We used comparative genomic hybridization (CGH) to identify recurrent chromosomal imbalances in tumor DNA from 25 malignant ovarian carcinomas and two ovarian tumors of low malignant potential (LMP). Many of the carcinoma specimens displayed numerous imbalances. The most common sites of copy number
Comparative genomic hybridization reveals frequent chromosome 13q and 4q losses in renal carcinomas with sarcomatoid transformation
โ Scribed by Jiang, Feng; Moch, Holger; Richter, Jan; Egenter, Carole; Gasser, Thomas; Bubendorf, Lukas; Gschwind, Rudolf; Sauter, Guido; Mihatsch, Michael J.
- Book ID
- 101222703
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 307 KB
- Volume
- 185
- Category
- Article
- ISSN
- 0022-3417
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โฆ Synopsis
Renal cell carcinomas (RCCs) with sarcomatoid transformation show the most malignant behaviour of all renal carcinoma types. In this study, comparative genomic hybridization was used to screen for losses and gains of DNA sequences along all chromosome arms in 12 sarcomatoid (S) RCCs. On average, there were 8โข6 aberrations per tumour. DNA sequence losses (5โข2 4โข4) were slightly more frequent than gains (3โข4 2โข6). DNA gains most often involved chromosomes 17 (33 per cent), 7, and 8q (25 per cent each). High-level co-amplification involving 11q22-23 and 7p21-22 in one SRCC was not present in adjacent non-sarcomatous tumour areas, raising the possibility of oncogene involvement at these loci for sarcomatoid transformation. DNA losses were most prevalent at 13q (75 per cent) and 4q (50 per cent), suggesting that inactivation of tumour suppressor genes at chromosomes 13q and 4q may be linked to sarcomatoid growth of RCC. It is concluded that SRCCs are genetically highly complex. Chromosomes 13q, 4q, 7p21-22, and 11q22-23 may carry genes with relevance for sarcomatoid growth in RCC. 1998 John Wiley & Sons, Ltd.
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Comparative genomic hybridization (CGH) was used to screen for genomic imbalances in 24 exocrine pancreatic carcinomas, including 11 low-passage cell lines (4-8 subcultures) and 13 uncultured samples. Aberrations were found in all cell lines and in seven of the 13 biopsies. The most frequent changes