Single-cell transcriptome analysis revealed a suppressive tumor immune microenvironment in EGFR mutant lung adenocarcinoma

BackgroundsImmunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important...

Full description

Saved in:
Bibliographic Details
Published inJournal for immunotherapy of cancer Vol. 10; no. 2; p. e003534
Main Authors Yang, Lei, He, Yun-Ting, Dong, Song, Wei, Xue-Wu, Chen, Zhi-Hong, Zhang, Bo, Chen, Wei-Dong, Yang, Xiao-Rong, Wang, Fen, Shang, Xue-Meng, Zhong, Wen-Zhao, Wu, Yi-Long, Zhou, Qing
Format Journal Article
LanguageEnglish
Published England BMJ Publishing Group Ltd 01.01.2022
BMJ Publishing Group LTD
BMJ Publishing Group
SeriesOriginal research
Subjects
Adenocarcinoma of Lung - genetics
Adenocarcinoma of Lung - pathology
Biomarkers, Tumor - metabolism
Cancer
Cancer therapies
Chemotherapy
Cytokines
Epidermal growth factor
ErbB Receptors - genetics
Female
Fibroblasts
Genes
Humans
Immune Checkpoint Inhibitors - pharmacology
Immune Checkpoint Inhibitors - therapeutic use
Immunotherapy
Immunotherapy - methods
Immunotherapy Biomarkers
Kinases
Lung cancer
lung neoplasms
Lung Neoplasms - genetics
Lung Neoplasms - pathology
Lymphocytes
Male
Mutation
Neutrophils
Ontology
Patients
Prognosis
Single-Cell Analysis - methods
Transcriptome - genetics
Tumor Microenvironment
lung neoplasms
immunotherapy
tumor microenvironment
Online AccessGet full text

Cover

Abstract BackgroundsImmunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important factor to affect the efficacy of immunotherapy, tumor microenvironment (TME) characteristics of this subgroup of NSCLC are not comprehensively understood up to date. Hence, we initiated this study to describe the specific TME of EGFR-mutant lung adenocarcinoma (LUAD) from cellular compositional and functional perspectives to better understand the immune landscape of this most common subtype of NSCLC.MethodsWe used single-cell transcriptome sequencing and multiplex immunohistochemistry to investigate the immune microenvironment of EGFR-mutant and EGFR wild-type LUADs and determined the efficacy of immunotherapy. We analyzed single cells from nine treatment-naïve samples and compared them to three post-immunotherapy samples previously reported from single cell perspective using bioinformatics methods.ResultsWe found that EGFR-mutant malignant epithelial cells had similar characteristics to the epithelial cells in non-responders. EGFR-mutant LUAD lacked CD8+ tissue-resident memory (TRM) cells, which could promote tertiary lymphoid structure generation by secreting CXCL13. In addition, other cell types, including tumor-associated macrophages and cancer-associated fibroblasts, which are capable of recruiting, retaining, and expanding CD8+ TRM cells in the TME, were also deficient in EGFR-mutant LUAD. Furthermore, EGFR-mutant LUAD had significantly less crosstalk between T cells and other cell types via programmed cell death-1 (PD-1) and PD-L1 or other immune checkpoints compared with EGFR wild-type LUAD.ConclusionsOur findings provide a comprehensive understanding of the immune landscape of EGFR-mutant LUAD at the single-cell level. Based on the results, many cellular components might have negative impact on the specific TME of EGFR-mutant LUAD through influencing CD8+ TRM. Lack of CD8+ TRM might be a key factor responsible for the suppressive TME of EGFR-mutant LUAD.
AbstractList BackgroundsImmunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important factor to affect the efficacy of immunotherapy, tumor microenvironment (TME) characteristics of this subgroup of NSCLC are not comprehensively understood up to date. Hence, we initiated this study to describe the specific TME of EGFR-mutant lung adenocarcinoma (LUAD) from cellular compositional and functional perspectives to better understand the immune landscape of this most common subtype of NSCLC.MethodsWe used single-cell transcriptome sequencing and multiplex immunohistochemistry to investigate the immune microenvironment of EGFR-mutant and EGFR wild-type LUADs and determined the efficacy of immunotherapy. We analyzed single cells from nine treatment-naïve samples and compared them to three post-immunotherapy samples previously reported from single cell perspective using bioinformatics methods.ResultsWe found that EGFR-mutant malignant epithelial cells had similar characteristics to the epithelial cells in non-responders. EGFR-mutant LUAD lacked CD8+ tissue-resident memory (TRM) cells, which could promote tertiary lymphoid structure generation by secreting CXCL13. In addition, other cell types, including tumor-associated macrophages and cancer-associated fibroblasts, which are capable of recruiting, retaining, and expanding CD8+ TRM cells in the TME, were also deficient in EGFR-mutant LUAD. Furthermore, EGFR-mutant LUAD had significantly less crosstalk between T cells and other cell types via programmed cell death-1 (PD-1) and PD-L1 or other immune checkpoints compared with EGFR wild-type LUAD.ConclusionsOur findings provide a comprehensive understanding of the immune landscape of EGFR-mutant LUAD at the single-cell level. Based on the results, many cellular components might have negative impact on the specific TME of EGFR-mutant LUAD through influencing CD8+ TRM. Lack of CD8+ TRM might be a key factor responsible for the suppressive TME of EGFR-mutant LUAD.
Immunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important factor to affect the efficacy of immunotherapy, tumor microenvironment (TME) characteristics of this subgroup of NSCLC are not comprehensively understood up to date. Hence, we initiated this study to describe the specific TME of EGFR-mutant lung adenocarcinoma (LUAD) from cellular compositional and functional perspectives to better understand the immune landscape of this most common subtype of NSCLC. We used single-cell transcriptome sequencing and multiplex immunohistochemistry to investigate the immune microenvironment of EGFR-mutant and EGFR wild-type LUADs and determined the efficacy of immunotherapy. We analyzed single cells from nine treatment-naïve samples and compared them to three post-immunotherapy samples previously reported from single cell perspective using bioinformatics methods. We found that EGFR-mutant malignant epithelial cells had similar characteristics to the epithelial cells in non-responders. EGFR-mutant LUAD lacked CD8 tissue-resident memory (TRM) cells, which could promote tertiary lymphoid structure generation by secreting CXCL13. In addition, other cell types, including tumor-associated macrophages and cancer-associated fibroblasts, which are capable of recruiting, retaining, and expanding CD8 TRM cells in the TME, were also deficient in EGFR-mutant LUAD. Furthermore, EGFR-mutant LUAD had significantly less crosstalk between T cells and other cell types via programmed cell death-1 (PD-1) and PD-L1 or other immune checkpoints compared with EGFR wild-type LUAD. Our findings provide a comprehensive understanding of the immune landscape of EGFR-mutant LUAD at the single-cell level. Based on the results, many cellular components might have negative impact on the specific TME of EGFR-mutant LUAD through influencing CD8 TRM. Lack of CD8 TRM might be a key factor responsible for the suppressive TME of EGFR-mutant LUAD.
Immunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important factor to affect the efficacy of immunotherapy, tumor microenvironment (TME) characteristics of this subgroup of NSCLC are not comprehensively understood up to date. Hence, we initiated this study to describe the specific TME of EGFR-mutant lung adenocarcinoma (LUAD) from cellular compositional and functional perspectives to better understand the immune landscape of this most common subtype of NSCLC.BACKGROUNDSImmunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important factor to affect the efficacy of immunotherapy, tumor microenvironment (TME) characteristics of this subgroup of NSCLC are not comprehensively understood up to date. Hence, we initiated this study to describe the specific TME of EGFR-mutant lung adenocarcinoma (LUAD) from cellular compositional and functional perspectives to better understand the immune landscape of this most common subtype of NSCLC.We used single-cell transcriptome sequencing and multiplex immunohistochemistry to investigate the immune microenvironment of EGFR-mutant and EGFR wild-type LUADs and determined the efficacy of immunotherapy. We analyzed single cells from nine treatment-naïve samples and compared them to three post-immunotherapy samples previously reported from single cell perspective using bioinformatics methods.METHODSWe used single-cell transcriptome sequencing and multiplex immunohistochemistry to investigate the immune microenvironment of EGFR-mutant and EGFR wild-type LUADs and determined the efficacy of immunotherapy. We analyzed single cells from nine treatment-naïve samples and compared them to three post-immunotherapy samples previously reported from single cell perspective using bioinformatics methods.We found that EGFR-mutant malignant epithelial cells had similar characteristics to the epithelial cells in non-responders. EGFR-mutant LUAD lacked CD8+ tissue-resident memory (TRM) cells, which could promote tertiary lymphoid structure generation by secreting CXCL13. In addition, other cell types, including tumor-associated macrophages and cancer-associated fibroblasts, which are capable of recruiting, retaining, and expanding CD8+ TRM cells in the TME, were also deficient in EGFR-mutant LUAD. Furthermore, EGFR-mutant LUAD had significantly less crosstalk between T cells and other cell types via programmed cell death-1 (PD-1) and PD-L1 or other immune checkpoints compared with EGFR wild-type LUAD.RESULTSWe found that EGFR-mutant malignant epithelial cells had similar characteristics to the epithelial cells in non-responders. EGFR-mutant LUAD lacked CD8+ tissue-resident memory (TRM) cells, which could promote tertiary lymphoid structure generation by secreting CXCL13. In addition, other cell types, including tumor-associated macrophages and cancer-associated fibroblasts, which are capable of recruiting, retaining, and expanding CD8+ TRM cells in the TME, were also deficient in EGFR-mutant LUAD. Furthermore, EGFR-mutant LUAD had significantly less crosstalk between T cells and other cell types via programmed cell death-1 (PD-1) and PD-L1 or other immune checkpoints compared with EGFR wild-type LUAD.Our findings provide a comprehensive understanding of the immune landscape of EGFR-mutant LUAD at the single-cell level. Based on the results, many cellular components might have negative impact on the specific TME of EGFR-mutant LUAD through influencing CD8+ TRM. Lack of CD8+ TRM might be a key factor responsible for the suppressive TME of EGFR-mutant LUAD.CONCLUSIONSOur findings provide a comprehensive understanding of the immune landscape of EGFR-mutant LUAD at the single-cell level. Based on the results, many cellular components might have negative impact on the specific TME of EGFR-mutant LUAD through influencing CD8+ TRM. Lack of CD8+ TRM might be a key factor responsible for the suppressive TME of EGFR-mutant LUAD.
