Advances of the Role of Lung Cancer Driver Gene and PD-1/PD-L1 Pathway Interaction in the Tumorigenesis and Progression of Non-small Cell Lung Cancer
Programmed death 1 (PD-1) and programmed death 1 ligand (PD-L1) pathway is a key mechanism of immune regulation, and its abnormal activation in tumor tissues suggests that PD-1/PD-L1 pathway may participate in the regulation of tumor immune escape. Driver gene mutation which is known as a key factor...
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Published in | Zhongguo fei ai za zhi Vol. 20; no. 11; pp. 781 - 786 |
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Main Authors | , , , |
Format | Journal Article |
Language | Chinese |
Published |
China
Chinese Anti-Cancer Association Chinese Antituberculosis Association
20.11.2017
Chinese Anti-Cancer Association; Chinese Antituberculosis Association |
Subjects | |
Online Access | Get full text |
ISSN | 1009-3419 1999-6187 1999-6187 |
DOI | 10.3779/j.issn.1009-3419.2017.11.10 |
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Summary: | Programmed death 1 (PD-1) and programmed death 1 ligand (PD-L1) pathway is a key mechanism of immune regulation, and its abnormal activation in tumor tissues suggests that PD-1/PD-L1 pathway may participate in the regulation of tumor immune escape. Driver gene mutation which is known as a key factor in the tumorigenesis of non-small cell lung cancer (NSCLC), was also reported to play a important role in the process of tumor immune escape. It indicates that there is an interaction between driver gene and PD-1/PD-L1 pathway. The purpose of this paper is to review the relationship between PD-1/PD-L1 pathway and lung cancer driver gene, such as epidermal growth factor receptor (EGFR), Kirsten rate sarcoma viral oncogene homolog (KRAS) and echinoderm microtubuleassociated protein-like 4 - anaplastic lymphoma kinase (EML4-ALK) and to summarize the role of lung cancer driver gene and PD-1/PD-L1 pathway interaction in the tumorigenesis and progression of NSCLC. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Review-3 content type line 23 |
ISSN: | 1009-3419 1999-6187 1999-6187 |
DOI: | 10.3779/j.issn.1009-3419.2017.11.10 |