may be formed by either a one-step or a two-step mechanism. Proper assessment of the prognostic significance of variant translocations requires better categorization of these translocations based on their mechanisms of genesis and the deletion status.
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              The cytogenetic scenario of chronic myeloid leukemia.

              F Mitelman (1992)
              The Philadelphia chromosome (Ph), i.e., the reciprocal translocation t(9;22)(q34;q11), is found with great specificity in bone marrow cells from patients with chronic myeloid leukemia (CML). Variant Ph-producing translocations, seen in 5-10% of all patients, are all complex and involve the same molecular rearrangement as the regular t(9;22). Patients with classic and variant Ph-producing translocations are clinically and hematologically identical, and as a group differ from Ph-negative CML patients. In all patient groups, the occurrence of additional chromosome changes is an ominous sign indicating that disease progression is imminent. The chromosome changes occurring in excess of the Ph in CML are clearly nonrandom and two pathways of cytogenetic evolution may be distinguished. Major route changes comprise trisomy 8, i(17q), trisomy 19, and an extra Ph; totally, 71% of Ph-positive CML patients have at least one of these four major route changes. Six minor route changes, including five numerical abnormalities (-7, -17, +17, +21, and -Y) but also one structural aberration, t(3;21) (q26;q22), have been identified. At least one of these changes is found in 15% of all Ph-positive CML cases. Altogether, the four major route aberrations and the six minor route changes are present as part of the clonal evolution in 86% of CML with cytogenetic abnormalities in addition to the Ph chromosome.
              Article 0 comments Cited 21 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Biomed Biotechnol
                Journal ID (publisher-id): JBB
                Title: Journal of Biomedicine and Biotechnology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1110-7243
                ISSN (Electronic): 1110-7251
                Publication date (Print): 2007
                Publication date (Electronic): 26 December 2007
                Volume: 2007
                Electronic Location Identifier: 92385
                Affiliations
                1Laboratoire de Cytogénétique, Institut Pasteur du Maroc, Casablanca 20100, Morocco
                2Neurosurgery and Neurooncology Section, Surgery Department, Faculty of medicine and health science, University of Shebrooke, Sherbrooke, PQ, Canada J1K2R1
                3Laboratoire d'Hématologie-Pr RAPHAEL, Cytogénétique, Pav BROCA - 4ème étage, 78 rue du Général Leclerc, 94275 Le Kremlin-Bicetre , France
                Author notes
                *Abdeljabar El Andaloussi: chromo8@ 123456hotmail.com

                Recommended by Hatem El Shanti

                Article
                DOI: 10.1155/2007/92385
                PMC ID: 2219519
                PubMed ID: 18273416
                SO-VID: fe3713ca-0366-4c95-9300-d42c51dcc614
                Copyright © Copyright © 2007 A. El Andaloussi and C. Bilhou-Nabera.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 16 August 2007
                Date accepted : 23 October 2007
                Categories
                Subject: Case Report

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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