Backgrounds Immunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell death-ligand 1 (PD-L1) expression and tumor mutation burden (TMB) are reported to be the underlying mechanism. Being another important factor to affect the efficacy of immunotherapy, tumor microenvironment (TME) characteristics of this subgroup of NSCLC are not comprehensively understood up to date. Hence, we initiated this study to describe the specific TME of EGFR-mutant lung adenocarcinoma (LUAD) from cellular compositional and functional perspectives to better understand the immune landscape of this most common subtype of NSCLC.Methods We used single-cell transcriptome sequencing and multiplex immunohistochemistry to investigate the immune microenvironment of EGFR-mutant and EGFR wild-type LUADs and determined the efficacy of immunotherapy. We analyzed single cells from nine treatment-naïve samples and compared them to three post-immunotherapy samples previously reported from single cell perspective using bioinformatics methods.Results We found that EGFR-mutant malignant epithelial cells had similar characteristics to the epithelial cells in non-responders. EGFR-mutant LUAD lacked CD8+ tissue-resident memory (TRM) cells, which could promote tertiary lymphoid structure generation by secreting CXCL13. In addition, other cell types, including tumor-associated macrophages and cancer-associated fibroblasts, which are capable of recruiting, retaining, and expanding CD8+ TRM cells in the TME, were also deficient in EGFR-mutant LUAD. Furthermore, EGFR-mutant LUAD had significantly less crosstalk between T cells and other cell types via programmed cell death-1 (PD-1) and PD-L1 or other immune checkpoints compared with EGFR wild-type LUAD.Conclusions Our findings provide a comprehensive understanding of the immune landscape of EGFR-mutant LUAD at the single-cell level. Based on the results, many cellular components might have negative impact on the specific TME of EGFR-mutant LUAD through influencing CD8+ TRM. Lack of CD8+ TRM might be a key factor responsible for the suppressive TME of EGFR-mutant LUAD.
Author Wu, Yi-Long
Zhou, Qing
Chen, Wei-Dong
He, Yun-Ting
Shang, Xue-Meng
Yang, Xiao-Rong
Yang, Lei
Zhang, Bo
Wang, Fen
Wei, Xue-Wu
Dong, Song
Chen, Zhi-Hong
Zhong, Wen-Zhao
AuthorAffiliation 1 Guangdong Lung Cancer Institute , Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences , Guangzhou , China
3 Novel Bioinformatics Co , Shanghai , China
2 The Second School of Clinical Medicine , Southern Medical University , Guangzhou , China
4 Panovue Biological Technology Co , Beijing , China
AuthorAffiliation_xml – name: 3 Novel Bioinformatics Co , Shanghai , China
– name: 4 Panovue Biological Technology Co , Beijing , China
– name: 1 Guangdong Lung Cancer Institute , Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences , Guangzhou , China
– name: 2 The Second School of Clinical Medicine , Southern Medical University , Guangzhou , China
Author_xml – sequence: 1
  givenname: Lei
  orcidid: 0000-0001-6888-2036
  surname: Yang
  fullname: Yang, Lei
  organization: The Second School of Clinical Medicine, Southern Medical University, Guangzhou, China
– sequence: 2
  givenname: Yun-Ting
  surname: He
  fullname: He, Yun-Ting
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 3
  givenname: Song
  surname: Dong
  fullname: Dong, Song
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 4
  givenname: Xue-Wu
  surname: Wei
  fullname: Wei, Xue-Wu
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 5
  givenname: Zhi-Hong
  surname: Chen
  fullname: Chen, Zhi-Hong
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 6
  givenname: Bo
  surname: Zhang
  fullname: Zhang, Bo
  organization: Novel Bioinformatics Co, Shanghai, China
– sequence: 7
  givenname: Wei-Dong
  surname: Chen
  fullname: Chen, Wei-Dong
  organization: Novel Bioinformatics Co, Shanghai, China
– sequence: 8
  givenname: Xiao-Rong
  surname: Yang
  fullname: Yang, Xiao-Rong
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 9
  givenname: Fen
  orcidid: 0000-0002-4876-710X
  surname: Wang
  fullname: Wang, Fen
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 10
  givenname: Xue-Meng
  surname: Shang
  fullname: Shang, Xue-Meng
  organization: Panovue Biological Technology Co, Beijing, China
– sequence: 11
  givenname: Wen-Zhao
  surname: Zhong
  fullname: Zhong, Wen-Zhao
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 12
  givenname: Yi-Long
  orcidid: 0000-0002-3611-0258
  surname: Wu
  fullname: Wu, Yi-Long
  organization: Guangdong Lung Cancer Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 13
  givenname: Qing
  orcidid: 0000-0002-0478-176X
  surname: Zhou
  fullname: Zhou, Qing
  email: gzzhouqing@126.com
  organization: The Second School of Clinical Medicine, Southern Medical University, Guangzhou, China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35140113$$D View this record in MEDLINE/PubMed
BookMark eNp9kstrFTEUxgep2Fq7dyUBNy4czWtmMhuhlLYWCoKPdTjJZK65TJJrkrlQ_3ozTq1tQVd5_b6Pc3K-59WBD95U1UuC3xHC2vdbm3VNMSU1xqxh_El1RHFDasJpe3Bvf1idpLTFGBPMmBDiWXXIGsJxMTmqfn6xfjOZWptpQjmCTzraXQ7OIPAw3SSbUDR7A5MZEKA073bRpGT3BuXZhYisc7M3yFkdg_F7G4N3xmdkPTq_vPiM3JyhHKfZbxAMxgcNUVsfHLyono4wJXNyux5X3y7Ov559rK8_XV6dnV7XqulZrnXDREc6EGPX9mToBQbVAVGiG6hglBPTD5yDZlzzlqimazmh0JtedGqkAthxdbX6DgG2chetg3gjA1j5-yLEjYSYrZ6MHNuGMqq0blTxVK3qqcLQM2gHPoxGF68Pq9duVs4MunQaYXpg-vDF2-9yE_ZSCIYZb4vBm1uDGH7MJmXpbFo-H7wJc5K0pR0vbWFR0NeP0G2YYxnKSuEC9U2hXt2v6K6UPyMuAF6BMqCUohnvEILlEiS5BEkuQZJrkIqkfSTRNkO2YenJTv8Tvl2Fym3_VvtP_BdzJN1C
CitedBy_id crossref_primary_10_1016_j_ctrv_2023_102602
crossref_primary_10_1007_s10238_023_01240_9
crossref_primary_10_3389_fimmu_2025_1555216
crossref_primary_10_3390_medicina59071277
crossref_primary_10_1155_2023_4689004
crossref_primary_10_18632_aging_204938
crossref_primary_10_2147_ITT_S494670
crossref_primary_10_3389_fimmu_2023_1238454
crossref_primary_10_3390_ijms24032943
crossref_primary_10_1002_advs_202405130
crossref_primary_10_1038_s41598_024_69020_3
crossref_primary_10_1111_cas_15848
crossref_primary_10_1007_s00432_022_04498_w
crossref_primary_10_3389_fonc_2024_1390523
crossref_primary_10_1016_j_biopha_2023_115513
crossref_primary_10_1016_j_heliyon_2024_e27586
crossref_primary_10_1002_mog2_70012
crossref_primary_10_1097_CM9_0000000000003187
crossref_primary_10_1007_s00109_022_02266_4
crossref_primary_10_1016_S1470_2045_24_00379_6
crossref_primary_10_1016_j_tranon_2024_102074
crossref_primary_10_1186_s40537_024_00945_2
crossref_primary_10_3892_ol_2024_14476
crossref_primary_10_18632_aging_204890
crossref_primary_10_3389_fmed_2023_1191019
crossref_primary_10_3390_ijms25179502
crossref_primary_10_3390_cancers16223765
crossref_primary_10_1002_cam4_6914
crossref_primary_10_1007_s10142_023_01245_3
crossref_primary_10_3390_biom13010185
crossref_primary_10_1007_s10142_023_01056_6
crossref_primary_10_1007_s12672_024_01325_1
crossref_primary_10_1111_jcmm_18346
crossref_primary_10_3389_fonc_2024_1331128
crossref_primary_10_1186_s12915_024_01866_5
crossref_primary_10_3389_fimmu_2023_1137880
crossref_primary_10_1016_j_semcancer_2025_01_001
crossref_primary_10_1016_j_cell_2024_02_005
crossref_primary_10_1080_14737140_2023_2170879
crossref_primary_10_1186_s12967_024_05135_5
crossref_primary_10_1080_2162402X_2024_2340154
crossref_primary_10_1186_s12885_025_13497_2
crossref_primary_10_1002_2211_5463_13970
crossref_primary_10_1186_s41065_023_00307_7
crossref_primary_10_1038_s41392_024_02045_2
