EML4-ALK enhances programmed cell death-ligand 1 expression in pulmonary adenocarcinoma via hypoxia-inducible factor (HIF)-1α and STAT3-Reference-Cited by-同舟云学术

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EML4-ALK enhances programmed cell death-ligand 1 expression in pulmonary adenocarcinoma via hypoxia-inducible factor (HIF)-1α and STAT3

Published:2015-10-29 Issue:3 Volume:5 Page:e1108514
ISSN:2162-402X
Container-title:OncoImmunology
language:en
Short-container-title:OncoImmunology

Author:

Koh Jaemoon,Jang Ji-Young,Keam Bhumsuk,Kim Sehui,Kim Moon-Young,Go Heounjeong,Kim Tae Min,Kim Dong-Wan,Kim Chul-Woo,Jeon Yoon Kyung,Chung Doo Hyun

Publisher

Informa UK Limited

Subject

Oncology,Immunology,Immunology and Allergy

Link

http://www.tandfonline.com/doi/pdf/10.1080/2162402X.2015.1108514

Reference39 articles.

1. Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology

2. Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer

3. Molecular Testing Guideline for Selection of Lung Cancer Patients for EGFR and ALK Tyrosine Kinase Inhibitors: Guideline from the College of American Pathologists, International Association for the Study of Lung Cancer, and Association for Molecular Pathology

4. Comparative analyses of overall survival in patients with anaplastic lymphoma kinase-positive and matched wild-type advanced nonsmall cell lung cancer

5. Anaplastic Lymphoma Kinase Inhibition in Non–Small-Cell Lung Cancer

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