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Wenfeng Fang

Researcher at Sun Yat-sen University

Publications -  233
Citations -  6222

Wenfeng Fang is an academic researcher from Sun Yat-sen University. The author has contributed to research in topics: Lung cancer & Medicine. The author has an hindex of 33, co-authored 175 publications receiving 3993 citations. Previous affiliations of Wenfeng Fang include Wuhan University & University of Illinois at Chicago.

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Upregulation of PD-L1 by EGFR Activation Mediates the Immune Escape in EGFR-Driven NSCLC: Implication for Optional Immune Targeted Therapy for NSCLC Patients with EGFR Mutation

TL;DR: The results imply that EGFR-TKIs could not only directly inhibit tumor cell viability but also indirectly enhance antitumor immunity through the downregulation of PD-L1.
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Camrelizumab (SHR-1210) alone or in combination with gemcitabine plus cisplatin for nasopharyngeal carcinoma: results from two single-arm, phase 1 trials

TL;DR: This work presents safety and preliminary antitumour activity of camrelizumab alone as second-line therapy in patients with recurrent or metastatic nasopharyngeal carcinoma and combined with gemcitabine and cisplatin as first-line Therapy in this patient population.
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EBV-driven LMP1 and IFN-γ up-regulate PD-L1 in nasopharyngeal carcinoma: Implications for oncotargeted therapy

TL;DR: It is found that EBV-induced latent membrane protein 1 (LMP1) and IFN-γ pathways cooperate to regulate programmed cell death protein 1 ligand (PD-L1), which was higher in EBV positive NPC cell lines compared with EBV negative cell lines.
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The association between PD-L1 and EGFR status and the prognostic value of PD-L1 in advanced non-small cell lung cancer patients treated with EGFR-TKIs

TL;DR: High PD-L1 expression was likely to be associated with the presence of EGFR mutation in advanced lung adenocarcinoma, and this can be considered as a poor prognostic indicator of OS for EGFR wild-type patients.
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KRAS mutation-induced upregulation of PD-L1 mediates immune escape in human lung adenocarcinoma

TL;DR: It is demonstrated that KRAS mutation could induce PD-L1 expression through p-ERK signaling in lung adenocarcinoma and blockade of PD-1/PD- L1 pathway may be a promising therapeutic strategy for human KRAS-mutant lungAdenocARCinoma.