crossref_primary_10_3390_biomedicines11112916
crossref_primary_10_3390_cells12071086
crossref_primary_10_1186_s40001_023_01195_3
crossref_primary_10_1016_j_tranon_2025_102364
crossref_primary_10_1016_j_tips_2024_04_006
crossref_primary_10_3389_fimmu_2023_1170321
crossref_primary_10_2174_0113862073282003240119064337
crossref_primary_10_1002_ctm2_1199
crossref_primary_10_1002_adbi_202300190
crossref_primary_10_18632_aging_204752
crossref_primary_10_18632_aging_205840
crossref_primary_10_3390_ijms23126489
crossref_primary_10_1186_s12957_025_03701_9
crossref_primary_10_1186_s13008_024_00112_2
crossref_primary_10_1016_j_lungcan_2024_107933
crossref_primary_10_1016_j_lungcan_2024_107815
crossref_primary_10_3389_fgene_2022_988703
crossref_primary_10_12677_ACM_2024_141027
crossref_primary_10_3389_fimmu_2022_983570
crossref_primary_10_3390_cancers15102858
crossref_primary_10_3389_fimmu_2024_1416751
crossref_primary_10_1177_17588359221144099
crossref_primary_10_3389_fimmu_2023_1094764
crossref_primary_10_1038_s41392_024_01799_z
crossref_primary_10_1007_s10142_023_01281_z
crossref_primary_10_3389_fimmu_2023_1119383
crossref_primary_10_1007_s11864_023_01132_w
crossref_primary_10_1038_s41698_025_00842_8
crossref_primary_10_1016_j_ejca_2024_114184
crossref_primary_10_1038_s41598_025_91401_5
crossref_primary_10_3389_fimmu_2022_940288
crossref_primary_10_1016_j_heliyon_2024_e35529
crossref_primary_10_1016_j_jncc_2024_06_004
crossref_primary_10_1038_s41571_022_00718_x
crossref_primary_10_1186_s12967_024_05400_7
crossref_primary_10_1016_j_canlet_2024_217278
crossref_primary_10_3233_CBM_230036
crossref_primary_10_1177_17588359231193726
crossref_primary_10_1111_crj_70037
crossref_primary_10_3389_fimmu_2024_1320244
crossref_primary_10_1016_j_ejca_2023_113469
crossref_primary_10_18632_aging_204923
crossref_primary_10_3390_cancers15102749
crossref_primary_10_3390_ijms26020583
crossref_primary_10_1016_j_jncc_2022_10_002
crossref_primary_10_3390_biom14121523
crossref_primary_10_1002_advs_202308892
crossref_primary_10_1186_s12885_024_12136_6
crossref_primary_10_1016_j_tranon_2025_102280
crossref_primary_10_3389_fgene_2022_986453
Cites_doi 10.1172/jci.insight.136417
10.1016/j.celrep.2018.07.097
10.1080/2162402X.2017.1328337
10.1002/stem.1251
10.1016/j.ccell.2019.02.008
10.1016/j.neo.2016.08.002
10.1080/2162402X.2017.1356145
10.1111/imr.12644
10.1158/0008-5472.CAN-17-0348
10.1016/S2213-2600(19)30084-0
10.1016/j.ccell.2019.05.004
10.1073/pnas.1320318110
10.1189/jlb.3MR1216-523R
10.1038/s41467-020-19973-6
10.1158/1078-0432.CCR-19-1868
10.3390/ijms19113595
10.1038/srep22288
10.1016/j.canlet.2006.12.012
10.1186/s13073-020-00780-z
10.1038/cr.2017.34
10.1038/s41571-020-0333-y
10.1158/1078-0432.CCR-18-4142
10.1038/s41591-020-1086-y
10.1001/jamaoncol.2019.2187
10.1016/j.jtho.2018.09.012
10.3109/08830185.2012.679989
10.1158/1078-0432.CCR-18-1294
10.1158/1078-0432.CCR-17-2257
10.1038/ni.3775
10.1038/s41590-020-0765-7
10.1016/j.stem.2014.06.008
10.1002/eji.200838289
10.1158/2326-6066.CIR-18-0517
10.1038/s41586-019-1922-8
10.1042/BSR20182361
10.4049/jimmunol.1400551
10.1016/j.yexmp.2015.11.021
10.1038/onc.2016.367
10.2217/fon-2018-0639
10.1002/ijc.23392
10.1016/j.xcrm.2020.100127
10.1186/s40425-018-0399-6
10.1016/j.bbrc.2009.02.149
10.7554/eLife.54542
10.1172/JCI77053
10.1136/jitc-2020-002312
10.1136/jitc-2020-000778
10.1172/JCI91561
10.1158/1078-0432.CCR-10-3346
10.1007/s12016-019-08753-w
10.1016/j.ccell.2018.01.011
10.1093/annonc/mdz394.029
ContentType Journal Article
Copyright Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
2022 Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. 2022
Copyright_xml – notice: Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
– notice: 2022 Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/ . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
– notice: Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ. 2022
DBID 9YT
ACMMV
AAYXX
CITATION
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7X7
7XB
88E
8FI
8FJ
8FK
ABUWG
AFKRA
AZQEC
BENPR
CCPQU
DWQXO
FYUFA
GHDGH
K9.
M0S
M1P
PHGZM
PHGZT
PIMPY
PJZUB
PKEHL
PPXIY
PQEST
PQQKQ
PQUKI
PRINS
7X8
5PM
DOA
DOI 10.1136/jitc-2021-003534
DatabaseName BMJ Open Access Journals
BMJ Journals:Open Access
CrossRef
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
ProQuest Central (Corporate)
Health & Medical Collection
ProQuest Central (purchase pre-March 2016)
Medical Database (Alumni Edition)
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
Proquest Central
ProQuest One
ProQuest Central
Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Health & Medical Complete (Alumni)
ProQuest Health & Medical Collection
Medical Database
ProQuest Central Premium
ProQuest One Academic (New)
Publicly Available Content Database
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Academic
ProQuest One Academic UKI Edition
ProQuest Central China
MEDLINE - Academic
PubMed Central (Full Participant titles)
DOAJ Directory of Open Access Journals
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Publicly Available Content Database
ProQuest One Academic Middle East (New)
ProQuest Central Essentials
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
ProQuest Central China
ProQuest Central
ProQuest Health & Medical Research Collection
Health Research Premium Collection
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
Health & Medical Research Collection
ProQuest Central (New)
ProQuest Medical Library (Alumni)
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
ProQuest Hospital Collection (Alumni)
ProQuest Health & Medical Complete
ProQuest Medical Library
ProQuest One Academic UKI Edition
ProQuest One Academic
ProQuest One Academic (New)
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList Publicly Available Content Database
MEDLINE
MEDLINE - Academic
Database_xml – sequence: 1
  dbid: DOA
  name: DOAJ Directory of Open Access Journals
  url: https://www.doaj.org/
  sourceTypes: Open Website
– sequence: 2
  dbid: NPM
  name: PubMed
  url: https://proxy.k.utb.cz/login?url=http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 3
  dbid: EIF
  name: MEDLINE
  url: https://proxy.k.utb.cz/login?url=https://www.webofscience.com/wos/medline/basic-search
  sourceTypes: Index Database
– sequence: 4
  dbid: ACMMV
  name: BMJ Journals:Open Access
  url: https://journals.bmj.com/
  sourceTypes: Publisher
– sequence: 5
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 2051-1426
ExternalDocumentID oai_doaj_org_article_f65232bcc5bd44b6b92b0a93a6d4dfec
PMC8830346
35140113
10_1136_jitc_2021_003534
jitc
Genre Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: The High-level Hospital Construction Project
  grantid: DFJH201810
– fundername: The National Natural Science Foundation of China
  grantid: 82072562
– fundername: GDPH Scientific Research Funds for Leading Medical Talents in Guangdong Province
  grantid: KJ012019428
– fundername: ;
  grantid: 82072562
– fundername: ;
  grantid: KJ012019428
– fundername: ;
  grantid: DFJH201810
GroupedDBID 4.4
53G
5VS
7X7
88E
8FI
8FJ
9YT
ABUWG
ACGFS
ACMMV
ADBBV
ADRAZ
AFKRA
AHBYD
AHYZX
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AMKLP
AOIJS
ASPBG
AVWKF
BAWUL
BCNDV
BENPR
BFQNJ
BMC
BPHCQ
BVXVI
C6C
CCPQU
DIK
EBS
FYUFA
GROUPED_DOAJ
HMCUK
HYE
IAO
IHR
IHW
INH
INR
KQ8
M1P
M48
M~E
OK1
PHGZT
PIMPY
PQQKQ
PROAC
PSQYO
RBZ
RMJ
RPM
RSV
SOJ
UKHRP
AAYXX
ADUKV
AHSBF
CITATION
EJD
H13
ITC
PHGZM
ROL
CGR
CUY
CVF
ECM
EIF
NPM
PJZUB
PPXIY
3V.
