February 1, 1997Genes Chromosomes and Cancer
Analysis of loss of heterozygosity andKRAS2 mutations in ovarian neoplasms: Clinicopathological correlations
Authors
Discussion
Loading...
Member takes
Implication
Observational genetic analysis uncovers distinct chromosomal losses and KRAS2 mutations across ovarian tumors, suggesting low-malignant-potential lesions rarely progress to frank malignancy.
Key Points
- To determine whether ovarian adenocarcinomas arise from benign or low malignant potential precursor lesions through the profiling of chromosomal loss of heterozygosity and KRAS2 mutations.
- Evaluated loss of heterozygosity (LOH) across multiple loci on 17 chromosomes in 25 benign, 31 low malignant potential (LMP), and 93 adenocarcinoma ovarian tumors.
- Screened tumors for KRAS2 mutations and correlated mutation status with tumor malignant potential and clinical stage.
- Performed univariate and multivariate survival analyses to identify prognostic associations with specific chromosomal alterations.
- Significant cooperative LOH associations were identified in adenocarcinomas between chromosomes 5 and 17 (P = 0.0002) and chromosomes 17 and 18 (P = 0.00007).
- KRAS2 mutations occurred significantly more often in LMP neoplasms than in malignant tumors (P = 0.004) and in Stage I/II compared with Stage III/IV cancers (P = 0.033).
- LOH on chromosomes 11 (P = 0.039) and 17 (P = 0.04) correlated with significantly worse survival in univariate analysis, while benign tumors exhibited LOH only on chromosomes 6 (14%), 9 (5%), and X (33%).
Cite This Study
Chenevix‐Trench et al. (1997) studied this question.