Abnormalities of Chromosomes 8, 11, 14, and X in T-Prolymphocytic Leukemia Studied by Fluorescence In Situ Hybridization

Abnormalities of Chromosomes 8, 11, 14, and X in T-Prolymphocytic Leukemia Studied by Fluorescence In Situ Hybridization

Twenty-one patients with T-prolymphocytic leukemia (T-PLL) were studied by FISH to characterize abnormalities of chromosomes 8, 11, 14, and X. A higher percentage of abnormalities of these chromosomes was detected by FISH than by cytogenetics. Seventy-one percent had inv(14) (q11q32)/t(14;14)(q11;q3...

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Bibliographic Details
Published in:Cancer genetics and cytogenetics Vol. 103; no. 2; pp. 110 - 116
Main Authors: Maljaei, Seyed Hoda, Brito-Babapulle, Vasantha, Hiorns, Lynne R, Catovsky, Daniel
Format: Journal Article
Language:English
Published: New York, NY Elsevier Inc 01-06-1998
Elsevier Science
Subjects:
Adult
Aged
Aged, 80 and over
Azure Stains - metabolism
Biological and medical sciences
Centromere - genetics
Chromosome Aberrations - genetics
Chromosome Banding
Chromosome Disorders
Chromosomes, Human, Pair 11 - genetics
Chromosomes, Human, Pair 14 - genetics
Chromosomes, Human, Pair 8 - genetics
Female
Genes, myc
Hematologic and hematopoietic diseases
Humans
In Situ Hybridization, Fluorescence
Karyotyping
Leukemia, Prolymphocytic - genetics
Leukemia, T-Cell - genetics
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Male
Medical sciences
Middle Aged
X Chromosome - genetics
Chromosomal aberration
Human
Sporadic
In situ
Fluorescence
Malignant hemopathy
Hybridization
Chronic
Lymphoproliferative syndrome
Chromosome 8
T-Lymphocyte
Chromosome 11
Cytogenetics
Chromosome 14
X-Chromosome
Molecular biology
Prolymphocytic leukemia
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Summary:Twenty-one patients with T-prolymphocytic leukemia (T-PLL) were studied by FISH to characterize abnormalities of chromosomes 8, 11, 14, and X. A higher percentage of abnormalities of these chromosomes was detected by FISH than by cytogenetics. Seventy-one percent had inv(14) (q11q32)/t(14;14)(q11;q32). Four patients had abnormalities involving Xq28 (MTCP-1 locus) resulting from t(X;14)(q28;q11) or t(X;7)(q28;q35). These abnormalities have also been described in persistent expanding pre-malignant T-cell clones in patients with ataxia telangiectasia (AT). We have previously reported that in T-PLL and AT developing T-cell leukemia, the above abnormalities occur with additional abnormalities, mainly trisomy for 8q resulting predominantly from an i(8)(q10) and an increased expression of MYC. In this series, 81% of cases had chromosome 8 abnormalities including i(8)(q10)[43%]/t(8;8)(p12;q11)[14%],+8[14%], and 8p+[14%]. The use of probes for MYC (8q24) and chromosome 8 centromere on metaphase chromosomes revealed that cases with i(8)(q10) were dicentric and t(8;8) monocentric. These abnormalities are not only associated with increase in dosage of 8q and the MYC gene, but also involved 8p. 8p is known to have several suppressor genes associated with solid tumors. Our findings suggest that the possible loss of a tumor suppressor gene plus the increased dosage of the q arm and/or the high expression of TCL-1/MTCP-1, which results from inv(14)/t(14;14), allows the malignant phenotype to emerge.
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ISSN:0165-4608
1873-4456
DOI:10.1016/S0165-4608(97)00410-X