7XB
8FK
AZQEC
DWQXO
K9.
PKEHL
PQEST
PQUKI
PRINS
7X8
5PM
PUEGO
ID FETCH-LOGICAL-b593t-c538717a8f7691d980ab7a1b87d283241e9d44ac34c461b576412a9e987bf28a3
IEDL.DBID M48
ISSN 2051-1426
IngestDate Wed Aug 27 01:29:04 EDT 2025
Thu Aug 21 18:02:13 EDT 2025
Fri Jul 11 04:56:00 EDT 2025
Fri Jul 25 22:58:49 EDT 2025
Mon Jul 21 06:05:19 EDT 2025
Tue Jul 01 01:55:56 EDT 2025
Thu Apr 24 23:11:46 EDT 2025
Thu Apr 24 22:50:17 EDT 2025
IsDoiOpenAccess true
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords lung neoplasms
immunotherapy
tumor microenvironment
Language English
License This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.
Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-b593t-c538717a8f7691d980ab7a1b87d283241e9d44ac34c461b576412a9e987bf28a3
Notes Original research
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ORCID 0000-0001-6888-2036
0000-0002-3611-0258
0000-0002-0478-176X
0000-0002-4876-710X
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.1136/jitc-2021-003534
PMID 35140113
PQID 2627032095
PQPubID 2040222
ParticipantIDs doaj_primary_oai_doaj_org_article_f65232bcc5bd44b6b92b0a93a6d4dfec
pubmedcentral_primary_oai_pubmedcentral_nih_gov_8830346
proquest_miscellaneous_2627483208
proquest_journals_2627032095
pubmed_primary_35140113
crossref_primary_10_1136_jitc_2021_003534
crossref_citationtrail_10_1136_jitc_2021_003534
bmj_journals_10_1136_jitc_2021_003534
ProviderPackageCode CITATION
AAYXX
PublicationCentury 2000
PublicationDate 2022-01-01
PublicationDateYYYYMMDD 2022-01-01
PublicationDate_xml – month: 01
  year: 2022
  text: 2022-01-01
  day: 01
PublicationDecade 2020
PublicationPlace England
PublicationPlace_xml – name: England
– name: London
– name: BMA House, Tavistock Square, London, WC1H 9JR
PublicationSeriesTitle Original research
PublicationTitle Journal for immunotherapy of cancer
PublicationTitleAbbrev J Immunother Cancer
PublicationTitleAlternate J Immunother Cancer
PublicationYear 2022
Publisher BMJ Publishing Group Ltd
BMJ Publishing Group LTD
BMJ Publishing Group
Publisher_xml – name: BMJ Publishing Group Ltd
– name: BMJ Publishing Group LTD
– name: BMJ Publishing Group
References Andersson, Srivastava, Harris-White (R29) 2011; 17
Zhou, Yue, Murphy (R34) 2014; 15
Eruslanov, Bhojnagarwala, Quatromoni (R49) 2014; 124
(R4) 2019; 30
Han, Kim, Lee (R27) 2009; 382
Zhang, Yang, Wang (R33) 2020; 11
Dong, Yang, Li (R45) 2016; 100
Huang, Lei, Zhao (R24) 2007; 252
Reck, Mok, Nishio (R6) 2019; 7
Timperi, Focaccetti, Gallerano (R13) 2017; 6
Toki, Mani, Smithy (R3) 2018; 13
Tan, Hiwa, Mueller (R32) 2020; 21
Tremblay, Viala, Shafer (R40) 2020; 9
Ye, Kuang, Xie (R35) 2020; 12
Topalian, Hodi, Brahmer (R1) 2019; 5
Burkhardt, Maravillas-Montero, Carnevale (R22) 2014; 193
Feig, Jones, Kraman (R38) 2013; 110
Li, Gu (R2) 2019; 15
Byrne, Savas, Sant (R18) 2020; 17
Yarchoan, Ho, Mohan (R39) 2020; 5
Mizukami, Kono, Kawaguchi (R47) 2008; 122
Workel, Lubbers, Arnold (R19) 2019; 7
Papaccio, Della Corte, Viscardi (R41) 2018; 19
Ganesan, Clarke, Wood (R52) 2017; 18
House, Savas, Lai (R31) 2020; 26
Yang, Wang, Ren (R14) 2012; 31
Corgnac, Malenica, Mezquita (R17) 2020; 1
Apte, Voronov (R11) 2017; 102
Cham, Driessens, O'Keefe (R15) 2008; 38
Raeber, Zurbuchen, Impellizzieri (R12) 2018; 283
Komi, Redegeld (R50) 2020; 58
Garrido-Martin, Mellows, Clarke (R30) 2020; 8
Datar, Sanmamed, Wang (R51) 2019; 25
Dong, Zhang, Liu (R5) 2017; 6
Liao, Overman, Boutin (R9) 2019; 35
Maeda, Enomoto, Hara (R42) 2016; 6
Gao, Navai, Alhalabi (R46) 2020; 26
Zhu, Padgett, Dinh (R48) 2018; 24
Mami-Chouaib, Blanc, Corgnac (R44) 2018; 6
Su, Liao, Liu (R8) 2017; 27
Zhang, Ye, Li (R21) 2017; 36
Blattner, Fleming, Weber (R23) 2018; 78
Helmink, Reddy, Gao (R20) 2020; 577
Edwards, Wilmott, Madore (R16) 2018; 24
Costa, Kieffer, Scholer-Dahirel (R37) 2018; 33
Zhang, Yin, Liu (R7) 2021; 9
Sjöberg, Meyrath, Milde (R36) 2019; 25
Dangaj, Bruand, Grimm (R28) 2019; 35
Miyake, Hori, Morizawa (R10) 2016; 18
Gjorgjevski, Hannen, Carl (R25) 2019; 39
Ratnam, Peterson, Talbert (R26) 2017; 127
Shangguan, Ti, Krause (R43) 2012; 30
2024053111345217000_10.2.e003534.51
2024053111345217000_10.2.e003534.50
2024053111345217000_10.2.e003534.15
Tan (2024053111345217000_10.2.e003534.32) 2020; 21
2024053111345217000_10.2.e003534.12
2024053111345217000_10.2.e003534.11
2024053111345217000_10.2.e003534.10
2024053111345217000_10.2.e003534.52
Yarchoan (2024053111345217000_10.2.e003534.39) 2020; 5
Byrne (2024053111345217000_10.2.e003534.18) 2020; 17
2024053111345217000_10.2.e003534.49
Dong (2024053111345217000_10.2.e003534.45) 2016; 100
Helmink (2024053111345217000_10.2.e003534.20) 2020; 577
Zhang (2024053111345217000_10.2.e003534.21) 2017; 36
Zhang (2024053111345217000_10.2.e003534.33) 2020; 11
2024053111345217000_10.2.e003534.47
Su (2024053111345217000_10.2.e003534.8) 2017; 27
2024053111345217000_10.2.e003534.44
2024053111345217000_10.2.e003534.43
Garrido-Martin (2024053111345217000_10.2.e003534.30) 2020; 8
Tremblay (2024053111345217000_10.2.e003534.40) 2020; 9
2024053111345217000_10.2.e003534.38
Reck (2024053111345217000_10.2.e003534.6) 2019; 7
2024053111345217000_10.2.e003534.37
2024053111345217000_10.2.e003534.36
Toki (2024053111345217000_10.2.e003534.3) 2018; 13
2024053111345217000_10.2.e003534.34
Corgnac (2024053111345217000_10.2.e003534.17) 2020; 1
Topalian (2024053111345217000_10.2.e003534.1) 2019; 5
2024053111345217000_10.2.e003534.31
Gao (2024053111345217000_10.2.e003534.46) 2020; 26
Yang (2024053111345217000_10.2.e003534.14) 2012; 31
2024053111345217000_10.2.e003534.29
2024053111345217000_10.2.e003534.28
2024053111345217000_10.2.e003534.27
Maeda (2024053111345217000_10.2.e003534.42) 2016; 6
Ratnam (2024053111345217000_10.2.e003534.26) 2017; 127
Zhu (2024053111345217000_10.2.e003534.48) 2018; 24
Li (2024053111345217000_10.2.e003534.2) 2019; 15
2024053111345217000_10.2.e003534.25
2024053111345217000_10.2.e003534.24
2024053111345217000_10.2.e003534.23
2024053111345217000_10.2.e003534.22
2024053111345217000_10.2.e003534.19
Papaccio (2024053111345217000_10.2.e003534.41) 2018; 19
2024053111345217000_10.2.e003534.16
2024053111345217000_10.2.e003534.5
2024053111345217000_10.2.e003534.4
Timperi (2024053111345217000_10.2.e003534.13) 2017; 6
Ye (2024053111345217000_10.2.e003534.35) 2020; 12
2024053111345217000_10.2.e003534.9
2024053111345217000_10.2.e003534.7
References_xml – volume: 5
  year: 2020
  ident: R39
  article-title: Effects of B cell-activating factor on tumor immunity
  publication-title: JCI Insight
  doi: 10.1172/jci.insight.136417
– volume: 24
  start-page: 2329
  year: 2018
  ident: R48
  article-title: Identification of an early Unipotent neutrophil progenitor with pro-tumoral activity in mouse and human bone marrow
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2018.07.097
– volume: 6
  year: 2017
  ident: R13
  article-title: IL-18 receptor marks functional CD8+ T cells in non-small cell lung cancer
  publication-title: Oncoimmunology
  doi: 10.1080/2162402X.2017.1328337
– volume: 30
  start-page: 2810
  year: 2012
  ident: R43
