Analysis of lesions containing both premalignant and cancerous components suggested Type II-L-positive TSAs may develop into KRAS-mutated/CIMP-low/microsatellite stable cancers, while Type II-O-positive SSA/Ps develop into BRAF-mutated/CIMP-high/microsatellite unstable cancers.
Additionally, the results that benign pancreas are negative forKRAS mutations complement the findings of other relevant study that KRAS mutation-associated premalignant lesions do not appear to arise from acinar cells or Langerhans islets.
Although CA was observed in mammary tumors initiated by c-Myc or K-Ras(G12D), it was detected only in premalignant mammary lesions expressing K-Ras(G12D).
Our results suggest that mutational activation of K-ras gene is implicated in the development of premalignant cervical lesions and HPV infection may be an important step in the development of premalignant cervical lesions.
At year 3, the data indicated that individuals with KRAS mutations in their baseline premalignant stomach biopsies were 3.74 times as likely to progress to a higher premalignant stage than those who lacked baseline mutations (P = 0.04; C. Gong et al., Cancer Epidemiol.Biomark.Prevy.8:167-171, 1999).
Alterations of the p53 tumor suppressor gene and its association with activation of the c-K-ras-2 protooncogene in premalignant and malignant lesions of the human uterine endometrium.
The results of this study indicates no detectable mutations in the 12th codon of the first exon of the Ki-ras gene in any premalignant or malignant melanocytic lesion examined.