Evidence, Mechanism, and Clinical Relevance of the Transdifferentiation from Lung Adenocarcinoma to Squamous Cell Carcinoma
2017-05
发表期刊AMERICAN JOURNAL OF PATHOLOGY (IF:4.7[JCR-2023],4.8[5-Year])
ISSN0002-9440
卷号187期号:5页码:954-962
发表状态已发表
DOI10.1016/j.ajpath.2017.01.009
摘要Lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC) are two distinct subtypes of non-small-cell lung carcinoma. Interestingly, approximately 4% to 9% of human non small-cell lung carcinoma tumors contain mixed adenomatous and squamous pathologies in a single lesion, clinically termed adenosquamous cell carcinoma. More important, these two different pathological components frequently share identical oncogenic mutations, indicative of a potential transition. Indeed, recent data have provided convincing evidence in supporting the ADC to SCC transdifferentiation in lungs. In the liver kinase B1 (official name STK11)-deficient mouse model, lung ADC can progressively trans differentiate to SCC through pathologically mixed adenosquamous cell carcinoma as the intermediate status. Mechanistic studies further identify essential roles of extracellular matrix remodeling and metabolic reprogramming during this phenotypic transition. Small molecular compounds, including lysyl oxidase inhibitors and reactive oxygen species-inducing reagents such as phenformin, significantly accelerate the transition from Lung ADC to SCC and thus confer lung tumors with drug resistance. Consistent with these findings, recent clinical studies have shown that epidermal growth factor receptor mutant lung ADC can transdifferentate to SCC in relapsed cancer patients. Together, these data support that this phenotypic transition from lung ADC to SCC might represent a novel mechanism for drug resistance. This review will summarize our current understanding of the transdifferentiation from lung ADC to SCC.
收录类别SCI
语种英语
资助项目Science and Technology Commission of Shanghai Municipality grant[15XD1504000]
WOS研究方向Pathology
WOS类目Pathology
WOS记录号WOS:000400229600002
出版者ELSEVIER SCIENCE INC
WOS关键词TYROSINE KINASE INHIBITORS ; YES-ASSOCIATED PROTEIN ; PEUTZ-JEGHERS-SYNDROME ; ADENOSQUAMOUS CARCINOMA ; LYSYL OXIDASE ; EXTRACELLULAR-MATRIX ; CANCER PROGRESSION ; POOR-PROGNOSIS ; HISTOLOGIC TRANSFORMATION ; IMMUNOHISTOCHEMICAL PANEL
原始文献类型Review
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文献类型期刊论文
条目标识符https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/1396
专题生命科学与技术学院_特聘教授组_季红斌组
通讯作者Ji, Hongbin
作者单位
1.Chinese Acad Sci, Key Lab Syst Biol, Shanghai, Peoples R China
2.Chinese Acad Sci, Ctr Excellence Mol Cell Sci, Shanghai, Peoples R China
3.Chinese Acad Sci, Innovat Ctr Cell Signaling Network, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, Shanghai, Peoples R China
4.Univ Chinese Acad Sci, Beijing, Peoples R China
5.Shanghai Tech Univ, Sch Life Sci & Technol, Shanghai, Peoples R China
通讯作者单位生命科学与技术学院
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GB/T 7714
Hou, Shenda,Zhou, Shiyu,Qin, Zhen,et al. Evidence, Mechanism, and Clinical Relevance of the Transdifferentiation from Lung Adenocarcinoma to Squamous Cell Carcinoma[J]. AMERICAN JOURNAL OF PATHOLOGY,2017,187(5):954-962.
APA Hou, Shenda.,Zhou, Shiyu.,Qin, Zhen.,Yang, Liu.,Han, Xiangkun.,...&Ji, Hongbin.(2017).Evidence, Mechanism, and Clinical Relevance of the Transdifferentiation from Lung Adenocarcinoma to Squamous Cell Carcinoma.AMERICAN JOURNAL OF PATHOLOGY,187(5),954-962.
MLA Hou, Shenda,et al."Evidence, Mechanism, and Clinical Relevance of the Transdifferentiation from Lung Adenocarcinoma to Squamous Cell Carcinoma".AMERICAN JOURNAL OF PATHOLOGY 187.5(2017):954-962.
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