  article-title: Inhibition of TGF-β/Smad signaling by BAMBI blocks differentiation of human mesenchymal stem cells to carcinoma-associated fibroblasts and abolishes their protumor effects
  publication-title: Stem Cells
  doi: 10.1002/stem.1251
– volume: 35
  start-page: 559
  year: 2019
  ident: R9
  article-title: KRAS-IRF2 axis drives immune suppression and immune therapy resistance in colorectal cancer
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2019.02.008
– volume: 18
  start-page: 636
  year: 2016
  ident: R10
  article-title: CXCL1-mediated interaction of cancer cells with tumor-associated macrophages and cancer-associated fibroblasts promotes tumor progression in human bladder cancer
  publication-title: Neoplasia
  doi: 10.1016/j.neo.2016.08.002
– volume: 6
  year: 2017
  ident: R5
  article-title: EGFR mutation correlates with uninflamed phenotype and weak immunogenicity, causing impaired response to PD-1 blockade in non-small cell lung cancer
  publication-title: Oncoimmunology
  doi: 10.1080/2162402X.2017.1356145
– volume: 283
  start-page: 176
  year: 2018
  ident: R12
  article-title: The role of cytokines in T-cell memory in health and disease
  publication-title: Immunol Rev
  doi: 10.1111/imr.12644
– volume: 78
  start-page: 157
  year: 2018
  ident: R23
  article-title: CCR5+ myeloid-derived suppressor cells are enriched and activated in melanoma lesions
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-17-0348
– volume: 7
  start-page: 387
  year: 2019
  ident: R6
  article-title: Atezolizumab plus bevacizumab and chemotherapy in non-small-cell lung cancer (IMpower150): key subgroup analyses of patients with EGFR mutations or baseline liver metastases in a randomised, open-label phase 3 trial
  publication-title: Lancet Respir Med
  doi: 10.1016/S2213-2600(19)30084-0
– volume: 35
  start-page: 885
  year: 2019
  ident: R28
  article-title: Cooperation between constitutive and inducible chemokines enables T cell engraftment and immune attack in solid tumors
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2019.05.004
– volume: 110
  start-page: 20212
  year: 2013
  ident: R38
  article-title: Targeting CXCL12 from FAP-expressing carcinoma-associated fibroblasts synergizes with anti-PD-L1 immunotherapy in pancreatic cancer
  publication-title: Proc Natl Acad Sci U S A
  doi: 10.1073/pnas.1320318110
– volume: 102
  start-page: 293
  year: 2017
  ident: R11
  article-title: Immunotherapeutic approaches of IL-1 neutralization in the tumor microenvironment
  publication-title: J Leukoc Biol
  doi: 10.1189/jlb.3MR1216-523R
– volume: 11
  year: 2020
  ident: R33
  article-title: CCL7 recruits cDC1 to promote antitumor immunity and facilitate checkpoint immunotherapy to non-small cell lung cancer
  publication-title: Nat Commun
  doi: 10.1038/s41467-020-19973-6
– volume: 26
  start-page: 487
  year: 2020
  ident: R31
  article-title: Macrophage-derived CXCL9 and CXCL10 are required for antitumor immune responses following immune checkpoint blockade
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-19-1868
– volume: 19
  year: 2018
  ident: R41
  article-title: Hgf/Met and the immune system: relevance for cancer immunotherapy
  publication-title: Int J Mol Sci
  doi: 10.3390/ijms19113595
– volume: 6
  year: 2016
  ident: R42
  article-title: Identification of meflin as a potential marker for mesenchymal stromal cells
  publication-title: Sci Rep
  doi: 10.1038/srep22288
– volume: 252
  start-page: 86
  year: 2007
  ident: R24
  article-title: CCL2/CCR2 pathway mediates recruitment of myeloid suppressor cells to cancers
  publication-title: Cancer Lett
  doi: 10.1016/j.canlet.2006.12.012
– volume: 12
  year: 2020
  ident: R35
  article-title: Small-molecule MMP2/MMP9 inhibitor SB-3CT modulates tumor immune surveillance by regulating PD-L1
  publication-title: Genome Med
  doi: 10.1186/s13073-020-00780-z
– volume: 27
  start-page: 461
  year: 2017
  ident: R8
  article-title: Blocking the recruitment of naive CD4+ T cells reverses immunosuppression in breast cancer
  publication-title: Cell Res
  doi: 10.1038/cr.2017.34
– volume: 17
  start-page: 341
  year: 2020
  ident: R18
  article-title: Tissue-resident memory T cells in breast cancer control and immunotherapy responses
  publication-title: Nat Rev Clin Oncol
  doi: 10.1038/s41571-020-0333-y
– volume: 25
  start-page: 4663
  year: 2019
  ident: R51
  article-title: Expression analysis and significance of PD-1, LAG-3, and Tim-3 in human non-small cell lung cancer using spatially resolved and multiparametric single-cell analysis
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-18-4142
– volume: 26
  start-page: 1845
  year: 2020
  ident: R46
  article-title: Neoadjuvant PD-L1 plus CTLA-4 blockade in patients with cisplatin-ineligible operable high-risk urothelial carcinoma
  publication-title: Nat Med
  doi: 10.1038/s41591-020-1086-y
– volume: 5
  start-page: 1411
  year: 2019
  ident: R1
  article-title: Five-year survival and correlates among patients with advanced melanoma, renal cell carcinoma, or non-small cell lung cancer treated with nivolumab
  publication-title: JAMA Oncol
  doi: 10.1001/jamaoncol.2019.2187
– volume: 13
  start-page: 1884
  year: 2018
  ident: R3
  article-title: Immune marker profiling and programmed death ligand 1 expression across NSCLC mutations
  publication-title: J Thorac Oncol
  doi: 10.1016/j.jtho.2018.09.012
– volume: 31
  start-page: 177
  year: 2012
  ident: R14
  article-title: Amino acid metabolism related to immune tolerance by MDSCs
  publication-title: Int Rev Immunol
  doi: 10.3109/08830185.2012.679989
– volume: 25
  start-page: 3702
  year: 2019
  ident: R36
  article-title: A novel ACKR2-dependent role of fibroblast-derived CXCL14 in epithelial-to-mesenchymal transition and metastasis of breast cancer
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-18-1294
– volume: 24
  start-page: 3036
  year: 2018
  ident: R16
  article-title: CD103+ tumor-resident CD8+ T cells are associated with improved survival in immunotherapy-Naïve melanoma patients and expand significantly during anti-PD-1 treatment
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-17-2257
– volume: 18
  start-page: 940
  year: 2017
  ident: R52
  article-title: Tissue-resident memory features are linked to the magnitude of cytotoxic T cell responses in human lung cancer
  publication-title: Nat Immunol
  doi: 10.1038/ni.3775
– volume: 30
  start-page: v851
  year: 2019
  ident: R4
  article-title: Association between tissue TMB (tTMB) and clinical outcomes with pembrolizumab monotherapy (pembro) in PD-L1-positive advanced NSCLC in the KEYNOTE-010 and -042 trials
  publication-title: Ann Oncol
– volume: 21
  start-page: 1267
  year: 2020
  ident: R32
  article-title: NR4A nuclear receptors restrain B cell responses to antigen when second signals are absent or limiting
  publication-title: Nat Immunol
  doi: 10.1038/s41590-020-0765-7
– volume: 15
  start-page: 154
  year: 2014
  ident: R34
