ABSTRACT
A translocation (6;11)(q26-27;q23) was detected in four male patients diagnosed with acute T-cell lymphoblastic leukemia and acute myelomonocytic and monocytic leukemias. This acquired reciprocal translocation appears to be associated with acute leukemias in young men who present clinically with localized infection, and a moderate leukocytosis. There was a poor response to antileukemic chemotherapy and a short overall survival. Aggressive treatment strategies should be considered in the treatment of these high-risk leukemias.
Subject(s)
Chromosomes, Human, Pair 11 , Chromosomes, Human, Pair 6 , Leukemia, Monocytic, Acute/genetics , Leukemia, Myelomonocytic, Acute/genetics , Leukemia-Lymphoma, Adult T-Cell/genetics , Translocation, Genetic/genetics , Adolescent , Adult , Humans , Karyotyping , Male , Middle Aged , PrognosisABSTRACT
Assessment of cytogenetic patterns associated with chronic myelogenous leukemia (CML) suggests that genetic events at band q34 of chromosome nine are critical in the conversion of benign to malignant hematopoiesis. A break at this band is identified in almost all cases of Philadelphia chromosome (Ph1) positive CML, is also noted in some cases of Ph1 negative CML and cannot be excluded in the remaining cases. The human cellular homolog of the Abelson retrovirus oncogene (c-abl) is situated at band 9q34 and is translocated with the genetic sequences distal to the break point at this site in Ph1 positive disease. This oncogene has been shown experimentally to transform pre-B cells and it is expressed in primitive cells of the granulocytic series which are involved in CML. Although the break in CML chromosomes at 9q34 and the location of c-abl at 9q34 could be unrelated, it seems more likely that the two genetic events are associated with evolution of malignant hematopoiesis of man.
Subject(s)
Chromosomes, Human, 6-12 and X , Leukemia, Myeloid/genetics , Abelson murine leukemia virus/genetics , Chromosome Aberrations/genetics , Chromosome Disorders , Chromosomes, Human, 21-22 and Y , Humans , Karyotyping , Translocation, GeneticABSTRACT
The cytogenetic status of bone marrow stromal elements obtained from six patients with Ph1-positive chronic myelogenous leukemia (CML), two in blast crisis, was studied in vitro utilizing the potential of marrow to form surface-adherent colonies morphologically compatible with mesenchymal elements. We demonstrated the absence of both the marker chromosome and other chromosomal abnormalities in all the fibroblastic colonies studied, indicating that the progenitors of such colonies (plaque-forming units in culture, PFU-C) are not closely related to hematopoietic elements including macrophages. This supports previous reports suggesting that the stromal elements in myelofibrosis associated with CML are not derived from the primary Ph1-positive malignant clone but represent a stromal reactive component of benign or independent malignant potential.