Targeting NTRK1 Enhances Immune Checkpoint Inhibitor Efficacy in NTRK1 Wild-Type Non–Small Cell Lung Cancer Article Swipe
Margaret Smith
,
Caroline B. Dixon
,
Yuezhu Wang
,
Yin Liu
,
Ralph B. D’Agostino
,
Jimmy Ruiz
,
George Watson Oliver
,
Lance D. Miller
,
Ümit Topaloğlu
,
Michael D. Chan
,
Michael Farris
,
Jing Su
,
Kathryn F. Mileham
,
Dawen Zhao
,
Wencheng Li
,
Tammy Sexton
,
Thomas Lycan
,
Karen M. Haas
,
Jason M. Grayson
,
Fei Xing
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1158/0008-5472.can-24-0658
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1158/0008-5472.can-24-0658
Treatment of non–small cell lung cancer (NSCLC) has drastically changed in recent years owing to the robust anticancer effects of immune checkpoint inhibitors (ICI). However, only 20% of the patients with NSCLC benefit from ICIs, highlighting the need to uncover the mechanisms mediating resistance. By analyzing the overall survival (OS) and mutational profiles of 424 patients with NSCLC who received ICI treatments between 2015 and 2021, we determined that patients carrying a loss-of-function mutation in neurotrophic tyrosine kinase receptor 1 (NTRK1) had a prolonged OS when compared with patients with wild-type NTRK1. Notably, suppression of the NTRK1 pathway by knockdown or entrectinib treatment significantly enhanced ICI efficacy in mouse NSCLC models. Comprehensive T-cell population analyses demonstrated that stem-like CD4+ T cells and effector CD4+ and CD8+ T cells were highly enriched in anti–PD-1–treated mice bearing tumors with decreased NTRK1 signaling. RNA sequencing revealed that suppression of NTRK1 signaling in tumor cells increased complement C3 expression, which enhanced the recruitment of T cells and myeloid cells and stimulated M1-like macrophage polarization in the tumor. Together, this study demonstrates a role for NTRK1 signaling in regulating cross-talk between tumor cells and immune cells in the tumor microenvironment and provides a potential therapeutic approach to overcome immunotherapy resistance in patients with NSCLC with NTRK1 wild-type. Significance: Inhibition of NTRK1 signaling confers sensitivity to immunotherapy by enhancing complement C3-mediated T-cell and macrophage functions, leading to improved responses to immune checkpoint inhibitors in patients with lung cancer with NTRK1 mutations.
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Metadata
- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1158/0008-5472.can-24-0658
- OA Status
- green
- Cited By
- 5
- References
- 73
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4402355222
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
-
https://openalex.org/W4402355222Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1158/0008-5472.can-24-0658Digital Object Identifier
- Title
-
Targeting NTRK1 Enhances Immune Checkpoint Inhibitor Efficacy in NTRK1 Wild-Type Non–Small Cell Lung CancerWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-09-09Full publication date if available
- Authors
-
Margaret Smith, Caroline B. Dixon, Yuezhu Wang, Yin Liu, Ralph B. D’Agostino, Jimmy Ruiz, George Watson Oliver, Lance D. Miller, Ümit Topaloğlu, Michael D. Chan, Michael Farris, Jing Su, Kathryn F. Mileham, Dawen Zhao, Wencheng Li, Tammy Sexton, Thomas Lycan, Karen M. Haas, Jason M. Grayson, Fei XingList of authors in order
- Landing page
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https://doi.org/10.1158/0008-5472.can-24-0658Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
greenOpen access status per OpenAlex
- OA URL
-
https://www.ncbi.nlm.nih.gov/pmc/articles/11611666Direct OA link when available
- Concepts
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Cancer research, Immunotherapy, Immune system, Lung cancer, CD8, Medicine, Cancer, Biology, Tumor microenvironment, Immunology, Internal medicineTop concepts (fields/topics) attached by OpenAlex
- Cited by
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5Total citation count in OpenAlex
- Citations by year (recent)
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2025: 5Per-year citation counts (last 5 years)
- References (count)
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73Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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