  article-title: Leptin-receptor-expressing mesenchymal stromal cells represent the main source of bone formed by adult bone marrow
  publication-title: Cell Stem Cell
  doi: 10.1016/j.stem.2014.06.008
– volume: 38
  start-page: 2438
  year: 2008
  ident: R15
  article-title: Glucose deprivation inhibits multiple key gene expression events and effector functions in CD8+ T cells
  publication-title: Eur J Immunol
  doi: 10.1002/eji.200838289
– volume: 7
  start-page: 784
  year: 2019
  ident: R19
  article-title: A transcriptionally distinct CXCL13+CD103+CD8+ T-cell population is associated with B-cell recruitment and neoantigen load in human cancer
  publication-title: Cancer Immunol Res
  doi: 10.1158/2326-6066.CIR-18-0517
– volume: 577
  year: 2020
  ident: R20
  article-title: B cells and tertiary lymphoid structures promote immunotherapy response
  publication-title: Nature
  doi: 10.1038/s41586-019-1922-8
– volume: 39
  year: 2019
  ident: R25
  article-title: Molecular profiling of the tumor microenvironment in glioblastoma patients: correlation of microglia/macrophage polarization state with metalloprotease expression profiles and survival
  publication-title: Biosci Rep
  doi: 10.1042/BSR20182361
– volume: 193
  start-page: 1468
  year: 2014
  ident: R22
  article-title: CXCL17 is a major chemotactic factor for lung macrophages
  publication-title: J Immunol
  doi: 10.4049/jimmunol.1400551
– volume: 100
  start-page: 17
  year: 2016
  ident: R45
  article-title: PGRN promotes migration and invasion of epithelial ovarian cancer cells through an epithelial mesenchymal transition program and the activation of cancer associated fibroblasts
  publication-title: Exp Mol Pathol
  doi: 10.1016/j.yexmp.2015.11.021
– volume: 36
  start-page: 2095
  year: 2017
  ident: R21
  article-title: CXCL2/MIF-CXCR2 signaling promotes the recruitment of myeloid-derived suppressor cells and is correlated with prognosis in bladder cancer
  publication-title: Oncogene
  doi: 10.1038/onc.2016.367
– volume: 15
  start-page: 1667
  year: 2019
  ident: R2
  article-title: PD-L1 expression and EGFR status in advanced non-small-cell lung cancer patients receiving PD-1/PD-L1 inhibitors: a meta-analysis
  publication-title: Future Oncol
  doi: 10.2217/fon-2018-0639
– volume: 122
  start-page: 2286
  year: 2008
  ident: R47
  article-title: CCL17 and CCL22 chemokines within tumor microenvironment are related to accumulation of Foxp3+ regulatory T cells in gastric cancer
  publication-title: Int J Cancer
  doi: 10.1002/ijc.23392
– volume: 1
  year: 2020
  ident: R17
  article-title: CD103+CD8+ T RM cells accumulate in tumors of Anti-PD-1-responder lung cancer patients and are tumor-reactive lymphocytes enriched with Tc17
  publication-title: Cell Rep Med
  doi: 10.1016/j.xcrm.2020.100127
– volume: 6
  year: 2018
  ident: R44
  article-title: Resident memory T cells, critical components in tumor immunology
  publication-title: J Immunother Cancer
  doi: 10.1186/s40425-018-0399-6
– volume: 382
  start-page: 124
  year: 2009
  ident: R27
  article-title: CCL23 up-regulates expression of KDR/Flk-1 and potentiates VEGF-induced proliferation and migration of human endothelial cells
  publication-title: Biochem Biophys Res Commun
  doi: 10.1016/j.bbrc.2009.02.149
– volume: 9
  year: 2020
  ident: R40
  article-title: Regulation of stem/progenitor cell maintenance by BMP5 in prostate homeostasis and cancer initiation
  publication-title: Elife
  doi: 10.7554/eLife.54542
– volume: 124
  start-page: 5466
  year: 2014
  ident: R49
  article-title: Tumor-associated neutrophils stimulate T cell responses in early-stage human lung cancer
  publication-title: J Clin Invest
  doi: 10.1172/JCI77053
– volume: 9
  year: 2021
  ident: R7
  article-title: Multiomics analysis reveals a distinct response mechanism in multiple primary lung adenocarcinoma after neoadjuvant immunotherapy
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-002312
– volume: 8
  year: 2020
  ident: R30
  article-title: M1 hot tumor-associated macrophages boost tissue-resident memory T cells infiltration and survival in human lung cancer
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-000778
– volume: 127
  start-page: 3796
  year: 2017
  ident: R26
  article-title: NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development
  publication-title: J Clin Invest
  doi: 10.1172/JCI91561
– volume: 17
  start-page: 3660
  year: 2011
  ident: R29
  article-title: Role of CXCR3 ligands in IL-7/IL-7R alpha-Fc-mediated antitumor activity in lung cancer
  publication-title: Clin Cancer Res
  doi: 10.1158/1078-0432.CCR-10-3346
– volume: 58
  start-page: 313
  year: 2020
  ident: R50
  article-title: Role of mast cells in shaping the tumor microenvironment
  publication-title: Clin Rev Allergy Immunol
  doi: 10.1007/s12016-019-08753-w
– volume: 33
  start-page: 463
  year: 2018
  ident: R37
  article-title: Fibroblast heterogeneity and immunosuppressive environment in human breast cancer
  publication-title: Cancer Cell
  doi: 10.1016/j.ccell.2018.01.011
– volume: 100
  start-page: 17
  year: 2016
  ident: 2024053111345217000_10.2.e003534.45
  article-title: PGRN promotes migration and invasion of epithelial ovarian cancer cells through an epithelial mesenchymal transition program and the activation of cancer associated fibroblasts
  publication-title: Exp Mol Pathol
  doi: 10.1016/j.yexmp.2015.11.021
– volume: 31
  start-page: 177
  year: 2012
  ident: 2024053111345217000_10.2.e003534.14
  article-title: Amino acid metabolism related to immune tolerance by MDSCs
  publication-title: Int Rev Immunol
  doi: 10.3109/08830185.2012.679989
– volume: 15
  start-page: 1667
  year: 2019
  ident: 2024053111345217000_10.2.e003534.2
  article-title: PD-L1 expression and EGFR status in advanced non-small-cell lung cancer patients receiving PD-1/PD-L1 inhibitors: a meta-analysis
  publication-title: Future Oncol
  doi: 10.2217/fon-2018-0639
– volume: 7
  start-page: 387
  year: 2019
  ident: 2024053111345217000_10.2.e003534.6
  article-title: Atezolizumab plus bevacizumab and chemotherapy in non-small-cell lung cancer (IMpower150): key subgroup analyses of patients with EGFR mutations or baseline liver metastases in a randomised, open-label phase 3 trial
  publication-title: Lancet Respir Med
  doi: 10.1016/S2213-2600(19)30084-0
– volume: 12
  year: 2020
  ident: 2024053111345217000_10.2.e003534.35
  article-title: Small-molecule MMP2/MMP9 inhibitor SB-3CT modulates tumor immune surveillance by regulating PD-L1
  publication-title: Genome Med
  doi: 10.1186/s13073-020-00780-z
– ident: 2024053111345217000_10.2.e003534.11
  doi: 10.1189/jlb.3MR1216-523R
– ident: 2024053111345217000_10.2.e003534.23
  doi: 10.1158/0008-5472.CAN-17-0348
– volume: 13
  start-page: 1884
  year: 2018
  ident: 2024053111345217000_10.2.e003534.3
  article-title: Immune marker profiling and programmed death ligand 1 expression across NSCLC mutations
  publication-title: J Thorac Oncol
  doi: 10.1016/j.jtho.2018.09.012
