Only 10 CGH array assays were contributive and concluded in complex chromosomal patterns as hallmarks of malignancy in 5 melanomas, single isolated imbalances in 3 nevi, and no chromosomal gain or loss in 2 nevi.
The main databases devoted stricto sensu to cancer cytogenetics are the "Mitelman Database of Chromosome Aberrations and Gene Fusions in Cancer" ( http://cgap.nci.nih.gov/Chromosomes/Mitelman ), the "Atlas of Genetics and Cytogenetics in Oncology and Haematology" ( http://atlasgeneticsoncology.org ), and COSMIC ( http://cancer.sanger.ac.uk/cosmic ).However, being a complex multistep process, cancer cytogenetics are broadened to "cytogenomics," with complementary resources on: general databases (nucleic acid and protein sequences databases; cartography browsers: GenBank, RefSeq, UCSC, Ensembl, UniProtKB, and Entrez Gene), cancer genomic portals associated with recent international integrated programs, such as TCGA or ICGC, other fusion genes databases, array CGH databases, copy number variation databases, and mutation databases.
The results of our CGH analysis and validation by alternative methods indicate that oncogenic signals driving growth of metastatic tumors exist in the original cancer.
Array CGH or aCGH probes provide a reliable, consistent, and economical method of profiling genome-wide copy number alterations (CNAs) of cancer specimens at fairly robust resolution.
Our results demonstrate the utility of array CGH and cross-species comparisons to identify candidate oncogenes essential for the pathogenesis of human cancer.
Using a custom CGH-like oligonucleotide array to measure the global microsatellite content in the genomes of 72 cancer, cancer-free, and high risk patient and cell line samples (56 germline DNA and 16 in tumor or tumor cell line DNA) we found a unique, reproducible, and statistically significant pattern of 18 motif-specific microsatellite families (out of 962 possible 1-6 mer repeats) in breast cancer patient germline and tumor DNA, but not in germline DNA of cancer-free volunteer controls or in breast cancer patients with BRCA1/2 mutations.
This case demonstrates the need to carefully assess regions found to be deleted in individuals, referred for dysmorphia and/or developments delay, by array-CGH for the presence of genes known to be implicated in malignancy.
With the extension of this analysis to an Array-CGH dataset (glioblastomas) from The Cancer Genome Atlas we demonstrate the validity of this approach to investigate the functional impact of CNAs.
Microarray-CGH facilitates analysis of cancer-associated genomic differences between normal and tumor tissues and provides a genome-wide assessment of copy number variations (CNVs).
The developed methodology was fit to and validated using data from the Cancer Metastasis Research Center at Yonsei University; 30 pairs of gastric tumors and normal gastric tissues were used in the cDNA microarray-based CGH.
Recent CGH microarray studies have revealed several regions that are recurrently amplified in pancreatic cancer; these are thus likely to contain genes that contribute to cancer pathogenesis and thereby could serve as novel diagnostic and therapeutic targets.
This methodology was fit to and validated using cDNA microarray-based CGH data obtained from the Cancer Metastasis Research Center at Yonsei University.
Combined analysis of gene expression profiling and array-CGH data indicated that 12 to 25% of the genes that are targeted by genomic amplification are actually over-expressed in tumor cells, several of them having already been implicated in cancer.
Therefore the biologists and clinicians involved in cancer research urgently need such an integrative tool, which motivated us to undertake the construction of a database for array-CGH and other DNA copy number data for tumors (ACTuDB).
The LH/hCG receptor expression in several cancer cells provides new possibilities for developing new strategies for targeted cancer therapy based on lytic LH/hCG conjugates.