Project description:Dysfunction in type I interferon (IFN) signaling occurs in patients with stage II or more advanced cancer. After screening the effects of a panel of 12 melanoma cell lines on PBMCs of healthy volunteers of IFNalpha signal pathway, two groups of melanoma cell lines could be identified one with stronger suppression (low pSTAT-1 group) than the other (high pSTAT-1 group). Comparative genomic hybridization (CGH) identified consistent amplification of 12q22-24 as a genomic marker for the immune suppressive melanoma cell lines. This region corresponded to higher transcription of the NOS1 gene located in that region in the low pSTAT1 group and NOS1 expression was identified as causal factor in melanoma induced immune suppression.
Project description:Array Comparative Genomic Hybridization (CGH) profiling of Oral Leukoplakia (OPL) and early stage Oral Squamous Cell Carcinoma (OSCC) was performed to delineate candidate non-random chromosomal loci associated with disease progression and clinico-pathological parameters. The array CGH hybridizations were performed for 24 OPL and 38 OSCC samples with pooled gender matched controls. All tissue samples were collected after obtaining written informed consent.
Project description:Unbalanced chromosomal abnormalities might play a major role in the leukemogenesis of AML-M5 Oligonucelotide array CGH were performed on 24 patients with AML-M5
Project description:Biological material: One solid mouse tumor "Colon 26A" was routinely maintained by successive transplantation. A subset of mice with this tumor was treated at the maximum tolerable dosage of Gemcitabine and successively transplanted 5 times and similarly treated. The last passage was completly resistant and designated, "Colon 26G". Oligo array CGH microarray: DNA from tumor and normal liver samples were isolated using the Wizard Genomic DNA purification kit according to the manufactures protocol (Promega Benelux BV, Leiden, NL). Labeling and hybridization procedures for the oligo array CGH were performed as previously described (Carvalho et al, 2004, J. Clin. Pathol., 57:644-649) with the following modifications: a mouse oligo library version 2.0 (Compugen/Sigma-Aldrich Chemie B.V., Zwijndrecht, NL) containing 21,997 oligonucleotides (65bp) representing 21,587 exon regions on all chromosomes were spotted on the arrays. Prehybridisation was omitted and Cot-1 concentrations during the hybridization were reduced to 100 µg. Hybridizations were done using a Hybstation12 (Perkin-Elmer, Zaventem, BE). CGH arrays were scanned using a laser scanner (Agilent Technologies, Amstelveen, NL) and analyzed using Bluefuse Software v.2.0 (Bluegnome Ltd, Cambridge, UK). Images show fused values; values with confidence higher then 0.35 with the overall Cy3 and Cy5 channels normalized to a log2ratio of 0. Tumor 26G was hybridized twice and Bluefuse confidence based average values are given. No further normalizations were performed. For interpretation and visualization purposes,smoothing was performed by version 2 of aCGH smooth, with λ set to 2.0. Keywords: other
Project description:A series of studies have been published that evaluate the chromosomal copy number changes of different tumor classes using array Comparative Genomic Hybridization (array CGH), however the chromosomal aberrations that distinguish the different tumor classes have not been fully characterized. Therefore, we performed a meta-analysis of different array CGH data sets in an attempt to classify samples tested across different platforms. As opposed to RNA expression a common reference is used in dual channel CGH arrays: normal human DNA, theoretically facilitating cross-platform analysis. To this aim, cell line and primary cancer data sets from three different dual channel array CGH platforms obtained by four different institutes were integrated. The cell line data were used to develop preprocessing methods which performed noise reduction and transformed samples into a common format. The transformed array CGH profiles allowed perfect clustering by cell line, but importantly not by platform or institute. The same preprocessing procedures used for the cell line data were applied to data from 373 primary tumors profiled by array CGH, including controls. Results indicated that there is no apparent feature related to the institute or platform and that array CGH allows for unambiguous cross-platform meta-analysis. Major clusters with common tissue origin were identified. Interestingly, tumors of hematopoietic and mesenchymal origins cluster separately from tumors of epithelial origin. Therefore it can be concluded that chromosomal aberrations of tumors from hematopoietic and mesenchymal origin versus tumors of epithelial origin are distinct, and these differences can be picked up by metaanalysis of array CGH data. This suggests the possibility of prospectively using combined analysis of diverse copy number datasets for cancer subtype classification. Keywords: comparative genomic hybridization, meta-analysis, cancer
Project description:In this study, we extend array CGH technology by making the accurate detection of segmental aneusomies possible from a single lymphoblast and fibroblast following Phi29 DNA polymerase amplification Keywords: array CGH, aCGH