– ident: 2024053111345217000_10.2.e003534.5
  doi: 10.1080/2162402X.2017.1356145
– ident: 2024053111345217000_10.2.e003534.36
  doi: 10.1158/1078-0432.CCR-18-1294
– ident: 2024053111345217000_10.2.e003534.9
  doi: 10.1016/j.ccell.2019.02.008
– volume: 26
  start-page: 1845
  year: 2020
  ident: 2024053111345217000_10.2.e003534.46
  article-title: Neoadjuvant PD-L1 plus CTLA-4 blockade in patients with cisplatin-ineligible operable high-risk urothelial carcinoma
  publication-title: Nat Med
  doi: 10.1038/s41591-020-1086-y
– volume: 5
  year: 2020
  ident: 2024053111345217000_10.2.e003534.39
  article-title: Effects of B cell-activating factor on tumor immunity
  publication-title: JCI Insight
  doi: 10.1172/jci.insight.136417
– volume: 27
  start-page: 461
  year: 2017
  ident: 2024053111345217000_10.2.e003534.8
  article-title: Blocking the recruitment of naive CD4+ T cells reverses immunosuppression in breast cancer
  publication-title: Cell Res
  doi: 10.1038/cr.2017.34
– ident: 2024053111345217000_10.2.e003534.38
  doi: 10.1073/pnas.1320318110
– volume: 11
  year: 2020
  ident: 2024053111345217000_10.2.e003534.33
  article-title: CCL7 recruits cDC1 to promote antitumor immunity and facilitate checkpoint immunotherapy to non-small cell lung cancer
  publication-title: Nat Commun
  doi: 10.1038/s41467-020-19973-6
– volume: 577
  year: 2020
  ident: 2024053111345217000_10.2.e003534.20
  article-title: B cells and tertiary lymphoid structures promote immunotherapy response
  publication-title: Nature
  doi: 10.1038/s41586-019-1922-8
– ident: 2024053111345217000_10.2.e003534.43
  doi: 10.1002/stem.1251
– ident: 2024053111345217000_10.2.e003534.44
  doi: 10.1186/s40425-018-0399-6
– ident: 2024053111345217000_10.2.e003534.47
  doi: 10.1002/ijc.23392
– ident: 2024053111345217000_10.2.e003534.4
  doi: 10.1093/annonc/mdz394.029
– ident: 2024053111345217000_10.2.e003534.10
  doi: 10.1016/j.neo.2016.08.002
– volume: 127
  start-page: 3796
  year: 2017
  ident: 2024053111345217000_10.2.e003534.26
  article-title: NF-κB regulates GDF-15 to suppress macrophage surveillance during early tumor development
  publication-title: J Clin Invest
  doi: 10.1172/JCI91561
– ident: 2024053111345217000_10.2.e003534.22
  doi: 10.4049/jimmunol.1400551
– volume: 1
  year: 2020
  ident: 2024053111345217000_10.2.e003534.17
  article-title: CD103+CD8+ T RM cells accumulate in tumors of Anti-PD-1-responder lung cancer patients and are tumor-reactive lymphocytes enriched with Tc17
  publication-title: Cell Rep Med
  doi: 10.1016/j.xcrm.2020.100127
– ident: 2024053111345217000_10.2.e003534.25
  doi: 10.1042/BSR20182361
– ident: 2024053111345217000_10.2.e003534.28
  doi: 10.1016/j.ccell.2019.05.004
– volume: 17
  start-page: 341
  year: 2020
  ident: 2024053111345217000_10.2.e003534.18
  article-title: Tissue-resident memory T cells in breast cancer control and immunotherapy responses
  publication-title: Nat Rev Clin Oncol
  doi: 10.1038/s41571-020-0333-y
– ident: 2024053111345217000_10.2.e003534.15
  doi: 10.1002/eji.200838289
– ident: 2024053111345217000_10.2.e003534.16
  doi: 10.1158/1078-0432.CCR-17-2257
– ident: 2024053111345217000_10.2.e003534.37
  doi: 10.1016/j.ccell.2018.01.011
– ident: 2024053111345217000_10.2.e003534.27
  doi: 10.1016/j.bbrc.2009.02.149
– volume: 24
  start-page: 2329
  year: 2018
  ident: 2024053111345217000_10.2.e003534.48
  article-title: Identification of an early Unipotent neutrophil progenitor with pro-tumoral activity in mouse and human bone marrow
  publication-title: Cell Rep
  doi: 10.1016/j.celrep.2018.07.097
– ident: 2024053111345217000_10.2.e003534.34
  doi: 10.1016/j.stem.2014.06.008
– ident: 2024053111345217000_10.2.e003534.51
  doi: 10.1158/1078-0432.CCR-18-4142
– ident: 2024053111345217000_10.2.e003534.7
  doi: 10.1136/jitc-2020-002312
– ident: 2024053111345217000_10.2.e003534.31
  doi: 10.1158/1078-0432.CCR-19-1868
– volume: 6
  year: 2016
  ident: 2024053111345217000_10.2.e003534.42
  article-title: Identification of meflin as a potential marker for mesenchymal stromal cells
  publication-title: Sci Rep
  doi: 10.1038/srep22288
– volume: 6
  year: 2017
  ident: 2024053111345217000_10.2.e003534.13
  article-title: IL-18 receptor marks functional CD8+ T cells in non-small cell lung cancer
  publication-title: Oncoimmunology
  doi: 10.1080/2162402X.2017.1328337
– ident: 2024053111345217000_10.2.e003534.50
  doi: 10.1007/s12016-019-08753-w
– ident: 2024053111345217000_10.2.e003534.19
  doi: 10.1158/2326-6066.CIR-18-0517
– volume: 36
  start-page: 2095
  year: 2017
  ident: 2024053111345217000_10.2.e003534.21
  article-title: CXCL2/MIF-CXCR2 signaling promotes the recruitment of myeloid-derived suppressor cells and is correlated with prognosis in bladder cancer
  publication-title: Oncogene
  doi: 10.1038/onc.2016.367
– volume: 9
  year: 2020
  ident: 2024053111345217000_10.2.e003534.40
  article-title: Regulation of stem/progenitor cell maintenance by BMP5 in prostate homeostasis and cancer initiation
  publication-title: Elife
  doi: 10.7554/eLife.54542
– ident: 2024053111345217000_10.2.e003534.24
  doi: 10.1016/j.canlet.2006.12.012
– ident: 2024053111345217000_10.2.e003534.49
  doi: 10.1172/JCI77053
– ident: 2024053111345217000_10.2.e003534.12
  doi: 10.1111/imr.12644
– ident: 2024053111345217000_10.2.e003534.29
  doi: 10.1158/1078-0432.CCR-10-3346
– volume: 8
  year: 2020
  ident: 2024053111345217000_10.2.e003534.30
  article-title: M1 hot tumor-associated macrophages boost tissue-resident memory T cells infiltration and survival in human lung cancer
  publication-title: J Immunother Cancer
  doi: 10.1136/jitc-2020-000778
– volume: 5
  start-page: 1411
  year: 2019
  ident: 2024053111345217000_10.2.e003534.1
  article-title: Five-year survival and correlates among patients with advanced melanoma, renal cell carcinoma, or non-small cell lung cancer treated with nivolumab
  publication-title: JAMA Oncol
  doi: 10.1001/jamaoncol.2019.2187
– volume: 21
  start-page: 1267
  year: 2020
  ident: 2024053111345217000_10.2.e003534.32
  article-title: NR4A nuclear receptors restrain B cell responses to antigen when second signals are absent or limiting
  publication-title: Nat Immunol
  doi: 10.1038/s41590-020-0765-7
– ident: 2024053111345217000_10.2.e003534.52
  doi: 10.1038/ni.3775
– volume: 19
  year: 2018
  ident: 2024053111345217000_10.2.e003534.41
  article-title: Hgf/Met and the immune system: relevance for cancer immunotherapy
  publication-title: Int J Mol Sci
  doi: 10.3390/ijms19113595
SSID ssj0001033888
Score 2.5624049
Snippet BackgroundsImmunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed...
Immunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower programmed cell...
Backgrounds Immunotherapy is less effective in patients with epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer (NSCLC). Lower...
SourceID doaj
pubmedcentral
proquest
pubmed
crossref
bmj
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage e003534
SubjectTerms Adenocarcinoma of Lung - genetics
