• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
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
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
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 @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

p53 和表皮生长因子受体在胶质母细胞瘤中的表达。

Expression of p53 & epidermal growth factor receptor in glioblastoma.

机构信息

Department of Pathology & Neurosurgery, Sri Venkateswara Institute of Medical Sciences, Tirupati, India.

出版信息

Indian J Med Res. 2017 Dec;146(6):738-745. doi: 10.4103/ijmr.IJMR_1179_15.

DOI:10.4103/ijmr.IJMR_1179_15
PMID:29664032
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5926345/
Abstract

BACKGROUND & OBJECTIVES: Glioblastoma (GB) is the most frequent brain tumour, manifesting at any age, with a peak incidence between 45 and 75 years. Primary and secondary GBs constitute relatively distinct disease entities in evolution, in expression profiles and in therapeutic response. Histopathologically, primary and secondary GBs are indistinguishable. The aim of this investigation was to study the immunohistochemical (IHC) expression of p53 and epidermal growth factor receptor (EGFR) in GB with the objective of categorizing the morphological variants of GB into primary and secondary based on the presence of low-grade areas and knowing the variable expression of p53 and EGFR in primary and secondary GB.

METHODS

A total of 28 patients with GB were studied and categorized into primary and secondary based on the presence of low-grade areas, i.e. discernible astrocytic morphology, gemistocyte and oligodendroglia. Tumours with the presence of combination of the above features or any one of the above features were taken as secondary GB, whereas tumours with highly pleomorphic areas were considered as primary GB. IHC was done on the representative tissue blocks for p53 and EGFR.

RESULTS

Majority of the patients were in the fifth and sixth decades of life with a mean age of 46.96±13 yr with male preponderance (male:female 2.5:1). Mean age of presentation was 48.93±12 yr in primary and 44.69±15 yr in secondary GB. All cases of GB were classified into primary (53.57%) and secondary (46.43%) based on morphology. EGFR was more frequently expressed than p53. Based on IHC, 50 per cent of cases were classified into primary, three per cent into secondary and 47 per cent as unclassified.

INTERPRETATION & CONCLUSIONS: Histopathological features, i.e. presence of low-grade areas, may play a role in classifying GB into primary and secondary. EGFR has a pivotal role in gliomagenesis. Combination of p53 and EGFR alone may not be sufficient to clarify GB into primary and secondary.

摘要

背景与目的

胶质母细胞瘤(GB)是最常见的脑肿瘤,可发生于任何年龄,但在 45 至 75 岁之间发病率最高。原发性和继发性 GB 在演化、表达谱和治疗反应方面是相对不同的疾病实体。组织病理学上,原发性和继发性 GB 无法区分。本研究旨在研究胶质母细胞瘤中 p53 和表皮生长因子受体(EGFR)的免疫组织化学(IHC)表达,目的是根据低级别区域的存在将 GB 的形态变异体分为原发性和继发性,并了解原发性和继发性 GB 中 p53 和 EGFR 的可变表达。

方法

共研究了 28 例胶质母细胞瘤患者,并根据低级别区域(即可识别的星形胶质细胞形态、巨星形细胞瘤和少突胶质细胞瘤)的存在将其分为原发性和继发性。存在上述特征组合或任何一种特征的肿瘤被认为是继发性胶质母细胞瘤,而高度多形性区域的肿瘤被认为是原发性胶质母细胞瘤。对 p53 和 EGFR 的代表性组织块进行了免疫组化检测。

结果

大多数患者年龄在 50 至 60 岁之间,平均年龄为 46.96±13 岁,男性居多(男:女为 2.5:1)。原发性和继发性胶质母细胞瘤的平均发病年龄分别为 48.93±12 岁和 44.69±15 岁。所有胶质母细胞瘤病例均根据形态学分为原发性(53.57%)和继发性(46.43%)。EGFR 的表达频率高于 p53。根据免疫组化,50%的病例被归类为原发性,3%的病例被归类为继发性,47%的病例为未分类。

解释与结论

组织病理学特征,即低级别区域的存在,可能在将胶质母细胞瘤分为原发性和继发性方面发挥作用。EGFR 在神经胶质瘤发生中起关键作用。单独使用 p53 和 EGFR 的组合可能不足以将胶质母细胞瘤分为原发性和继发性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/1c47db82e764/IJMR-146-738-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/62b85b39625e/IJMR-146-738-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/27e61a422bd8/IJMR-146-738-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/5bf439d05e6d/IJMR-146-738-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/45646be676b3/IJMR-146-738-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/31a59113cbe2/IJMR-146-738-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/65e1f89f31ef/IJMR-146-738-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/4ffc1b1cbe9f/IJMR-146-738-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/b59160a9f76d/IJMR-146-738-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/849b50cd8a5b/IJMR-146-738-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/010101209a75/IJMR-146-738-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/844c073eed41/IJMR-146-738-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/1c47db82e764/IJMR-146-738-g012.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/62b85b39625e/IJMR-146-738-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/27e61a422bd8/IJMR-146-738-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/5bf439d05e6d/IJMR-146-738-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/45646be676b3/IJMR-146-738-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/31a59113cbe2/IJMR-146-738-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/65e1f89f31ef/IJMR-146-738-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/4ffc1b1cbe9f/IJMR-146-738-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/b59160a9f76d/IJMR-146-738-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/849b50cd8a5b/IJMR-146-738-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/010101209a75/IJMR-146-738-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/844c073eed41/IJMR-146-738-g011.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0f4b/5926345/1c47db82e764/IJMR-146-738-g012.jpg

