Hepatic Sarcomatoid Carcinoma Is an Aggressive Hepatic Neoplasm Sharing Common Molecular Features With Its Conventional Carcinomatous Counterparts

肉瘤样癌 肝细胞癌 病理 血液病理学 免疫组织化学 ARID1A型 生物 癌症研究 医学 突变 基因 生物化学 细胞遗传学 染色体
作者
Naomi Yoshuantari,Yung‐Ming Jeng,Jau‐Yu Liau,Chia-Hsiang Lee,Jia‐Huei Tsai
出处
期刊:Modern Pathology [Elsevier BV]
卷期号:36 (1): 100042-100042 被引量:4
标识
DOI:10.1016/j.modpat.2022.100042
摘要

Hepatic sarcomatoid carcinoma is a rare hepatic tumor with an aggressive clinical behavior and dismal outcome. However, the molecular pathogenesis is incompletely defined. In this study, we analyzed 59 hepatic sarcomatoid carcinomas using targeted next-generation sequencing and immunohistochemistry. A panel of 14 genes commonly mutated in primary liver carcinomas was examined. PD-L1 and loss of expression for switch/sucrose nonfermenting complexes, including BAP1, ARID1A, ARID2, and PBRM1, were detected by immunohistochemistry. The 59 hepatic sarcomatoid carcinomas encompass various carcinomatous subtypes and tumors with complete sarcomatoid transformation. Mutations in TP53 and promoter of TERT (pTERT) were frequently identified in sarcomatoid hepatocellular carcinoma, sarcomatoid combined hepatocellular cholangiocarcinoma, and hepatic sarcomatoid carcinomas with complete sarcomatoid transformation but rarely in sarcomatoid cholangiocarcinoma. Alterations involving switch/sucrose nonfermenting complexes were uncommon in hepatic sarcomatoid carcinoma (n = 2). PD-L1 expressed in tumor-associated immune cells in 67% of the tumors and in tumor cells in 33% of the tumors. A multivariate survival analysis indicated that PD-L1 expression in immune cells served as an independent favorable predictive factor of patient survival (P = .036). In conclusion, hepatic sarcomatoid carcinoma displays molecular similarity with its conventional carcinomatous counterparts. This finding suggests persistent genetic characteristics during sarcomatous evolution. PD-L1 expression in immune cells is a favorable prognostic factor for patient outcomes and may be a potential biomarker for immunotherapeutic treatment.
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
Akim应助风趣的梦露采纳,获得10
1秒前
白桃乌龙发布了新的文献求助10
4秒前
ccx981166完成签到,获得积分10
7秒前
111完成签到,获得积分10
8秒前
兼听则明应助AaronDP采纳,获得100
9秒前
小六子123完成签到,获得积分10
9秒前
宗师算个瓢啊完成签到 ,获得积分10
11秒前
fire完成签到 ,获得积分10
11秒前
雨齐完成签到,获得积分10
12秒前
13秒前
堀江真夏完成签到 ,获得积分10
14秒前
科研小裴完成签到 ,获得积分10
14秒前
折耳根完成签到 ,获得积分10
15秒前
卿卿完成签到,获得积分10
17秒前
Youlu发布了新的文献求助10
19秒前
帕尼灬尼完成签到,获得积分10
22秒前
ALIVE_STAR完成签到,获得积分10
23秒前
小二郎应助Youlu采纳,获得10
23秒前
中岛悠斗完成签到,获得积分10
24秒前
朴素的紫安完成签到 ,获得积分10
27秒前
无奈的铅笔完成签到,获得积分20
27秒前
30秒前
pluto应助无奈的铅笔采纳,获得10
31秒前
锦秋完成签到 ,获得积分10
32秒前
沉静大有发布了新的文献求助10
35秒前
所所应助夜猫酱酱子采纳,获得10
36秒前
Lucas应助高手采纳,获得10
38秒前
淡然珍完成签到,获得积分10
38秒前
沅宝完成签到 ,获得积分10
39秒前
可以的完成签到,获得积分10
44秒前
perfect完成签到 ,获得积分10
44秒前
务实的绝悟完成签到,获得积分10
46秒前
46秒前
科目三应助二甲亚砜2022采纳,获得10
47秒前
清颜完成签到 ,获得积分10
49秒前
50秒前
坦率完成签到,获得积分10
50秒前
阳光c完成签到 ,获得积分10
57秒前
58秒前
852应助科研通管家采纳,获得10
58秒前
高分求助中
【此为提示信息,请勿应助】请按要求发布求助,避免被关 20000
Technologies supporting mass customization of apparel: A pilot project 450
Mixing the elements of mass customisation 360
Периодизация спортивной тренировки. Общая теория и её практическое применение 310
the MD Anderson Surgical Oncology Manual, Seventh Edition 300
Nucleophilic substitution in azasydnone-modified dinitroanisoles 300
Political Ideologies Their Origins and Impact 13th Edition 260
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 物理 生物化学 纳米技术 计算机科学 化学工程 内科学 复合材料 物理化学 电极 遗传学 量子力学 基因 冶金 催化作用
热门帖子
关注 科研通微信公众号,转发送积分 3780920
求助须知:如何正确求助?哪些是违规求助? 3326387
关于积分的说明 10226987
捐赠科研通 3041612
什么是DOI,文献DOI怎么找? 1669520
邀请新用户注册赠送积分活动 799081
科研通“疑难数据库(出版商)”最低求助积分说明 758734