Traditional serrated adenoma of the colorectum: clinicopathologic implications and endoscopic findings of the precursor lesions.

Traditional serrated adenoma of the colorectum: clinicopathologic implications and endoscopic findings of the precursor lesions.
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结直肠的传统锯齿状腺瘤:前体病变的临床病理学意义和内镜检查结果。

DOI:
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发表时间:
2013
影响因子:
3.5
通讯作者:
E. Youk
E. Youk
中科院分区:
医学4区
文献类型:
--
作者:
Mi;Eun;J. Suh;S. Chun;S. Jang;D. S. Kim;D. Lee;Suk Hee Lee;E. Youk

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目标 目的探讨与传统锯齿状腺瘤相关的前驱病变的临床病理和内窥镜特点。 方法 对104例患者107例TSA进行了BRAF、KRAS、PIK3CA、EGFR基因突变检测和Ki-67免疫组织化学染色。 结果 56例(52.3%)TSA发现非增生性增生性息肉(HP)或静止性锯齿状腺瘤/息肉(SSA/P)前驱病变,其中32例(57.1%)镜下表现为平坦隆起的II型凹陷型病变。有SSA/P前驱病变的TSA多见于近端结肠,而有Hp或无前驱病变的TSA主要位于远端结肠和直肠(P&lt;.001)。有前驱病变的TSA与无前驱病变的TSA相比,常规上皮异型增生和KRAS突变的发生率较低,而BRAF突变的发生率较高(分别为P=0.002,P<0.01和P<0.01)。 结论 根据Hp或SSA/P前驱病变合并TSA的胃镜检查,可根据其平坦隆起的生长和II型凹陷模式发现相当大比例的Hp或SSA/P前驱病变。TSA在临床病理和分子特征方面的异质性与前驱病变的状态或类型有关。
OBJECTIVES To investigate the clinicopathologic and endoscopic features of precursor lesions associated with traditional serrated adenomas (TSAs). METHODS Mutation studies for BRAF, KRAS, PIK3CA, and EGFR and immunohistochemical staining for Ki-67 were performed on 107 TSAs from 104 patients. RESULTS Nondysplastic hyperplastic polyp (HP) or sessile serrated adenoma/polyp (SSA/P) precursor lesions were found in 56 (52.3%) TSAs, among which 32 (57.1%) cases showed a flat-elevated lesion with a type II pit pattern during endoscopy. TSAs with an SSA/P precursor lesion were usually found in the proximal colon, while TSAs with an HP or with no precursor lesion were mainly located in the distal colon and rectum (P < .001). TSAs with a precursor lesion showed a lower frequency of conventional epithelial dysplasia and KRAS mutation as well as a higher frequency of BRAF mutation compared with those with no precursor lesion (P = .002, P < .001, and P < .001, respectively). CONCLUSIONS A significant proportion of HP or SSA/P precursor lesions accompanied by TSAs can be detected by endoscopy based on both their flat-elevated growth and type II pit patterns. The heterogeneity of TSAs in terms of clinicopathologic and molecular features correlated with the status or type of precursor lesions.