PubMed · 15595189
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Bryan T Lin. 2004. Sorting cytogenetic data.. https://pubmed.ncbi.nlm.nih.gov/15595189/
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Comparative genomic hybridization (CGH) allows the analysis of chromosomal imbalances without requiring cell cultures and is more reliable than conventional cytogenetic studies for detecting gains, losses, and amplified regions. To perform CGH on cervical lesions, some authors obtain the tumoral DNA from frozen or paraffin-embedded biopsies. Others use laser microdissected material from paraffin-embedded samples, followed by degenerate oligonucleotide primer-polymerase chain reaction (DOP-PCR). In all these cases, surgery is required to obtain the sample. In our study, we obtained DNA from a cotton-lint cervical sample obtained from the pathological zone using a colposcopy technique. Chromosomal alterations were found in 9 (81%) of the 11 cases analyzed. The most frequent alterations affected the 3p12, 4q25, 5q15 approximately q21, and 18p11 regions. Satisfactory results have been observed when the cotton-lint cervical sample has been used as the source for obtaining DNA. In the laboratory, the manipulation of this type of sample obtained by a noninvasive system is much simpler, easier, and faster than the obtained with a conventional biopsy.
To identify chromosomal aberrations that differentiate among the Dukes' stages of colorectal cancer (CRC) as well as those that are responsible for the progression into liver metastases, we performed a meta-analysis of data obtained from 31 comparative genomic hybridization (CGH) studies comprising a total of 859 CRCs. Individual copy number profiles for 373 primary tumors and 102 liver metastases were recorded and several statistical analyses, such as frequency, multivariate logistic regression, and trend tests, were performed. In addition, time of occurrence analysis was applied for the first time to copy number changes identified by CGH, and each genomic imbalance was thereby classified as an early or late event in colorectal tumorigenesis. By combining data from the different statistical tests, we present a novel genetic pathway for CRC progression that distinguishes the Dukes' stages and identifies early and late events in both primary carcinomas and liver metastases. Results from the combined analyses suggest that losses at 17p and 18 and gains of 8q, 13q, and 20 occur early in the establishment of primary CRCs, whereas loss of 4p is associated with the transition from Dukes' A to B-D. Deletion of 8p and gains of 7p and 17q are correlated with the transition from primary tumor to liver metastasis, whereas losses of 14q and gains of 1q, 11, 12p, and 19 are late events. We supplement these findings with a list of potential target genes for the specific alterations from a publicly available microarray expression dataset of CRC.