Correlation of polypoid colorectal adenocarcinoma with pre-existing adenomatous polyps and KRAS mutation

被引:7
作者
Chen, Hui
Lefferts, Joel A.
Schwab, Mary C.
Suriawinata, Arief A.
Tsongalis, Gregory J. [1 ]
机构
[1] Dartmouth Hitchcock Med Ctr, Dept Pathol, Lebanon, NH 03766 USA
关键词
KRAS; colorectal adenocarcinoma; villous adenoma; adenomatous polyp with villous architecture; K-RAS MUTATIONS; SERRATED POLYPS; CANCER; CETUXIMAB; GROWTH; PROTOONCOGENE; PATHWAY; GENE; CARCINOMA; FEATURES;
D O I
10.1016/j.cancergen.2011.04.002
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cetuximab is an anti-epidermal growth factor receptor that helps effectively treat patients with advanced colorectal adenocarcinoma without KRAS activating mutations. KRAS mutations are associated with 16% to 50% of isolated villous adenomas and approximately 30% of colorectal cancer. Correlation between the gross and histological subset of colorectal adenocarcinoma with KRAS mutation is unknown. Archived surgical resection specimens of colorectal adenocarcinoma (n = 42) and villous adenoma (n = 9) were collected. The gross appearance and histopathological features of these lesions were thoroughly reviewed, including the presence of a pre-existing adenomatous polyp. DNA was extracted from formalin-fixed, paraffin-embedded tissue sections and then subjected to TaqMan real-time polymerase chain reaction to detect the seven most common KRAS mutations. KRAS mutations were found in 13 of 42 cases (31%) of colorectal adenocarcinoma and 7 of 9 cases (78%) of villous adenoma. All 13 cases of colorectal carcinoma with a KRAS mutation showed a gross polypoid configuration, compared to no KRAS mutation in the colorectal carcinomas with ulcerative configuration. In addition, 13 of 17 of these cases (76%) had histological features of adenocarcinoma with a persistent preexisting adenomatous polyp with villous architecture. In summary, grossly polypoid colorectal adenocarcinomas with a persistent pre-existing adenomatous polyp with villous architecture are strongly associated with KRAS mutations.
引用
收藏
页码:245 / 251
页数:7
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