NONRANDOM PATTERN OF TELOMERIC ASSOCIATIONS IN ATYPICAL LIPOMATOUS TUMORS WITH RING AND GIANT MARKER CHROMOSOMES

Citation
N. Mandahl et al., NONRANDOM PATTERN OF TELOMERIC ASSOCIATIONS IN ATYPICAL LIPOMATOUS TUMORS WITH RING AND GIANT MARKER CHROMOSOMES, Cancer genetics and cytogenetics, 103(1), 1998, pp. 25-34
Citations number
56
Categorie Soggetti
Oncology,"Genetics & Heredity
ISSN journal
01654608
Volume
103
Issue
1
Year of publication
1998
Pages
25 - 34
Database
ISI
SICI code
0165-4608(1998)103:1<25:NPOTAI>2.0.ZU;2-L
Abstract
Atypical lipomatous tumors (ALTs) are cytogenetically characterized by supernumerary ring and giant marker chromosomes. Another common findi ng in ALT is that the tumor cells are cytogenetically heterogeneous wi th a variety of mostly nonclonal numerical and structural chromosome a berrations, including telomeric associations. In a series of 48 cytoge netically investigated ALTs, all chromosomal aberrations, clonal as we ll as nonclonal, were registered. Clonal ring chromosomes were present in 47 cases and giant markers in 11 cases. In 7 cases, 12 clonal telo meric associations were found and 37 cases showed nonclonal associatio ns involving 344 identified telomeres. The telomere associations were nonrandomly distributed, with the telomeres of 11p, 20p, 20q, 9q, 15p, 19q, and 22q being most frequently (8.7-4.1% of all associations) inv olved; only Xp and Xq were never affected. The pattern of telomeric as sociations in ALT was compared with literature data on 47 giant cell t umors (880 telomeres), previously reported to show a nonrandom distrib ution of associations, and 36 sporadic cases of a variety of other hum an neoplasms (583 telomeres). The analysis indicated that the telomere s of 11p, 19q, and 20q are preferentially involved in associations in several tumor types. Among other structural aberrations in the ALT ser ies, 221 nonclonal and 52 clonal breakpoints were identified, as well as 342 nonclonal and 14 clonal numerical aberrations. The combined dat a suggest that telomeric associations may predispose to acquired chrom osome aberrations in neoplasia. (C) Elsevier Science Inc., 1998.