CGH-Explorer: a program for analysis of array-CGH data

Lingjærde, Ole Christian; Baumbusch, Lars Oliver; Liestøl, Knut; Glad, Ingrid K.; Børresen‐Dale, Anne‐Lise

doi:10.1093/bioinformatics/bti113

Cited by 131 publications

(121 citation statements)

References 5 publications

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“…Nine patients who had tumor recurrence/progression for less than 12 months were defined as short term recurrence group (STR), and 13 patients who progressed after more than 12 months were called long term recurrence group. The coordinates of the deletion in clinical specimens were assessed via processing of the representation oligonucleotide microarray analysis data using CGH-Explorer software (23). Mapping the boundaries of homozygous 9p21.3 deletions in DNA specimens isolated from MM cell lines was done via genomic PCR on the CDKN2A-flanking areas using primers listed in supplemental Table S1.…”

Section: Methodsmentioning

confidence: 99%

Pro-tumorigenic Effects of miR-31 Loss in Mesothelioma

Ivanov

Goparaju

Lopez

et al. 2010

Journal of Biological Chemistry

120

113

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The human genome encodes several hundred microRNA (miRNA) genes that produce small (21-23n) single strand regulatory RNA molecules. Although abnormal expression of miRNAs has been linked to cancer progression, the mechanisms of this dysregulation are poorly understood. Malignant mesothelioma (MM) of pleura is an aggressive and highly lethal cancer resistant to conventional therapies. We and others previously linked loss of the 9p21.3 chromosome in MM with short time to tumor recurrence. In this study, we report that MM cell lines derived from patients with more aggressive disease fail to express miR-31, a microRNA recently linked with suppression of breast cancer metastases. We further demonstrate that this loss is due to homozygous deletion of the miR-31-encoding gene that resides in 9p21.3. Functional assessment of miR-31 activity revealed its ability to inhibit proliferation, migration, invasion, and clonogenicity of MM cells. Re-introduction of miR-31 suppressed the cell cycle and inhibited expression of multiple factors involved in cooperative maintenance of DNA replication and cell cycle progression, including pro-survival phosphatase PPP6C, which was previously associated with chemotherapy and radiation therapy resistance, and maintenance of chromosomal stability. PPP6C, whose mRNA is distinguished with three miR-31-binding sites in its 3-untranslated region, was consistently down-regulated by miR-31 introduction and upregulated in clinical MM specimens as compared with matched normal tissues. Taken together, our data suggest that tumorsuppressive propensity of miR-31 can be used for development of new therapies against mesothelioma and other cancers that show loss of the 9p21.3 chromosome.

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Section: Methodsmentioning

confidence: 99%

Pro-tumorigenic Effects of miR-31 Loss in Mesothelioma

Ivanov

Goparaju

Lopez

et al. 2010

Journal of Biological Chemistry

120

113

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“…Three olfactory neuroblastomas were studied by Riazimand et al 5 using conventional CGH, and amplification of whole chromosome 19, partial gains of 1p, 8q, 15q, and 22q, and deletions of 4q and 6p were detected. Szymas et al 6 studied a single olfactory neuroblastoma and found gains of whole chromosomes 4,8,11, and 14, partial gains of 1q and 17q, partial deletions of 5q and 17q, and whole chromosome losses of 16,18,19, and X. In our study, we applied for the first time an oligonucleotide-based array CGH (aCGH) to identify the most frequently occurring DNA copy number changes in 13 cases of olfactory neuroblastoma.…”

mentioning

confidence: 87%

“…To obtain a global view of the copy number alteration frequencies in olfactory neuroblastoma, we also analyzed the data using GeneSpring (Agilent Technologies) and CGH Explorer software 3.1. 8 The raw data from the Feature Extraction software were imported into the GeneSpring software and normalized using the Feature Extraction data import plugin (Agilent Technologies). Outlier probes marked by Feature Extraction were ignored in normalization.…”

Section: Array Cgh Experimentsmentioning

confidence: 99%

Array comparative genomic hybridization analysis of olfactory neuroblastoma

et al. 2008

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Olfactory neuroblastoma is an unusual neuroectodermal malignancy, which is thought to arise at the olfactory membrane of the sinonasal tract. Due to its rarity, little is understood regarding its molecular and cytogenetic abnormalities. The aim of the current study is to identify specific DNA copy number changes in olfactory neuroblastoma. Thirteen dissected tissue samples were analyzed using array comparative genomic hybridization. Our results show that gene copy number profiles of olfactory neuroblastoma samples are complex. The most frequent changes included gains at 7q11.22-q21.11, 9p13.3, 13q, 20p/q, and Xp/q, and losses at 2q31.1, 2q33.3, 2q37.1, 6q16.3, 6q21.33, 6q22.1, 22q11.23, 22q12.1, and Xp/q. Gains were more frequent than losses, and high-stage tumors showed more alterations than low-stage olfactory neuroblastoma. Frequent changes in high-stage tumors were gains at 13q14.2-q14.3, 13q31.1, and 20q11.21-q11.23, and loss of Xp21.1 (in 66% of cases). Gains at 5q35, 13q, and 20q, and losses at 2q31.1, 2q33.3, and 6q16-q22, were present in 50% of cases. The identified regions of gene copy number change have been implicated in a variety of tumors, especially carcinomas. In addition, our results indicate that gains in 20q and 13q may be important in the progression of this cancer, and that these regions possibly harbor genes with functional relevance in olfactory neuroblastoma.

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“…First, duplicate BAC spot values were averaged, and then all values were normalized to the mean of all control (non-HSA21) BACs. Second, samples were analyzed using CGHexplorer 35 to determine ploidy and to identify breakpoints. Figure S2).…”

Section: Array Analysismentioning

confidence: 99%

Genotype–phenotype correlations in Down syndrome identified by array CGH in 30 cases of partial trisomy and partial monosomy chromosome 21

et al. 2008

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Down syndrome (DS) is one of the most frequent congenital birth defects, and the most common genetic cause of mental retardation. In most cases, DS results from the presence of an extra copy of chromosome 21. DS has a complex phenotype, and a major goal of DS research is to identify genotype -phenotype correlations. Cases of partial trisomy 21 and other HSA21 rearrangements associated with DS features could identify genomic regions associated with specific phenotypes. We have developed a BAC array spanning HSA21q and used array comparative genome hybridization (aCGH) to enable high-resolution mapping of pathogenic partial aneuploidies and unbalanced translocations involving HSA21. We report the identification and mapping of 30 pathogenic chromosomal aberrations of HSA21 consisting of 19 partial trisomies and 11 partial monosomies for different segments of HSA21. The breakpoints have been mapped to within B85 kb. The majority of the breakpoints (26 of 30) for the partial aneuploidies map within a 10-Mb region. Our data argue against a single DS critical region. We identify susceptibility regions for 25 phenotypes for DS and 27 regions for monosomy 21. However, most of these regions are still broad, and more cases are needed to narrow down the phenotypic maps to a reasonable number of candidate genomic elements per phenotype.

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CGH-Explorer: a program for analysis of array-CGH data

Cited by 131 publications

References 5 publications

Pro-tumorigenic Effects of miR-31 Loss in Mesothelioma

Pro-tumorigenic Effects of miR-31 Loss in Mesothelioma

Array comparative genomic hybridization analysis of olfactory neuroblastoma

Genotype–phenotype correlations in Down syndrome identified by array CGH in 30 cases of partial trisomy and partial monosomy chromosome 21

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