We have investigated by high resolution array-CGH a series of 29 chromosome 19 markers after previous microdissection of ovarian carcinoma metaphases followed by FISH to determine where in chromosome 19 the rearrangements took place as well as from which partner chromosomes the additional material stems, obtaining informative results on 23 markers from 18 carcinomas.
Mammalian comparative genome hybridization on microarrays (array-CGH) has been applied to the study of many carcinomas, identifying common copy number changes in key regions including known oncogenes.
In this study, we subjected 27 primary tumors (15 myoepitheliomas and 12 myoepithelial carcinomas) to genome-wide microarray-based comparative genomic hybridization (array CGH).
We carried out an exhaustive search for regions susceptible to such mechanisms using a combination of transcriptome correlation map analysis and array CGH data for a series of bladder carcinomas.
The analysis of 12 mixed gastric carcinomas showed no significant differences in array CGH profiles between the diffuse and intestinal components of mixed carcinomas.
Interestingly, the array-CGH (CGHa) profile showed an increase in copy number along most of 19q including the AKT2 oncogene and the KLKs gene family, which have previously been shown to be amplified in pancreatic carcinomas and upregulated in several tumors, respectively.
Newer technology, such as array-CGH, when combined with cDNA microarrays and tissue microarrays, will facilitate the integration of genomic and gene expression data and pave the way toward a molecular classification of lung carcinomas.
Here, we have studied chromosomal changes in 12 locally recurrent, hormone-refractory prostate carcinomas using karyotyping and CGH that revealed genetic aberrations in all tumors.
The findings that normal rat prostates express functional LH/hCG receptors led us to test the hypothesis that benign prostatic hyperplasia (BPH) and prostate carcinomas may also express this receptor gene.