Two‐color FISH characterization of i(1q) and der(1;16) in human breast cancer cells

Kokalj-Vokac, Nadja; Alemeida, Anna; Gerbault‐Seureau, Michèle; Malfoy, Bernard; Dutrillaux, Bernard

doi:10.1002/gcc.2870070103

Cited by 53 publications

(33 citation statements)

References 13 publications

(10 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This reproducibility suggests an underlying mechanism in which regions containing highly repetitive DNA sequences are strategically implicated. An analogous situation is perhaps found in breast cancer, where a reproducible translocation affecting chromosomes 1 and 16 has been observed (Kokalj-Vokac et al, 1993). The breakpoints were found to span the heterochromatic regions, with the significant event considered to be the ensuing imbalance (KokaljVokac et al, 1993).…”

Section: Discussionmentioning

confidence: 82%

Association of specific chromosome alterations with tumour phenotype in posterior uveal melanoma

Sisley

Parsons

Garnham³

et al. 2000

Br J Cancer

View full text Add to dashboard Cite

Posterior uveal melanomas have recurrent alterations of chromosomes 1, 3, 6 and 8. In particular, changes of chromosomes 3 and 8 occur in association, appear to characterize those tumours with a ciliary body component, and have been shown to be of prognostic significance. The relevance of other chromosome alterations is less certain. We have performed cytogenetic analysis on 42 previously untreated primary posterior uveal melanomas. Of interest was the observation that as tumour size increased the involvement of specific chromosome changes, and the amount of chromosome abnormalities likewise increased. Loss, or partial deletions, of the short arm of chromosome 1 were found to associate with larger ciliary body melanomas; typically, loss of the short arm resulted from unbalanced translocations, the partners of which varied. Trisomy of chromosome 21 occurred more often in ciliary body melanomas, whilst rearrangements of chromosomes 6 and 11 were primarily related to choroidal melanomas. Our results imply that alterations of chromosome 1 are important in the progression of some uveal melanomas, and that other chromosome abnormalities, besides those of chromosomes 3 and 8, are associated with ocular tumours of particular locations. © 2000 Cancer Research Campaign

show abstract

Section: Discussionmentioning

confidence: 82%

Association of specific chromosome alterations with tumour phenotype in posterior uveal melanoma

Sisley

Parsons

Garnham³

et al. 2000

Br J Cancer

View full text Add to dashboard Cite

show abstract

“…According to cytogenetic studies, these chromosome imbalances are thought to occur as a consequence of breakage and recombination of alfa and beta satellite DNA located at chromosome regions 1q12, 16cen and 16q11.2. 17 These repetitive DNA sequences are prone to anomalous recombination and fusion because of a high homology degree. As they are not transcribed, it is rather difficult to speculate about specific genes affected by these chromosome changes.…”

Section: Discussionmentioning

confidence: 99%

Simultaneous chromosome 1q gain and 16q loss is associated with steroid receptor presence and low proliferation in breast carcinoma

et al. 2004

View full text Add to dashboard Cite

We applied comparative genomic hybridization (CGH) to 46 breast carcinoma samples, collected from 1993 to 1995, in order to detect chromosome 1q gains and 16q losses and to define whether samples showing both these alterations had distinct biopathologic features and different clinical outcome. A total of 22 samples (48%) had simultaneous chromosome 1q gain and 16q loss, which was always associated with other genetic changes. In total, 23 samples had various chromosome imbalances (including chromosome 1q gain independent of chromosome 16q loss and vice versa) and one sample did not show detectable alterations. Samples having chromosome 1q gain/16q loss were compared to the other samples with regard to neoplasm size, lymph-node status, histologic and nuclear grade, estrogen and progesterone receptor presence, Ki-67, pRB, Cyclin D1, Cyclin A, p53, p21 and p27 expression as detected by immunohistochemistry. The samples showing chromosome 1q gain/16q loss had high steroid hormone receptor expression (P ¼ 0.02), low cell growth fraction (Ki-67, P ¼ 0.03) and high p27 expression (Po0.001). No statistical correlation with disease-free survival and overall survival or response to hormonal therapy was found. We conclude that simultaneous chromosome 1q gain/16q loss is a frequent event in invasive breast cancer, which occurs in a subset of both intermediateand high-grade breast carcinomas. Although the final chromosome 1q and 16q imbalances might have originated from different chromosome alterations in low-and high-grade samples, the gene-dosage effect might be important in conferring peculiar biopathologic characteristics to this subset of samples. The cytogenetic and molecular mechanisms underlying these chromosome changes deserve further investigations.

show abstract

“…Rearrangements of 1q with similar breakpoints have been suggested in a number of human cancers, including multiple myeloma, breast cancer, and Wilms' tumor. [26][27][28][29] Recent studies of breast cancer and Wilms' tumor postulated that common heterochromatin breakage on chromosome 1 was attributable, as noted above, to hypomethylation, which led to chromatin decondensation, juxtacentromeric fragility, and finally chromosome breakage. 30,31 These events could have served as precursors to subsequent whole chromosome 1q translocations.…”

Section: Resultsmentioning

confidence: 99%

A Comprehensive Karyotypic Study on Human Hepatocellular Carcinoma by Spectral Karyotyping

Wong

2000

Hepatology

View full text Add to dashboard Cite

The current paucity of cytogenetic information on hepatocellular carcinoma (HCC) reflects the difficulties in culturing hepatocytes in vitro. Here, we report on the successful culture of 15 HCC cases. Chromosome aneuploidy ranging from a near-diploid to hyperhexaploid karyotype was found, but their complete karyotypic interpretations were hampered by the presence of many unidentifiable rearrangements. Spectral karyotyping (SKY) was used to elucidate structural changes in these HCC samples and 3 liver cancer cell lines (PLC/PRF/5, Hep3B, and HepG2). Frequent structural abnormalities were found on chromosomes 1 (13 of 15 cases; 3 of 3 cell lines), 8 (10 of 15 cases; 2 of 3 cell lines), 17 (9 of 15 cases; 3 of 3 cell lines), and 19 (9 of 15 cases; 1 of 3 cell lines). In particular, the chromosome regions 1p13-q21, 8p12-q21, 17p11-q12, 17q22, and 19p10-q13.1 were involved in multiple rearrangements. SKY analysis also suggested several previously undescribed breakpoints in HCC. These breakpoints, predominantly pericentromeric, clustered around the chromosome bands 2q33-q34, 3p13-q12, 4p14-q12, 5p10-q11, 7p12-q11, 10q10-q11, 11q10, 11q13-q21, 12q10-q13, 12q22-q23, 13q10-q14, 15q10, 16q10-q13, 18p11-q11, 20p11-q13.1, 21q10, and 22q10. When tumor sizes were compared, a significantly higher number of structural abnormalities was found in tumors larger than 4 cm (P ‫؍‬ .007). Rearrangements such as t(1;8), t(1;11), t(1;19), and t(17;21) that were identified in both primary tumors and cell lines might represent markers that reflect proliferative advantages. Although SKY analysis did not indicate consistent translocations, it suggested nonrandom breakpoints, predominantly in the pericentromeric region, on a number of chromosomes. These breakpoint clusters may thus prove to be more important in the liver carcinogenesis and targets for further molecular investigations. (HEPATOLOGY 2000;32:1060-1068.) Hepatocellular carcinoma (HCC) is a highly malignant tumor that is prevalent in China, Southeast Asia, and subSaharan Africa. 1 The incidence of HCC varies widely from less than 1 of 100,000 in parts of Northern Europe, to over 100 of 100,000 in parts of Southern Africa and China. 1 Such variation is presumably attributable to the difference in prevalence of various etiologic factors, particularly chronic viral hepatitis types B and C, aflatoxin exposure, and alcohol-induced liver disease. [2][3] Genetic aberrations associated with HCC have been mainly detected by microsatellite analysis, which has suggested frequent loss of heterozygosity (LOH) on chromosomes 1p, 4q, 8p, 13q, and 16q. [4][5][6][7] Using comparative genomic hybridization (CGH), we and others have shown the presence of recurring 1q, 8q, 17q, and 20q 8-10 copy number gains in HCC. The ability to elucidate structural abnormalities, however, is limited in CGH and LOH, and remains the strength of karyotypic analysis. Cytogenetic information on HCC has, on the other hand, been very limited because of the suboptimal tumor growth in vitro and the frequent poor chromosome...

show abstract

Two‐color FISH characterization of i(1q) and der(1;16) in human breast cancer cells

Cited by 53 publications

References 13 publications

Association of specific chromosome alterations with tumour phenotype in posterior uveal melanoma

Association of specific chromosome alterations with tumour phenotype in posterior uveal melanoma

Simultaneous chromosome 1q gain and 16q loss is associated with steroid receptor presence and low proliferation in breast carcinoma

A Comprehensive Karyotypic Study on Human Hepatocellular Carcinoma by Spectral Karyotyping

Contact Info

Product

Resources

About