Apoptosis-Related (Survivin, Bcl-2), Tumor Suppressor Gene (p53), Proliferation (Ki-67), and Non-Receptor Tyrosine Kinase (Src) Markers Expression and Correlation With Clinicopathologic Variables in 60 Thymic Neoplasms

生存素 胸腺癌 医学 酪氨酸激酶 病理 阶段(地层学) 胸腺瘤 精确检验 原癌基因酪氨酸蛋白激酶Src 免疫组织化学 肿瘤科 内科学 癌症研究 受体 生物 癌症 古生物学
作者
Thaer Khoury,Ainan Arshad,Paul N. Bogner,Nithya Ramnath,Shaozeng Zhang,Rameela Chandrasekhar,Gregory E. Wilding,Sadir Alrawi,Dongfeng Tan
出处
期刊:Chest [Elsevier BV]
卷期号:136 (1): 220-228 被引量:27
标识
DOI:10.1378/chest.08-2482
摘要

Our objective was to investigate the expression of survivin, Bcl-2, p53, Ki-67, and Src in thymic neoplasms and analyze their interrelationship with clinicopathologic variables.A series of 60 thymic neoplasms was reviewed and classified according to the World Health Organization (WHO) scheme. Key clinical information, including Masaoka stage, recurrence-free survival (RFS), and overall survival (OS) was obtained. The percentage and staining intensity of listed markers were recorded. The correlation of markers and clinicopathologic variables was statistically analyzed using the Fisher exact test and log-rank test.There were 7 type A, 15 type AB, 8 type B1, 5 type B2, 17 type B3 thymomas, and 8 thymic carcinomas. Seven patients (11.7%) died of the disease. Tumors recurred in eight patients (13.3%). Although p53 expression alone was found to be correlated with RFS with borderline significance (p = 0.056), patients with Src-positive and p53-positive coexpression had a shorter OS time than the other groups (p < 0.008). Cytoplasmic expression of survivin was present in 5 of 60 thymic neoplasms (8.3%), 4 of which were thymic carcinomas that all recurred.Regardless of WHO type and/or tumor stage, although p53 expression may predict recurrence in thymomas, p53 and Src coexpression can predict shorter OS, and cytoplasmic localization of survivin may predict recurrence in thymic carcinoma. These findings make thymic tumors a prime target for newly developed anti-Src and anti-survivin therapies.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
科目三应助加油女王采纳,获得10
刚刚
121完成签到,获得积分10
1秒前
G1234发布了新的文献求助10
1秒前
minyun完成签到,获得积分10
1秒前
ySX应助wzy采纳,获得10
1秒前
NexusExplorer应助支付宝采纳,获得10
2秒前
3秒前
3秒前
3秒前
尹英宇完成签到,获得积分10
3秒前
科研通AI6.4应助Mixrror采纳,获得10
3秒前
科研通AI6.4应助Mixrror采纳,获得10
4秒前
科研通AI6.2应助Mixrror采纳,获得10
4秒前
Morgan_Ruijie应助艺玲采纳,获得10
4秒前
大个应助Mixrror采纳,获得10
4秒前
科研通AI6.4应助Mixrror采纳,获得10
4秒前
科研通AI6.4应助Mixrror采纳,获得10
4秒前
折木浮华发布了新的文献求助10
4秒前
友好盼易完成签到 ,获得积分10
4秒前
李健应助Mixrror采纳,获得10
4秒前
科研通AI6.4应助Mixrror采纳,获得10
5秒前
NexusExplorer应助Mixrror采纳,获得10
5秒前
科研通AI6.4应助Mixrror采纳,获得10
5秒前
无花果应助Lipuer采纳,获得10
6秒前
科研通AI6.4应助轩轩采纳,获得10
6秒前
zhangyumi完成签到,获得积分10
7秒前
G1234完成签到,获得积分20
7秒前
微白完成签到,获得积分20
8秒前
Bean发布了新的文献求助200
8秒前
张经纬发布了新的文献求助10
9秒前
Ruo完成签到,获得积分10
9秒前
SEVEN驳回了bkagyin应助
9秒前
10秒前
甜美的谷云完成签到 ,获得积分10
10秒前
10秒前
11秒前
11秒前
13秒前
破罐子发布了新的文献求助20
13秒前
顽石发布了新的文献求助10
16秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Principles of town planning: translating concepts to applications 1000
Management and the Arts 510
Matrix Methods in Data Mining and Pattern Recognition Second Edition 510
核安全综合知识2024版 500
Photothermal Science and Techniques 500
Digital Displacement Hydrostatic Transmission for Rotorcraft and Distributed Propulsion 500
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 内科学 物理 复合材料 催化作用 细胞生物学 无机化学 光电子学 物理化学 电极 基因
热门帖子
关注 科研通微信公众号,转发送积分 7707755
求助须知:如何正确求助?哪些是违规求助? 9265209
关于积分的说明 20053372
捐赠科研通 7284216
什么是DOI,文献DOI怎么找? 3296106
关于科研通互助平台的介绍 2451002
邀请新用户注册赠送积分活动 2303106