Adenocarcinoma of Lung - pathology
Biomarkers, Tumor - metabolism
Cancer
Cancer therapies
Chemotherapy
Cytokines
Epidermal growth factor
ErbB Receptors - genetics
Female
Fibroblasts
Genes
Humans
Immune Checkpoint Inhibitors - pharmacology
Immune Checkpoint Inhibitors - therapeutic use
Immunotherapy
Immunotherapy - methods
Immunotherapy Biomarkers
Kinases
Lung cancer
lung neoplasms
Lung Neoplasms - genetics
Lung Neoplasms - pathology
Lymphocytes
Male
Mutation
Neutrophils
Ontology
Patients
Prognosis
Single-Cell Analysis - methods
Transcriptome - genetics
Tumor Microenvironment
SummonAdditionalLinks – databaseName: BMJ Open Access Journals
  dbid: 9YT
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwjV1Lb9QwEB5BkapeEG8CBRkJDhzSTRzHsY-AulRI5QCtVE6R7Thlq01SbRMO_HpmnOy2i1DFNbbjxDP2PDzzDcBbr1PvtSlim3ryVrk81rqoYq4tKrcyq4oQm3P8VR6dii9n-dlkKFIuzMWidwe2uRjTGQigqSVE-Rmfebr0ysQBuaXvwj0qTEJcrH-cXPtUEjS4lFrfRmYyvA4ZgaPJHEbvwS6FriNTE0wgzrMljgJq_79Uzb8jJm-IoPkDuD_pjuzDSOyHcMe3j2D3eLodfwy_v6McWvqYnPGsJyEUjoSu8cxM2COMEJtQJlTMsKvhcoyC_eVZPzTdii0oWcSzhoL0bmTAsUXLDj_Pv7FmoJrDbIkHBDN4YKEcXOHUXWOewOn88OTTUTzVVohtrrM-dnjQoSVnVF1InVZaJcYWJrWqqKh4kUi9roQwLhNOyNSiVSJSbrTXqrA1VyZ7Cjtt1_rnwFCFqlNeIDegquAk13nC8V2ebmRrpX0E73Chy2lvXJXB7MhkSbQpiTblSJsIZmtSlG4CKKc6GctbRrzfjLgcwTlu6fuRqLvpR7Da4UG3Oi-nXVrWEu1ybp3LLf69lVZzmxidGVmJqvYugv01b1z_D5e8oDL0Oo_gzaYZdylR27S-G8Y-Atc1URE8G1lp8yVrhoyg2GKyrU_dbmkXPwMSuFKogQj54j9X-CXsccreCB6kfdjpV4N_hTpVb1-HjfQHhyoczg
  priority: 102
  providerName: BMJ Publishing Group Ltd
– databaseName: DOAJ Directory of Open Access Journals
  dbid: DOA
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrR3LbtQw0IIeEBcE5ZW2ICPBgUO0ie34cSyo2wqpHIBKvUW244itNkm1TTj06zvjZJddhMqFa2In9sx4Xp4HIe-DyUMwVqUuD-it8kVqjKpSZhwot5JXKsbmnH-VZxfiy2VxudXqC2PCxvLAI-BmtQRTiTnvC1cJ4aQzzGXWcCsrUdXBI_cFmbdlTEXvSgaml9bre0kuZ1eL3gNJMDCeM15gn-SHrrnakUaxaP_fNM0_Aya3JND8KXkyqY70eFzyM_IgtPvk0fl0Of6c3H4HMbQMKfriaY8yKHKErgnUTqVHKBZsApFQUUtvhusxCPZXoP3QdCu6wFyRQBuM0dtKgKOLlp6czr_RZsCWw3QJ_IFa4FcgBlfw666xL8jF_OTH57N0aq2QusLwPvXA58CQs7pW0uSV0Zl1yuZOqwp7F4k8GIC29Vx4IXMHRonImTXBaOVqpi1_Sfbarg2vCQUNqs6ZAmIATcFLZoqMwbcCXsjW2oSEfABAl9PRuCmj1cFliQgpESHliJCEzNaoKP1UnxzbZCzvmfFxM-N6rM1xz9hPiN3NOKyqHR8ArZUTrZX_orWEHK1p4_d-mGQKu9CbIiHvNq_hkCK2bRu6YRwjAK6ZTsirkZQ2K8FUCmCyPCFqh8h2lrr7pl38jIXAtQYFRMiD_7G3Q_KYYWZH9C4dkb1-NYQ3oG_17m08WncTfyov
  priority: 102
  providerName: Directory of Open Access Journals
– databaseName: Health & Medical Collection
  dbid: 7X7
  link: http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfR1Nb9Mw1GJDQlwQ3wQGMhIcOERNHMcfJwRoZUIaB2BSb5HtOKxTk5Q22WG_nvcSt10R6jWxE9vv-X1_EPLO69R7bWRsU4_WKpfHWssyZtqCcCuyUg6xOeffxdkF_zbLZ8Hgtg5hlRuaOBDqsnVoI58wwSQ2-9b5x-WfGLtGoXc1tNA4InexdBlitZzJnY0lAQVMqY13MhOTq3nnADEYqNBJlmO35CNbX-3xpKF0___kzX_DJm_xoelD8iAIkPTTCPFH5I5vHpN758FF_oTc_ARmtPAxWuRph5xooAtt7akJBUgolm0CxlBSQ9f9cgyFvfa06-t2ReeYMeJpjZF6t9Lg6Lyhp1-nP2jdY-NhugAqQQ1QLWCGK_h1W5un5GJ6-uvLWRwaLMQ211kXO6B2oM4ZVUmh01KrxFhpUqtkiR2MeOp1yblxGXdcpBZUE54yo71W0lZMmewZOW7axr8gFOSoKmUSUALkBSeYzhMG3_Lolq2U9hF5DwddhAuyLgbdIxMFAqRAgBQjQCIy2YCicKFKOTbLWByY8WE7YzlW6Dgw9jNCdzsOa2sPD9rV7yJc1aISoJwz61xuYfdWWM1sYnRmRMnLyruInGxwY7efHXpG5O32NVxVhLZpfNuPYzica6Ii8nxEpe1KMKECSG0WEbmHZHtL3X_TzC-HcuBKgRjCxcvDy3pF7jPM3BisRyfkuFv1_jXIU519M1yavyN_ICM
  priority: 102
  providerName: ProQuest
Title Single-cell transcriptome analysis revealed a suppressive tumor immune microenvironment in EGFR mutant lung adenocarcinoma
URI https://jitc.bmj.com/content/10/2/e003534.full
https://www.ncbi.nlm.nih.gov/pubmed/35140113
https://www.proquest.com/docview/2627032095
https://www.proquest.com/docview/2627483208
https://pubmed.ncbi.nlm.nih.gov/PMC8830346
https://doaj.org/article/f65232bcc5bd44b6b92b0a93a6d4dfec
Volume 10
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
link http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwfR3bbtMw1GKbNO0FcScwKiPBAw9hieP48oDQNrVMSJ3QWFF5iuzEgU5NMrIUAV_POUnarajsJZHiS2yfY5-Lz4WQV06HzmkjfRs61Falsa-1zHymLTC3Ispka5szPhUnE_5xGk-v3aP7BbzaKNphPqlJPX_768fv97Dh3_UZSQ4uZk0K0GYgFwdRHPEtsgN0SWI-g3HP7LcalwDEMaWWd5UbGu6RXTRsB5THIIK2uFgjVm1M_02M6L_2lDcI1OgeudtzlvSwQ4X75I4rH5DdcX93_pD8-QxUau58VNXTBklUe2BUhaOmj0xCMZ4TUIyMGnq1uOxsZH862iyKqqYzdCVxtEATvhv-cXRW0uGH0RktFpiRmM7h-KAGjjOgkjX8uirMIzIZDc-PT_w-84JvYx01fgrHIMh5RuVS6DDTKjBWmtAqmWFqIx46nXFu0oinXIQWZBYeMqOdVtLmTJnoMdkuq9I9JRQYrDxkEnAFGIlUMB0HDPpyeF-bK-088hoWOlkCPmmFkkgkCJsEYZN0sPHIwRIUSdqHL8csGvNbWrxZtbjsQnfcUvcIobuqh0G32w9V_S3p93CSC5DamU3T2MLsrbCa2cDoyIiMZ7lLPbK_xI3r-TDBJCap17FHXq6KYQ8jtE3pqkVXh8O6BsojTzpUWo1kiZAekWtItjbU9ZJy9r2NE64U8CdcPPtvn8_JHkNvjlajtE-2m3rhXgCP1dgB2ZJTCU_99XxAdg6Px-Mv8D4ann46G7R6i0G7uf4CvwEpSw
linkProvider Scholars Portal
linkToHtml http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtR1Lb9Mw2NqGBFwQbzIGGIkdOERNnMSODwjxWOnYugNsUm-Z7TisU5OUNgXBj-I38n15tCtCve2a2Int7-3vRcgrK31rpRKu9i3eVpnIlVKkLpMalFsepKKOzRme8MFZ-HkUjbbIny4XBsMqO55YM-q0NHhH3mOcCWz2LaO30-8udo1C72rXQqNBiyP76yeYbPM3hx8BvvuM9Q9OPwzctquAqyMZVK4BEgcbRsWZ4NJPZewpLZSvY5Fi257QtzINQ2WC0ITc16CPhz5T0oJxrjMWqwC-u01ugOD10NgTI7G60_HA4Ivjzhsa8N7luDKAiAxMdi-IsDvzts4v12Rg3Srgf_rtv2GaV-Re_y650yqs9F2DYffIli3uk5vD1iX_gPz-CsJvYl30ANAKJV_Nh8rcUtUWPKFYJgoEUUoVnS-mTejtD0urRV7O6BgzVCzNMTLwStodHRf04FP_C80X2OiYToArUQVcEoTvDH5d5uohObuWo39EdoqysE8IBb0t85kAFAT9xHAmI4_Btyy6gbNYWofsw0EnLUHOk9rWCXiCAEkQIEkDEIf0OlAkpq2Kjs05JhtmvF7OmDYVQTaMfY_QXY7DWt71g3L2LWlZQ5LxCNRabUykYfeaa8m0p2SgeBqmmTUO2etwY7WfFTk45OXyNbAGhLYqbLloxoRwrl7skMcNKi1XggkcwNoDh4g1JFtb6vqbYnxRlx-PY1B7Qr67eVkvyK3B6fA4OT48OXpKbjPMGqlvrvbITjVb2Gegy1X6eU1AlJxfN8X-BVc8W3Q
linkToPdf http://utb.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwtR1Nb9Mw9GnrpIkL4pvAACOxA4eoiZM48QEhxlo2xqppMGm3zE4c6NQkpU1B8NP4dbyXj3ZFaLddEzux_b79vgBeGekaI1Voa9fQbVUS2FKGqc2lRuVWeGlYx-Ycj8TBmf_xPDjfgD9dLgyFVXY8sWbUaZnQHXmfCx5Ss28Z9LM2LOJkf_h2-t2mDlLkae3aaTQocmR-_UTzbf7mcB9hvcv5cPDl_YHddhiwdSC9yk6Q3NGeUVEWCummMnKUDpWrozClFj6-a2Tq-yrx_MQXrkbd3He5kgYNdZ3xSHn43U3YCskq6sHW3mB0crq64XHQ_Iuizjfqif7luEoQLTka8I4XUK_mTZ1frknEunHA_7Tdf4M2r0jB4R243aqv7F2Db3dhwxT3YPu4ddDfh9-fURROjE3-AFaRHKy5UpkbptryJ4yKRqFYSpli88W0CcT9YVi1yMsZG1O-imE5xQleScJj44INPgxPWb6gtsdsgjyKKeSZKIpn-OsyVw_g7EYO_yH0irIwj4GhFpe5PESERG0lEVwGDsdvGXIKZ5E0FuziQcctec7j2vLxREwAiQkgcQMQC_odKOKkrZFOrTom18x4vZwxbeqDXDN2j6C7HEeVvesH5exr3DKKOBMBKrk6SQKNu9dCS64dJT0lUj_NTGLBTocbq_2siMOCl8vXyCgI2qow5aIZ4-O5OpEFjxpUWq6E0jmQ0XsWhGtItrbU9TfF-FtdjDyKUAnyxZPrl_UCtpFa40-Ho6OncItTCkl9jbUDvWq2MM9Qsav085aCGFzcNNH-BXnBYQ8
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Single-cell+transcriptome+analysis+revealed+a+suppressive+tumor+immune+microenvironment+in+EGFR+mutant+lung+adenocarcinoma&rft.jtitle=Journal+for+immunotherapy+of+cancer&rft.au=Yang%2C+Lei&rft.au=He%2C+Yun-Ting&rft.au=Dong%2C+Song&rft.au=Wei%2C+Xue-Wu&rft.date=2022-01-01&rft.eissn=2051-1426&rft.volume=10&rft.issue=2&rft_id=info:doi/10.1136%2Fjitc-2021-003534&rft_id=info%3Apmid%2F35140113&rft.externalDocID=35140113
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=2051-1426&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=2051-1426&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=2051-1426&client=summon