文献检索文档翻译深度研究
Suppr Zotero 插件Zotero 插件
邀请有礼套餐&价格历史记录

新学期，新优惠

限时优惠:9月1日-9月22日

30天高级会员仅需29元

1天体验卡首发特惠仅需5.99元

了解详情
不再提醒
插件&应用
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
高级版
套餐订阅购买积分包
AI 工具
文献检索文档翻译深度研究
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利：CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2025

MLH1、BRAF 和 p53-寻找预测结直肠无蒂锯齿状病变向腺癌进展的显著标志物。

MLH1, BRAF and p53 - searching for significant markers to predict evolution towards adenocarcinoma in colonic sessile serrated lesions.

机构信息

Department of Pathology, Colentina University Hospital, Bucharest, Romania;

出版信息

Rom J Morphol Embryol. 2021 Oct-Dec;62(4):971-979. doi: 10.47162/RJME.62.4.09.

DOI:10.47162/RJME.62.4.09
PMID:35673816
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9289700/
Abstract

BACKGROUND AND AIM: Colonic serrated lesions are premalignant lesions, using an alternative malignization pathway, including multiple genetic and epigenetic alterations, as: mismatch repair deficiency due to MutL homolog 1 (MLH1) promoter methylation, tumor protein p53 (TP53) mutations, activating mutations of v-Raf murine sarcoma viral oncogene homolog B (BRAF) and Kirsten rat sarcoma viral oncogene homolog (KRAS). Our study aims to evaluate MLH1, BRAF and p53 immunohistochemical (IHC) status in sessile serrated lesions (SSLs), with and without dysplasia. MATERIALS AND METHODS: This is a retrospective case-control study including 20 SSLs with dysplasia and 20 SSLs without dysplasia (matching sex and age). IHC expression of MLH1, BRAF and p53 was evaluated as the percent of nuclear loss of MLH1, cytoplasmic positivity of BRAF and nuclear positivity of p53. Data concerning age, sex, localization of the lesion, dysplasia and IHC results were statistically processed using Microsoft Excel. RESULTS: We had very polymorphous patterns of IHC expression for BRAF, MLH1 and p53, especially in the dysplastic group. Thus, two patients were BRAF+∕MLH1-∕p53+, three were BRAF+∕MLH1-∕p53-, one was BRAF+∕MLH1+∕p53- and six were BRAF+∕MLH1+∕p53+. Dysplastic lesions without BRAF mutation exhibited the following phenotype: one case BRAF-∕MLH1-∕p53+, four BRAF-∕MLH1-∕p53- and three BRAF-∕MLH1+∕p53+. In the control group (SSLs without dysplasia), there was a more homogenous distribution of cases: eight cases BRAF+∕MLH1+∕p53-, seven BRAF-∕MLH1+∕p53-, one BRAF-∕MLH1-∕p53+, two BRAF-∕MLH1-∕p53- and two BRAF-∕MLH1+∕p53+. CONCLUSIONS: There are more routes on the serrated pathway, with different mutations and time of acquisition of each genetic or epigenetic lesion with the same morphological result. These lesions should be stratified according to their risk to poor outcome and their need to further surveillance.

摘要

背景与目的：结肠锯齿状病变是癌前病变，通过一种替代的恶性转化途径，包括多种遗传和表观遗传改变，如：由于 MutL 同源物 1（MLH1）启动子甲基化导致错配修复缺陷、肿瘤蛋白 p53（TP53）突变、v-Raf 鼠肉瘤病毒癌基因同源物 B（BRAF）和 Kirsten 大鼠肉瘤病毒癌基因同源物（KRAS）的激活突变。本研究旨在评估无或有锯齿状不典型增生的无蒂锯齿状病变（SSLs）中 MLH1、BRAF 和 p53 的免疫组织化学（IHC）状态。 材料与方法：这是一项回顾性病例对照研究，纳入 20 例有锯齿状不典型增生的 SSL 患者和 20 例无锯齿状不典型增生的 SSL 患者（性别和年龄匹配）。通过核 MLH1 缺失的百分比、细胞质 BRAF 阳性和核 p53 阳性评估 MLH1、BRAF 和 p53 的 IHC 表达。使用 Microsoft Excel 统计处理有关年龄、性别、病变部位、不典型增生和 IHC 结果的数据。 结果：我们发现 BRAF、MLH1 和 p53 的 IHC 表达模式非常多样，尤其是在有锯齿状不典型增生的组中。因此，有 2 例患者 BRAF+∕MLH1-∕p53+，3 例患者 BRAF+∕MLH1-∕p53-，1 例患者 BRAF+∕MLH1+∕p53-，6 例患者 BRAF+∕MLH1+∕p53+。无 BRAF 突变的锯齿状不典型增生病变表现为以下表型：1 例患者 BRAF-∕MLH1-∕p53+，4 例患者 BRAF-∕MLH1-∕p53-，3 例患者 BRAF-∕MLH1+∕p53+。在对照组（无锯齿状不典型增生的 SSLs）中，病例分布更为均匀：8 例患者 BRAF+∕MLH1+∕p53+，7 例患者 BRAF-∕MLH1+∕p53+，1 例患者 BRAF-∕MLH1-∕p53+，2 例患者 BRAF-∕MLH1-∕p53-，2 例患者 BRAF-∕MLH1+∕p53+。 结论：锯齿状途径有更多的途径，每种遗传或表观遗传改变的发生时间和突变不同，但具有相同的形态学结果。这些病变应根据其不良预后的风险和进一步监测的需要进行分层。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/f7d32d620af8/RJME-62-4-971-fig14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/8ad5a995eac9/RJME-62-4-971-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/ac6a06911bdd/RJME-62-4-971-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/0a0eca77cacf/RJME-62-4-971-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/ec5bf8568b15/RJME-62-4-971-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/fc27c545e019/RJME-62-4-971-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/5309a3b1fc6f/RJME-62-4-971-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/ee733a4dd5e1/RJME-62-4-971-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/9314c37cf161/RJME-62-4-971-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/3a3adfdb4c6a/RJME-62-4-971-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/845b1dcdb450/RJME-62-4-971-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/704d87efb680/RJME-62-4-971-fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/33b21977b828/RJME-62-4-971-fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/3c9a5f4410d3/RJME-62-4-971-fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/f7d32d620af8/RJME-62-4-971-fig14.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/8ad5a995eac9/RJME-62-4-971-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/ac6a06911bdd/RJME-62-4-971-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/0a0eca77cacf/RJME-62-4-971-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/ec5bf8568b15/RJME-62-4-971-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/fc27c545e019/RJME-62-4-971-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/5309a3b1fc6f/RJME-62-4-971-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/ee733a4dd5e1/RJME-62-4-971-fig7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/9314c37cf161/RJME-62-4-971-fig8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/3a3adfdb4c6a/RJME-62-4-971-fig9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/845b1dcdb450/RJME-62-4-971-fig10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/704d87efb680/RJME-62-4-971-fig11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/33b21977b828/RJME-62-4-971-fig12.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/3c9a5f4410d3/RJME-62-4-971-fig13.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d505/9289700/f7d32d620af8/RJME-62-4-971-fig14.jpg

