scispace - formally typeset
S

Si-Yang Liu

Researcher at South China University of Technology

Publications -  59
Citations -  1762

Si-Yang Liu is an academic researcher from South China University of Technology. The author has contributed to research in topics: Lung cancer & Medicine. The author has an hindex of 13, co-authored 31 publications receiving 1003 citations. Previous affiliations of Si-Yang Liu include Peking Union Medical College & Guangdong General Hospital.

Papers
More filters
Journal ArticleDOI

EGFR mutation correlates with uninflamed phenotype and weak immunogenicity, causing impaired response to PD-1 blockade in non-small cell lung cancer

TL;DR: Evidence is provided of a correlation between EGFR mutations and an uninflamed tumor microenvironment with immunological tolerance and weak immunogenicity, which caused an inferior response to PD-1 blockade in NSCLCs.
Journal ArticleDOI

Strong Programmed Death Ligand 1 Expression Predicts Poor Response and De Novo Resistance to EGFR Tyrosine Kinase Inhibitors Among NSCLC Patients With EGFR Mutation.

TL;DR: The adverse effects of PD‐L1 expression on EGFR‐TKI efficacy, especially in NSCLC patients with de novo resistance, are revealed, indicating the reshaping of an inflamed immune phenotype characterized by PD‐ L1 and CD8 dual positivity and suggest potential therapeutic sensitivity to programmed death 1 blockade.
Journal ArticleDOI

Specific TP53 subtype as biomarker for immune checkpoint inhibitors in lung adenocarcinoma

TL;DR: This study demonstrated that not all TP53 mutations are equal in predicting efficacy in patients with LUAD treated with ICIs, and showed that TP53 missense and nonsense mutations were significantly different in associations with PD-L1 expression, IFN-γ signatures and TME composition.
Journal ArticleDOI

Acquired MET Y1248H and D1246N Mutations Mediate Resistance to MET Inhibitors in Non–Small Cell Lung Cancer

TL;DR: Insight is provided into the diversity of mechanisms underlying MET-TKI–induced resistance and the potential of sequential use ofMET-TKIs and it is discovered that EGFR amplification may act as an alternative MET- TKI resistance mechanism.