By G. Stenman, J. Bullerdiek, S. Bartnitzke, P. Sahlin, E. Röijer, J. Mark (auth.), Prof. Dr. J. Bullerdiek, Dr. S. Bartnitzke (eds.)
Researchers serious about the cytogenetics and molecular genetics of human tumors will welcome this accomplished review of the kind of aberrations that chromosome 12 offers in human good tumors. The authors examine the consequences for a cytogenetic subtyping of the tumors concerned and techniques for deciding upon the molecular adjustments which underlie the karyotypic adjustments.
The aberrations of chromosome 12 which the booklet offers with are very common chromosomal changes in human tumors occuring in common benign mesenchymal tumors, equivalent to uterine leiomyomas and lipomas, and in tumors of epithelial starting place, comparable to pleomorphic adenomas of the salivary glands.
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Extra info for Chromosome 12 Aberrations in Human Solid Tumors: Cytogenetics and Molecular Genetics
Report of fourty cases. Cancer Genet Cytogenet 53:247-256 Vanni R, Van Roy N, Lecca U, SpeIeman F (1992) Uterine leiomyoma cytogenetics. IH. Interphase cytogenetic analysis of karyotypically normal uterine leiomyomas excJudes possibility of undetected trisomy 12. Cancer Genet Cytogenet 62:40-42 Zaloudek CJ, Norris HJ (1987) Mesenchymal turmors of the uterus. In: Kurman RJ (ed) Blaustein's pathology of the female tract, 3rd edn. Springer, Berlin Heidelberg New York Lipoma Cytogenetics N. Mandahl 1 Introduction The occurrence of nonrandom clonal cytogenetic abnormalities in tumor cells has been unequivocally demonstrated (Heim and Mitelman 1987; Sandberg 1990).
Before the mid 1980s, a substantial proportion of cytogenetic data was obtained from direct preparations and established celilines. Chromosome preparations made directly from fresh tumor tissue yield frequently condensed chromosomes with suboptimal banding patterns and require tumor tissue with a reasonably high mitotic activity. Hence, many slowly growing benign tumors, for example lipomas, are not suitable for direct preparations. During the latest decade, improved methods for cytogenetic analysis of solid tumors have been developed.
The chromosome number in these tumors ranged from 42 to 51, but the majority of cases were hyperdiploid. Rings and markers were the sole changes in at least one clone in the majority of cases, but in eight tumors different, additional, numerical and/or structural changes were found. The origin of the ring and marker chromosomes has not been possible to identify. Some of the tumors with these aberrations also showed multiple telomeric associations and a relatively high frequency of nonclonal aberrations.