相似文献

[1]
MLH1, BRAF and p53 - searching for significant markers to predict evolution towards adenocarcinoma in colonic sessile serrated lesions.

Rom J Morphol Embryol. 2021

[2]
Clinicopathological and molecular features of sessile serrated adenomas with dysplasia or carcinoma.

Gut. 2015-10-15

[3]
MLH1-deficient Colorectal Carcinoma With Wild-type BRAF and MLH1 Promoter Hypermethylation Harbor KRAS Mutations and Arise From Conventional Adenomas.

Am J Surg Pathol. 2016-10

[4]
BRAF V600E immunohistochemistry demonstrates that some sessile serrated lesions with adenomatous dysplasia may represent collision lesions.

Histopathology. 2019-5-16

[5]
MLH1-93 G/a polymorphism is associated with MLH1 promoter methylation and protein loss in dysplastic sessile serrated adenomas with BRAF mutation.

BMC Cancer. 2018-1-5

[6]
Phenotype and polyp landscape in serrated polyposis syndrome: a series of 100 patients from genetics clinics.

Am J Surg Pathol. 2012-6

[7]
RNF43 germline and somatic mutation in serrated neoplasia pathway and its association with BRAF mutation.

Gut. 2016-6-21

[8]
[Immunophenotypes and gene mutations in colorectal precancerous lesions and adenocarcinoma].

Zhonghua Bing Li Xue Za Zhi. 2013-10

[9]
Serrated polyps of the large intestine: a molecular study comparing sessile serrated adenomas and hyperplastic polyps.

Histopathology. 2009-8

[10]
Molecular Profiling Based on KRAS/BRAF Mutation, Methylation, and Microsatellite Statuses in Serrated Lesions.

Dig Dis Sci. 2018-7-5

引用本文的文献

[1]
Comparative Expression Analysis of Tumor Suppressor and Oncogene in Colorectal Adenocarcinoma.

Cancer Diagn Progn. 2024-3-3

[2]
The histopathological features and their prognostic impact in the postoperative follow-up of colorectal cancer patients.

Rom J Morphol Embryol. 2022

[3]
Clinical and morphopathological assay in vulvovaginal candidiasis.

Rom J Morphol Embryol. 2022

本文引用的文献

[1]
Serrated lesions of the colon and rectum: Emergent epidemiological data and molecular pathways.

Open Med (Wars). 2020-11-9

[2]
Evolving pathologic concepts of serrated lesions of the colorectum.

J Pathol Transl Med. 2020-7

[3]
Serrated polyps of the colon and rectum: Remove or not?

World J Gastroenterol. 2020-5-21

[4]
Molecular Features of the Serrated Pathway to Colorectal Cancer: Current Knowledge and Future Directions.

Gut Liver. 2021-1-15

[5]
Association Between Molecular Subtypes of Colorectal Tumors and Patient Survival, Based on Pooled Analysis of 7 International Studies.

Gastroenterology. 2020-6

[6]
The heterogeneous clinical and pathological landscapes of metastatic -mutated colorectal cancer.

Cancer Cell Int. 2020-1-29

[7]
Alterations in signaling pathways that accompany spontaneous transition to malignancy in a mouse model of BRAF mutant microsatellite stable colorectal cancer.

Neoplasia. 2020-2

[8]
Colorectal sessile serrated lesion with large size or synchronous neoplasm: a prospective study.

Eur J Gastroenterol Hepatol. 2020-2

[9]
Serrated Colorectal Cancer: The Road Less Travelled?

Trends Cancer. 2019-11

[10]
Pathways of Colorectal Carcinogenesis.

Gastroenterology. 2019-10-14

文献AI研究员

20分钟写一篇综述，助力文献阅读效率提升50倍

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

推荐工具

医学文档翻译智能文献检索