相似文献

1
Expression of p53 & epidermal growth factor receptor in glioblastoma.p53 和表皮生长因子受体在胶质母细胞瘤中的表达。
Indian J Med Res. 2017 Dec;146(6):738-745. doi: 10.4103/ijmr.IJMR_1179_15.
2
[Study on the expression of epidermal growth factor receptor and p53 in astrocytic gliomas: evidence for a distinct genetic pathway].[星形胶质细胞瘤中表皮生长因子受体和p53的表达研究:不同遗传途径的证据]
Zhonghua Bing Li Xue Za Zhi. 2006 Apr;35(4):232-6.
3
Overexpression of the EGF receptor and p53 mutations are mutually exclusive in the evolution of primary and secondary glioblastomas.表皮生长因子受体的过表达与p53突变在原发性和继发性胶质母细胞瘤的发展过程中相互排斥。
Brain Pathol. 1996 Jul;6(3):217-23; discussion 23-4. doi: 10.1111/j.1750-3639.1996.tb00848.x.
4
Molecular analysis of microdissected de novo glioblastomas and paired astrocytic tumors.显微切割的原发性胶质母细胞瘤和配对星形细胞瘤的分子分析。
J Neuropathol Exp Neurol. 1999 Feb;58(2):120-8. doi: 10.1097/00005072-199902000-00002.
5
Dynamic Contrast-Enhanced T1-Weighted Perfusion Magnetic Resonance Imaging Identifies Glioblastoma Immunohistochemical Biomarkers via Tumoral and Peritumoral Approach: A Pilot Study.动态对比增强 T1 加权灌注磁共振成像通过肿瘤和瘤周两种方法识别胶质母细胞瘤免疫组织化学标志物:一项初步研究。
World Neurosurg. 2019 Aug;128:e195-e208. doi: 10.1016/j.wneu.2019.04.089. Epub 2019 Apr 16.
6
Frequent LOH at chromosome 12q22-23 and Apaf-1 inactivation in glioblastoma.胶质母细胞瘤中12号染色体q22 - 23区域的频繁杂合性缺失及凋亡蛋白酶激活因子1(Apaf-1)失活
Brain Pathol. 2003 Oct;13(4):431-9. doi: 10.1111/j.1750-3639.2003.tb00474.x.
7
Glioblastoma multiforme in an Asian population: evidence for a distinct genetic pathway.亚洲人群中的多形性胶质母细胞瘤:独特遗传途径的证据
J Neurooncol. 2002 Nov;60(2):117-25. doi: 10.1023/a:1020622415786.
8
Amplification and overexpression of epidermal growth factor receptor gene in glioblastomas of Chinese patients correlates with patient's age but not with tumor's clinicopathological pathway.中国患者胶质母细胞瘤中表皮生长因子受体基因的扩增和过表达与患者年龄相关,但与肿瘤的临床病理途径无关。
Acta Neuropathol. 2005 Nov;110(5):481-9. doi: 10.1007/s00401-005-1072-y. Epub 2005 Sep 7.
9
p53 mutations versus EGF receptor expression in giant cell glioblastomas.巨细胞胶质母细胞瘤中p53突变与表皮生长因子受体表达的关系
J Neuropathol Exp Neurol. 1997 Nov;56(11):1236-41. doi: 10.1097/00005072-199711000-00008.
10
Molecular genetics of radiographically defined de novo glioblastoma multiforme.影像学确诊的原发性多形性胶质母细胞瘤的分子遗传学
Neuropathol Appl Neurobiol. 2000 Dec;26(6):544-52. doi: 10.1046/j.0305-1846.2000.00290.x.

引用本文的文献

1
Endothelial transdifferentiation of glioma stem cells: a literature review.胶质瘤干细胞的内皮转分化:文献综述
Acta Neuropathol Commun. 2025 Aug 21;13(1):181. doi: 10.1186/s40478-025-02031-x.
2
Study of Molecular Markers in Glioma and Their Association with Clinicopathological Features.胶质瘤分子标志物及其与临床病理特征的相关性研究。
Ann Afr Med. 2024 Nov 8;24(1):28-36. doi: 10.4103/aam.aam_127_23.
3
Parkinson's disease relevant pathological features are manifested in male Pink1/Parkin deficient rats.帕金森病相关病理特征在雄性Pink1/Parkin基因缺陷大鼠中表现出来。

