Integration of amplified BCR/ABL fusion genes into the short arm of chromosome 17 as a novel mechanism of disease progression in chronic myeloid leukemia

Medientyp: E-Artikel
Titel: Integration of amplified BCR/ABL fusion genes into the short arm of chromosome 17 as a novel mechanism of disease progression in chronic myeloid leukemia
Beteiligte: Metzke‐Heidemann, Simone; Harder, Lana; Gesk, Stefan; Schoch, Robert; Jenisch, Stefan; Grote, Werner; Siebert, Reiner; Schlegelberger, Brigitte
Erschienen: Wiley, 2001
Erschienen in: Genes, Chromosomes and Cancer
Sprache: Englisch
DOI: 10.1002/gcc.1112
ISSN: 1045-2257; 1098-2264
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Beschreibung: <jats:title>Abstract</jats:title><jats:p>We describe the cases of two patients with Philadelphia chromosome–positive chronic myeloid leukemia (CML), in whom the extramedullary blastic phase developed during disease progression. The similar clinical presentations of these patients was accompanied by gain of identical secondary chromosome abnormalities, that is, monosomies 9, 14, and 22, and by a clustered amplification of the <jats:italic>BCR/ABL</jats:italic> fusion gene. The additional copies of the <jats:italic>BCR/ABL</jats:italic> fusion gene were integrated into the short arm of structurally abnormal chromosomes 17 in both patients. The conformity of these genetic features in two patients with a rare disease manifestation leads us to the assumption that either the clustered amplification of the <jats:italic>BCR/ABL</jats:italic> fusion gene or the integration of this cluster into the short arm of chromosome 17 or both are associated with extramedullar disease progression in CML. Furthermore, the insertion of amplified <jats:italic>BCR/ABL</jats:italic> fusion genes into structurally abnormal chromosomes provides a novel mechanism of disease progression in <jats:italic>BCR/ABL</jats:italic>‐positive CML. © 2001 Wiley‐Liss, Inc.</jats:p>

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