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Clustering of aberrations to specific chromosomes in human neoplasms

Identifieur interne : 000D18 ( Main/Exploration ); précédent : 000D17; suivant : 000D19

Clustering of aberrations to specific chromosomes in human neoplasms

Auteurs : Felix Mitelman [Suède] ; Göran Levan [Suède]

Source :

RBID : ISTEX:6EECA21CC39A6736BA40B083F8B6AB58932D66B7

English descriptors

Abstract

This survey of chromosomal aberrations in human neoplasms comprises 1,871 cases distributed on 15 groups of malignant disease, viz. 4 groups of myeloproliferative disorders with 1,328 cases, 5 groups of lymphoproliferative disorders with 369 cases and 6 groups of solid tumors with 174 cases. The material is presented in 17 tables, in which the variation of each chromosome is listed separately for each geographic region. In the discussion part a number of special problems are looked into. The difference in variation between the individual chromosomes was highly signifcant statistically. Within each tumor, all chromosomes which exceeded the average variation with more than 1 standard deviation were considered selectively involved. In all neoplasms taken together, the chromosomes selectively involved clustered to 15 of the 24 human chromosome types. Other topics taken up for discussion were the following: possible differences in chromosome variation between geographic regions; the specificity of certain marker chromosomes; the hypothesis of 2 essentially different kinds of chromosome aberration in cancer. The phenomena of genic amplification and recurrent translocation often found in cancer require the assumption of unorthodox cytogenetic mechanisms. One main conclusion of the paper is that the aberrations of the selectively involved chromosomes influence cancer development because of the genes they carry.

Url:
DOI: 10.1111/j.1601-5223.1981.tb01331.x


Affiliations:


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Le document en format XML

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<term>Acta</term>
<term>Alimena</term>
<term>Berghe</term>
<term>Cancer genet</term>
<term>Causation</term>
<term>Chromosomal</term>
<term>Chromosomal aberrations</term>
<term>Chromosome</term>
<term>Chromosome aberrations</term>
<term>Chronic myelocytic leukemia</term>
<term>Chronic myeloid leukemia</term>
<term>Comm</term>
<term>Complex translocations</term>
<term>Cytogenet</term>
<term>Cytogenetic</term>
<term>Deletion</term>
<term>Different chromosome types</term>
<term>Engl</term>
<term>Fukuhara</term>
<term>Gahrton</term>
<term>Genet</term>
<term>Haematol</term>
<term>Hematol</term>
<term>Hereditas</term>
<term>Hossfeld</term>
<term>Human cancer</term>
<term>Human neoplasms</term>
<term>Kakati</term>
<term>Karyotype</term>
<term>Lable</term>
<term>Lancet</term>
<term>Lawler</term>
<term>Leukaemia</term>
<term>Leukemia</term>
<term>Levan</term>
<term>Lymphoma</term>
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<term>Myeloproliferative</term>
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<term>Rowley</term>
<term>Sakurai</term>
<term>Sandberg</term>
<term>Scand</term>
<term>Tanzer</term>
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<div type="abstract" xml:lang="en">This survey of chromosomal aberrations in human neoplasms comprises 1,871 cases distributed on 15 groups of malignant disease, viz. 4 groups of myeloproliferative disorders with 1,328 cases, 5 groups of lymphoproliferative disorders with 369 cases and 6 groups of solid tumors with 174 cases. The material is presented in 17 tables, in which the variation of each chromosome is listed separately for each geographic region. In the discussion part a number of special problems are looked into. The difference in variation between the individual chromosomes was highly signifcant statistically. Within each tumor, all chromosomes which exceeded the average variation with more than 1 standard deviation were considered selectively involved. In all neoplasms taken together, the chromosomes selectively involved clustered to 15 of the 24 human chromosome types. Other topics taken up for discussion were the following: possible differences in chromosome variation between geographic regions; the specificity of certain marker chromosomes; the hypothesis of 2 essentially different kinds of chromosome aberration in cancer. The phenomena of genic amplification and recurrent translocation often found in cancer require the assumption of unorthodox cytogenetic mechanisms. One main conclusion of the paper is that the aberrations of the selectively involved chromosomes influence cancer development because of the genes they carry.</div>
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