本文引用的文献

1
The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary.2016 年世界卫生组织中枢神经系统肿瘤分类:概述。
Acta Neuropathol. 2016 Jun;131(6):803-20. doi: 10.1007/s00401-016-1545-1. Epub 2016 May 9.
2
Epidermal growth factor receptor (EGFR) gene amplification in high-grade gliomas: Western Indian tertiary cancer center experience.高级别胶质瘤中表皮生长因子受体(EGFR)基因扩增:西印度三级癌症中心的经验
Neurol India. 2016 Jan-Feb;64(1):115-20. doi: 10.4103/0028-3886.173668.
3
EGFR, p53, IDH-1 and MDM2 immunohistochemical analysis in glioblastoma: therapeutic and prognostic correlation.
Brain Behav Immun Health. 2023 Jun 19;31:100656. doi: 10.1016/j.bbih.2023.100656. eCollection 2023 Aug.
4
EGFR suppresses p53 function by promoting p53 binding to DNA-PKcs: a noncanonical regulatory axis between EGFR and wild-type p53 in glioblastoma.表皮生长因子受体(EGFR)通过促进 p53 与 DNA 依赖性蛋白激酶催化亚基(DNA-PKcs)结合来抑制 p53 功能:胶质母细胞瘤中 EGFR 和野生型 p53 之间的非典型调控轴。
Neuro Oncol. 2022 Oct 3;24(10):1712-1725. doi: 10.1093/neuonc/noac105.
5
Loss of TRP53 (p53) accelerates tumorigenesis and changes the tumor spectrum of SJL/J mice.TRP53(p53)缺失会加速肿瘤发生,并改变SJL/J小鼠的肿瘤谱。
Genes Cancer. 2020;11(1-2):83-94. doi: 10.18632/genesandcancer.198.
6
Long noncoding RNA LINC00511 induced by SP1 accelerates the glioma progression through targeting miR-124-3p/CCND2 axis.长链非编码 RNA LINC00511 通过靶向 miR-124-3p/CCND2 轴被 SP1 诱导加速了胶质瘤的进展。
J Cell Mol Med. 2019 Jun;23(6):4386-4394. doi: 10.1111/jcmm.14331. Epub 2019 Apr 11.
胶质母细胞瘤中EGFR、p53、IDH-1和MDM2的免疫组织化学分析:治疗与预后的相关性
Arq Neuropsiquiatr. 2015 Jul;73(7):561-8. doi: 10.1590/0004-282X20150059.
4
Glioblastoma: pathology, molecular mechanisms and markers.胶质母细胞瘤:病理学、分子机制和标志物。
Acta Neuropathol. 2015 Jun;129(6):829-48. doi: 10.1007/s00401-015-1432-1. Epub 2015 May 6.
5
Genome-wide methylation profiling identifies an essential role of reactive oxygen species in pediatric glioblastoma multiforme and validates a methylome specific for H3 histone family 3A with absence of G-CIMP/isocitrate dehydrogenase 1 mutation.全基因组甲基化分析确定了活性氧在儿童多形性胶质母细胞瘤中的重要作用,并验证了一种针对H3组蛋白家族3A的甲基化组,该甲基化组不存在G-CIMP/异柠檬酸脱氢酶1突变。
Neuro Oncol. 2014 Dec;16(12):1607-17. doi: 10.1093/neuonc/nou113. Epub 2014 Jul 4.
6
Immunohistochemical classification of primary and secondary glioblastomas.原发性和继发性胶质母细胞瘤的免疫组织化学分类
Korean J Pathol. 2013 Dec;47(6):541-8. doi: 10.4132/KoreanJPathol.2013.47.6.541. Epub 2013 Dec 24.
7
Glioblastoma with oligodendroglioma component (GBM-O): molecular genetic and clinical characteristics.胶质母细胞瘤伴少突胶质细胞瘤成分(GBM-O):分子遗传学和临床特征。
Brain Pathol. 2013 Jul;23(4):454-61. doi: 10.1111/bpa.12018. Epub 2013 Jan 30.
8
Pathological significance of epidermal growth factor receptor expression and amplification in human gliomas.表皮生长因子受体表达和扩增在人类胶质瘤中的病理意义。
Histopathology. 2012 Oct;61(4):726-36. doi: 10.1111/j.1365-2559.2012.04354.x.
9
Genome-wide expression profiling identifies deregulated miRNAs in malignant astrocytoma.全基因组表达谱分析鉴定出恶性星形细胞瘤中失调的 miRNAs。
Mod Pathol. 2010 Oct;23(10):1404-17. doi: 10.1038/modpathol.2010.135. Epub 2010 Aug 13.
10
Heterozygosity status of 1p and 19q and its correlation with p53 protein expression and EGFR amplification in patients with astrocytic tumors: novel series from India.星形细胞瘤患者中1p和19q的杂合性状态及其与p53蛋白表达和表皮生长因子受体(EGFR)扩增的相关性:来自印度的新系列研究
Cancer Genet Cytogenet. 2010 Apr 15;198(2):126-34. doi: 10.1016/j.cancergencyto.2009.12.018.