File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Laminin γ2–mediating T cell exclusion attenuates response to anti–PD-1 therapy

TitleLaminin γ2–mediating T cell exclusion attenuates response to anti–PD-1 therapy
Authors
Issue Date2021
PublisherAmerican Association for the Advancement of Science: Science Advances. The Journal's web site is located at http://www.scienceadvances.org/
Citation
Science Advances, 2021, v. 7 n. 6, p. article no. eabc8346 How to Cite?
AbstractPD-1/PD-L1 blockade therapies provide notable clinical benefits for patients with advanced cancers, but the factors influencing the effectiveness of the treatment remain incompletely cataloged. Here, the up-regulation of laminin γ2 (Ln-γ2) predicted the attenuated efficacy of anti–PD-1 drugs and was associated with unfavorable outcomes in patients with lung cancer or esophageal cancer. Furthermore, Ln-γ2 was transcriptionally activated by transforming growth factor–β1 (TGF-β1) secreted from cancer-associated fibroblasts via JNK/AP1 signaling, which blocked T cell infiltration into the tumor nests by altering the expression of T cell receptors. Coadministration of the TGF-β receptor inhibitor galunisertib and chemotherapy drugs provoked vigorous antitumor activity of anti–PD-1 therapy in mouse tumor models. Therefore, Ln-γ2 may represent a useful biomarker to optimize clinical decisions and predict the response of cancer patients to treatment with anti–PD-1 drugs.
Persistent Identifierhttp://hdl.handle.net/10722/300779
ISSN
2020 Impact Factor: 14.136
2020 SCImago Journal Rankings: 5.928
PubMed Central ID

 

DC FieldValueLanguage
dc.contributor.authorLi, L-
dc.contributor.authorWei, JR-
dc.contributor.authorDong, J-
dc.contributor.authorLin, QG-
dc.contributor.authorTang, H-
dc.contributor.authorJia, YX-
dc.contributor.authorTan, W-
dc.contributor.authorChen, QY-
dc.contributor.authorZeng, TT-
dc.contributor.authorXing, S-
dc.contributor.authorQin, YR-
dc.contributor.authorZhu, YH-
dc.contributor.authorLi, Y-
dc.contributor.authorGuan, XY-
dc.date.accessioned2021-07-06T03:10:07Z-
dc.date.available2021-07-06T03:10:07Z-
dc.date.issued2021-
dc.identifier.citationScience Advances, 2021, v. 7 n. 6, p. article no. eabc8346-
dc.identifier.issn2375-2548-
dc.identifier.urihttp://hdl.handle.net/10722/300779-
dc.description.abstractPD-1/PD-L1 blockade therapies provide notable clinical benefits for patients with advanced cancers, but the factors influencing the effectiveness of the treatment remain incompletely cataloged. Here, the up-regulation of laminin γ2 (Ln-γ2) predicted the attenuated efficacy of anti–PD-1 drugs and was associated with unfavorable outcomes in patients with lung cancer or esophageal cancer. Furthermore, Ln-γ2 was transcriptionally activated by transforming growth factor–β1 (TGF-β1) secreted from cancer-associated fibroblasts via JNK/AP1 signaling, which blocked T cell infiltration into the tumor nests by altering the expression of T cell receptors. Coadministration of the TGF-β receptor inhibitor galunisertib and chemotherapy drugs provoked vigorous antitumor activity of anti–PD-1 therapy in mouse tumor models. Therefore, Ln-γ2 may represent a useful biomarker to optimize clinical decisions and predict the response of cancer patients to treatment with anti–PD-1 drugs.-
dc.languageeng-
dc.publisherAmerican Association for the Advancement of Science: Science Advances. The Journal's web site is located at http://www.scienceadvances.org/-
dc.relation.ispartofScience Advances-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleLaminin γ2–mediating T cell exclusion attenuates response to anti–PD-1 therapy-
dc.typeArticle-
dc.identifier.emailLi, L: lilei728@HKUCC-COM.hku.hk-
dc.identifier.emailGuan, XY: xyguan@hku.hk-
dc.identifier.authorityGuan, XY=rp00454-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1126/sciadv.abc8346-
dc.identifier.pmid33536206-
dc.identifier.pmcidPMC7857690-
dc.identifier.scopuseid_2-s2.0-85100974276-
dc.identifier.hkuros323257-
dc.identifier.volume7-
dc.identifier.issue6-
dc.identifier.spagearticle no. eabc8346-
dc.identifier.epagearticle no. eabc8346-
dc.publisher.placeUnited States-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats