Molecular biology of double‐minute chromosomes

Hahn, Peter

doi:10.1002/bies.950150707

Cited by 93 publications

(60 citation statements)

References 47 publications

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“…Double minute chromosomes (DMs) are the cytogenetic hallmark of extra-chromosomal genomic amplification (Hahn 1993). They are small, generally acentric, atelomeric, autonomously replicating chromatin bodies and are frequently detected in cytogenetic examinations of metaphase chromosomes in human tumor cells (Biedler et al 1983).…”

Section: Introductionmentioning

confidence: 99%

Frequency of double minute chromosomes and combined cytogenetic abnormalities and their characteristics

Fan

Mao

et al. 2010

J Appl Genetics

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Double minute chromosomes (DMs) are the cytogenetic hallmark of extra-chromosomal genomic amplification. The frequency of DMs in primary cancer and the cytogenetic features of DMs-positive primary cancer cases are largely unknown. To unravel these issues, we retrieved the Mitelman database and analyzed all DMs-positive primary cancerous karyotypes (787 karyotypes). The overall frequency of DMs is 1.4% (787 DMs-positive cases; total 54,398 cases). We found that DMs have the highest frequency in adrenal carcinoma (28.6%, topography) and neuroblastoma (31.7%, morphology). The frequencies of DMs in each tumor were much lower than in previous reports. The frequency of DMs in malignant cancers is significantly higher than in benign cancers, which confirms that DMs are malignant cytogenetic markers. DMs combined cytogenetic abnormalities are identified and sorted into two groups by principal component analysis (PCA), with one group containing −4, −5, −8, −9, −10, −13, −14, −15, −16, −17, −18, −20, −21, and −22, and the other containing −1p, −5q, +7, and +20. The prominent imbalance in DMs-positive cancer cases is chromosome loss. However, DMs-positive cancer cases, deriving from different morphologic cancers, cannot be clearly divided into subgroups. Our large database analysis provides novel knowledge of DMs and their combined cytogenetic abnormalities in primary cancer.

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Section: Introductionmentioning

confidence: 99%

Frequency of double minute chromosomes and combined cytogenetic abnormalities and their characteristics

Fan

Mao

et al. 2010

J Appl Genetics

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“…HSRs manifest as a ladder-like structure of inverted repeats within chromosomes (Schwab, 1998). Extrachromosomal amplicons appear as double minutes, which can be seen using conventional cytogenetics (Hahn, 1993), and episomes (B250 bp in length), which are only detectable using molecular biology methods (Maurer et al, 1987;Graux et al, 2004). HSRs, double minutes and episomes may contain fused genetic material from different chromosomal loci (Guan et al, 1994;Graux et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

DNA copy number amplification profiling of human neoplasms

et al. 2006

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DNA copy number amplifications activate oncogenes and are hallmarks of nearly all advanced tumors. Amplified genes represent attractive targets for therapy, diagnostics and prognostics. To investigate DNA amplifications in different neoplasms, we performed a bibliomics survey using 838 published chromosomal comparative genomic hybridization studies and collected amplification data at chromosome band resolution from more than 4500 cases. Amplification profiles were determined for 73 distinct neoplasms. Neoplasms were clustered according to the amplification profiles, and frequently amplified chromosomal loci (amplification hot spots) were identified using computational modeling. To investigate the site specificity and mechanisms of gene amplifications, colocalization of amplification hot spots, cancer genes, fragile sites, virus integration sites and gene size cohorts were tested in a statistical framework. Amplification-based clustering demonstrated that cancers with similar etiology, cell-oforigin or topographical location have a tendency to obtain convergent amplification profiles. The identified amplification hot spots were colocalized with the known fragile sites, cancer genes and virus integration sites, but global statistical significance could not be ascertained. Large genes were significantly overrepresented on the fragile sites and the reported amplification hot spots. These findings indicate that amplifications are selected in the cancer tissue environment according to the qualitative traits and localization of cancer genes.

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“…Notably, the additional ABL1 signals were extrachromosomal. Extrachromosomal amplification of oncogenes has been observed on double minute (dmin) chromosomes 11 , visible by standard cytogenetics, or on cytogenetically invisible units, called episomes 4 . In the cases we studied, no dmin chromosomes were visible by G or R banding ( Supplementary Fig.…”

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confidence: 99%