Project description:To analyze the global copy number aberrations of two nasopharyngeal carcinoma cell lines, TW01 and HONE1. Global copy number aberrations were analyzed by using high-resolution oligoarray CGH on two NPC cell lines, TW01 and HONE1. The overviews of array CGH profiles reveal high similarity between both NPC cell lines, but the degree of copy-number alterations were more severe in TW01 than in HONE1. There were 1204 and 1513 genes with copy-number gain (CNVs with aberration score > 0.5 and number of contiguous probes ≥ 3) in TW01 and HONE1, respectively. Among them, 850 were commonly amplified in both cell lines (Gain-TH). There were 3525 genes and 926 genes with copy-number loss (CNVs with aberration score < 0.5 and number of contiguous probe ≥ 3) in TW01 and HONE1, respectively. Among them, 582 were commonly deleted in both cell lines (Loss-TH). The most prominent CNVs observed including gain on 3q26.2-q26.31, loss on 3p21.2-q12.1, 9p24.3-p21.3, and nearly the whole Y chromosome.
Project description:Using Affymetrix Mapping 250K array, we studied copy number aberrations in oral squamous cell carcinoma (OSCC) to identified biomarkers associated with occult lymph node metastasis. We used frozen specimens from 60 OSCC patients.
Project description:Using Affymetrix Mapping 250K array, we studied copy number aberrations in oral squamous cell carcinoma (OSCC) to identified biomarkers associated with occult lymph node metastasis. We used frozen specimens from 60 OSCC patients. Copy number analysis was performed using homogenized samples of 60 oral squamous cell carcinoma patients by GeneChip Human Mapping 250k Sty arrays. As a reference, SNP array data set of 50 normal Asians (Japanese & Chinese) from HapMap database was used.
Project description:Abstract: BACKGROUND: The aim of this study was to characterize gene expression and DNA copy number profiles in androgen sensitive (AS) and androgen insensitive (AI) prostate cancer cell lines on a genome-wide scale. METHODS: Gene expression profiles and DNA copy number changes were examined using DNA microarrays in eight commonly used prostate cancer cell lines. Chromosomal regions with DNA copy number changes were identified using cluster along chromosome (CLAC). RESULTS: There were discrete differences in gene expression patterns between AS and AI cells that were not limited to androgen-responsive genes. AI cells displayed more DNA copy number changes, especially amplifications, than AS cells. The gene expression profiles of cell lines showed limited similarities to prostate tumors harvested at surgery. CONCLUSIONS: AS and AI cell lines are different in their transcriptional programs and degree of DNA copy number alterations. This dataset provides a context for the use of prostate cancer cell lines as models for clinical cancers. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
Project description:Genome wide copy number profiling of 20 PDAC cell lines to facilitate identification of novel tumor suppressor genes using an integrative genomics approach. Profiling of 20 commonly used PDAC cell lines
Project description:In order to identify biomarkers that contribute to genetic causes of OSCC, we attempt to identify copy number variation regions (CNV) in patients with OSCC. We identified and confirmed the clinical significance of amplification regions scattered from 8q22.2 to 8q24.3. Affymetrix SNP arrays were performed according to the manufacturer's directions on DNA extracted from normal oral tissues and OSCC specimens. Copy number analysis of Affymetrix SNP 6.0 arrays was performed for 112 OSCC specimens and 10 non-cancerous samples.
Project description:Abstract: BACKGROUND: The aim of this study was to characterize gene expression and DNA copy number profiles in androgen sensitive (AS) and androgen insensitive (AI) prostate cancer cell lines on a genome-wide scale. METHODS: Gene expression profiles and DNA copy number changes were examined using DNA microarrays in eight commonly used prostate cancer cell lines. Chromosomal regions with DNA copy number changes were identified using cluster along chromosome (CLAC). RESULTS: There were discrete differences in gene expression patterns between AS and AI cells that were not limited to androgen-responsive genes. AI cells displayed more DNA copy number changes, especially amplifications, than AS cells. The gene expression profiles of cell lines showed limited similarities to prostate tumors harvested at surgery. CONCLUSIONS: AS and AI cell lines are different in their transcriptional programs and degree of DNA copy number alterations. This dataset provides a context for the use of prostate cancer cell lines as models for clinical cancers. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
Project description:Over last decade several studies on oral cancer patients from eastern India have identified alterations in copy numbers in many regions of the chromosome such as 3p21.3, 8q24.21, 9p21, 9p22, 11q13, 11q21-24. However, all these studies employed microsatellite markers to map these CNV regions. This resulted in large map intervals (10-12 megabases) between the adjacent markers studied. As these regions contain a large number of genes, a high resolution CNV map of these regions was necessary to precisely identify novel genes affected by the amplifications and deletions. We thus used custom made Agilent 4X44K oligonucleotide array CGH platform to map the identified CNV regions in a resolution of 3 Kb in oral cancer patients from eastern India.
Project description:Comparative genomic hybridization (CGH) microarrays have been used to determine copy number variations (CNVs) and their effects on complex diseases. Detection of absolute CNVs independent of genomic variants of an arbitrary reference sample has been a critical issue in CGH array experiments. Whole genome analysis using massively parallel sequencing with multiple ultra-high resolution CGH arrays provides an opportunity to catalog highly accurate genomic variants of the reference DNA (NA10851). Using information on variants, we developed a new method, the CGH array reference-free algorithm (CARA), which can determine reference-unbiased absolute CNVs from any CGH array platform. The algorithm enables the removal and rescue of false positive and false negative CNVs, respectively, which appear due to the effects of genomic variants of the reference sample in raw CGH array experiments. We found that the CARA remarkably enhanced the accuracy of CGH array in determining absolute CNVs. Our method thus provides a new approach to interpret CGH array data for personalized medicine.