Chromogenic in situ hybridization detection of chromosome 7 and 17 abnormalities in renal cell carcinomas and comparison to flow cytometric DNA ploidy patterns

Abstract

Background and aim: The chromogenic in situ hybridization (CISH) is a new method in which chromosome aberration is determined by using a chromogenic reaction. We report the aberrations of chromosome 7 and 17 in three major subtypes of renal cell carcinomas (RCC), and compared these chromosomal changes with the flow cytometric DNA ploidy patterns. Methods: Aberrations of chromosomes 7 and 17 in 21 clear cell (c), 6 papillary (p) and 15 chromophobe (ch) RCCs were studied and compared with flow cytometric DNA ploidy. Results: Two of 14 chRCCs (14.3%) were monosomic for chromosome 7, but none of the cRCCs or pRCCs were monosomic. Twelve (85.7%) chRCCs showed monosomy for chromosome 17, but none of the pRCCs were monosomic. Three pRCCs (50%), 5 of 14 (35.7%) chRCCs and 2 (9.5%) cRCCs were polysomic for chromosome 7, whereas only one pRCC was polysomic. DNA aneuploidy was found in 2 pRCCs (33.3%), 2 cRCCs (9.5%), and 6 chRCCs (46.2%). Hypodiploidy was seen in one chRCC, and triploidy was seen in all types of RCCs. DNA aneuploidy was more frequent in cases with both chromosome 7 and 17 abnormalities (80%) than in cases with abnormality of one (38.5%) or neither (4.5%). Conclusion: The CISH method is useful in detecting chromosomal change in RCC, and the identification of chromosome 17 monosomy is helpful in diagnosis of chRCC.

Circulating biomarkers in renal cell carcinoma: the link between microRNAs and extracellular vesicles, where are we now?

“…The different RCC histological subtypes reflect differences in the molecular mechanisms involved in tumorigenesis as well as different prognosis. The papillary RCC is characterized by the gain of chromosome material (Trisomy 7, 17), chromophobe RCC is characterized by the loss of genetic material that included monosomy of chromosomes 1, 2, 6, 13, 17 or 21 ( 83 ), and the majority of cell RCC is characterized by loss of function of the von Hippel-Lindau (VHL) gene ( 84–87 ).…”