Chromosomes in adipose tissue tumors. An evaluation of 75 cases (original) (raw)
Related papers
Cancer Genetics and Cytogenetics, 1986
Detailed clinical histories and cytogenetic investigations using shart-term cultures are reported in three typical benign lipomas. Although a diploid (normal) karyotype was observed in two cases, a reciprocal chromosome translocation t(3;12)(q28;q14) was found in the third case, which was briefly reported previously. These data are discussed in light af a lipoma with similar karyotypic changes reported by Heim et al. and a similar translocation observed by us in malignant myxoid liposarcomas. The nanrandom involvement of segment 12q13-q14 in benign and malignant lipomatous tumors suggest a common basis for at least one of the possible multiple steps in the genesis of neoplastic processes.
International Journal of Cancer, 1996
Ordinary lipomas are cytogenetically characterized by a variety of balanced rearrangements involving chromosome segment I2q 13-15, and atypical lipomatous tumors (ALT) by supernumerary ring chromosomes or giant markers known to contain amplified I2q sequences. In a series of 228 cytogenetically analyzed and histopathologically reexamined ordinary lipomas and ALT, 10 tumors showed unbalanced chromosome-I2 aberrations. All 4 tumors with loss of segments from I2q were classified as ordinary lipomas, whereas 5 of the 6 tumors showing gain of I2q material were diagnosed as ALT.
Nonrandom Secondary Chromosome-Aberrations in Liposarcomas with T(12, 16)
International Journal of Oncology, 1994
Ten liposarcomas were analyzed cytogenetically after short-term culturing. Eight tumors had a t(12; 16) (ql3;pll) and two tumors had complex translocations involving chromosomes 7, 12, and 16 and 2, 9, 12, 16 and 20, respectively. Among the secondary aberrations seen in five tumors, +8 was found in two tumors and i(7)(ql0) in four tumors. Trisomy 8 has previously been described as a nonrandom secondary aberration in myxoid liposarcoma, but i(7q) has only been reported in a single case before. All recurrent chromosome aberrations reported in liposarcomas with recombination between 12ql3 and 16pll (42 cases) were surveyed and compared with their frequencies in liposarcomas without this recombination (33 cases). Trisomy 5 and 8 were found in both tumor groups, whereas +19, t(3;15)(p23;ql5), del(6)(q21), i(7q), and rearrangements of lpl 1 and 2q35 were found exclusively in tumors with 12ql3 and 16pll aberrations.
New discriminative chromosomal marker in adipose tissue tumors
Cancer Genetics and Cytogenetics, 1994
Specific chromosome abnormalities characterize benign and malignant adipose tissue tumors and are of great diagnostic and clinical importance. Lipoblastoma is a rare benign adipose tumor that mimics myxoid liposarcoma histologically. Although only a few lipablastomas have been investigated cytogenetically, it is increasingly clear that these adipose tissue tumor generally show rearrangements of Sq11-q13 region but lack the t(12;16
Deletion 6q in three cases of mixed type liposarcoma in addition to t(12;16)(q13;p11
Cancer Genetics and Cytogenetics, 1995
We report the cytogenetic findings in three mixed liposarcoma following short-term cultures. During the course ofcytogenetic investigation of various types ofliposarcomas, we observed an interstitial deletion of the long arm of chromosome 6 together with the translocation (12;16) (q13;p11) in three tumors. Translocation (12; is associated with myxoid and mixed (myxoid/round cell) liposarcomas, although deletion of chromosome 6 has been observed in only a few of these tumors. Our findings suggest that del , as an additional change in myxoid liposarcoma, is probably related to tumor progression.
Genes, Chromosomes and Cancer, 2007
Conventional lipomas harbor karyotypic changes that could be subdivided into four, usually mutually exclusive, categories: rearrangement, in particular through translocations, of chromosome bands 12q13-15, resulting in deregulation of the HMGA2 gene, loss of material from or rearrangement of chromosome 13, supernumerary ring or giant marker chromosomes, and aberrations of chromosome band 6p21. In the present study, 272 conventional lipomas, two-thirds of them deep-seated, with acquired clonal chromosome changes were assessed with regard to karyotypic and clinical features. A nonrandom distribution of breakpoints and imbalances could be confirmed, with 83% of the cases harboring one or more of the previously known cytogenetic hallmarks. Correlation with clinical features revealed that lipomas with rings/giant markers were larger, occurred in older patients, were more often deep-seated, and seemed to have an increased tendency to recur locally, compared with tumors with other chromosome aberrations. The possible involvement of the HMGA2 gene in cases that did not show any of the characteristic cytogenetic changes was further evaluated by locus-specific metaphase fluorescence in situ hybridization (FISH) and RT-PCR, revealing infrequent cryptic disruption of the gene but abundant expression of full length or truncated transcripts. By FISH, we could also show that breakpoints in bands 10q22-23 do not affect the MYST4 gene, whereas breakpoints in 6p21 or 8q11-12 occasionally target the HMGA1 or PLAG1 genes, respectively, also in conventional lipomas. This article contains Supplementary
Genes, Chromosomes and Cancer, 2009
Ring chromosomes are cytogenetic hallmarks of genomic amplification in several bone and soft tissue tumors, in particular atypical lipomatous tumors (ALT). In ALT, the ring chromosomes invariably contain amplified material from the central part of the long arm of chromosome 12, mainly 12q12!15, but often also segments from other chromosomes are involved. Previous studies have shown that one of the recurrent amplicons in ALT, located in 12q13.3-14.1 and harboring the candidate target genes TSPAN31 and CDK4, often has a sharp centromeric border. To characterize this breakpoint region in more detail, 12 cases of ALT with ring chromosomes were analyzed by array comparative genomic hybridization and fluorescence in situ hybridization. In the seven cases showing a sharply delineated amplicon in 12q13.3-14.1, the breakpoint region was further investigated by real time quantitative polymerase chain reaction and Vectorette PCR. The breakpoints clustered to a 146-kb region containing 11 genes. Whereas there was no indication that the breakpoints gave rise to fusion genes, in silico analysis revealed that the breakpoint region was enriched for repeated elements that could be important for ring chromosome formation in ALT.