Abstract
In this study, 23 low malignant potential (LMP) and 27 invasive epithelial ovarian tumours have been examined by microdissection and microsatellite polymerase chain reaction (PCR) for allelic imbalance (AI) at loci on the p and q arms of chromosomes 1, 11, 17, and X, and the data have been compared with interphase cytogenetics for numerical abnormalities (aneusomy) of these chromosomes. AI was uncommon in LMP tumours (5 of 23 at 9 of 146 informative loci) but was significantly more common (p < 0.001) in invasive carcinomas (21 of 27 at 47 of 168 informative loci). This difference remained when LMP tumours were compared specifically with stage I carcinomas (p < 0.001). A greater number of loci were involved in AI amongst serous than amongst mucinous carcinomas (p = 0.015). AI was present at significantly more loci in carcinomas showing aneusomy by interphase cytogenetics than in those showing no numerical chromosome abnormalities (p < 0.001). However, amongst the carcinomas showing aneusomy, AI was as frequent at loci on chromosomes with no numerical abnormality as at those with the numerical changes. These data demonstrate that aneusomy and AI are interrelated phenomena but that AI does not occur simply as a consequence of numerical chromosome changes. Copyright (C) 2001 John Wiley & Sons, Ltd.
Original language | English |
---|---|
Pages (from-to) | 443-450 |
Number of pages | 8 |
Journal | Journal of Pathology |
Volume | 195 |
Issue number | 4 |
DOIs | |
Publication status | Published - Nov 2001 |
Keywords
- allelic imbalance
- interphase cytogenetics
- ovarian tumours
- genetic instability
- tumour progression
- POLYMERASE CHAIN-REACTION
- SEROUS BORDERLINE TUMORS
- IN-SITU HYBRIDIZATION
- MICROSATELLITE INSTABILITY
- HISTOLOGICALLY BENIGN
- GENETIC INSTABILITY
- X-CHROMOSOME
- EARLY EVENT
- CARCINOMAS
- CANCER