Evidence map›Paper›PMID 36791109›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2023

ALK fusion NSCLC oncogenes promote survival and inhibit NK cell responses via

Tzu-Po Chuang, Wei-Yun Lai, Jonatan L Gabre, Dan E Lind, Ganesh Umapathy, Abdulmalik A Bokhari, Bengt Bergman, Linnea Kristenson, Fredrik B Thorén, Anh Le and 4 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
6.2field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Beyond ALK fusion positivity: structural complexity as a prognostic indicator in first-line ALK-TKI therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. ALK fusion NSCLC oncogenes promote survival and inhibit NK cell responses viaProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  18. Article
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 4 countries.

Tzu-Po ChuangDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.
Wei-Yun LaiDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.ORCID 0000-0001-8515-1358
Jonatan L GabreDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.
Dan E LindDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.
Ganesh UmapathyDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.
Abdulmalik A BokhariDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.
Bengt BergmanDepartment of Respiratory Medicine, Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Linnea KristensonDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.ORCID 0000-0003-0034-7875
Fredrik B ThorénDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.
Anh LeDivision of Medical Oncology, University of Colorado School of Medicine, Aurora, CO 80045.
Robert C DoebeleDivision of Medical Oncology, University of Colorado School of Medicine, Aurora, CO 80045.
Jimmy Van den EyndenDepartment of Human Structure and Repair, Anatomy and Embryology Unit, Ghent University, 9000 Ghent, Belgium.ORCID 0000-0003-0002-5614
Ruth H PalmerDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.ORCID 0000-0002-2735-8470
Bengt HallbergDepartment of Medical Biochemistry and Cell Biology, Institute of Biomedicine, Sahlgrenska Academy, Gothenburg University, 40530 Gothenburg, Sweden.ORCID 0000-0003-2032-2616
Institute of Biomedical Science · GBGhent University · BESahlgrenska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anaplastic lymphoma kinase (ALK) fusion variants in Non-Small Cell Lung Cancer (NSCLC) consist of numerous dimerizing fusion partners. Retrospective investigations suggest that treatment benefit in response to ALK tyrosine kinase inhibitors (TKIs) differs dependent on the fusion variant present in the patient tumor. Therefore, understanding the oncogenic signaling networks driven by different ALK fusion variants is important. To do this, we developed controlled inducible cell models expressing either Echinoderm Microtubule Associated Protein Like 4 (EML4)-ALK-V1, EML4-ALK-V3, Kinesin Family Member 5B (KIF5B)-ALK, or TRK-fused gene (TFG)-ALK and investigated their transcriptomic and proteomic responses to ALK activity modulation together with patient-derived ALK-positive NSCLC cell lines. This allowed identification of both common and isoform-specific responses downstream of these four ALK fusions. An inflammatory signature that included upregulation of the Serpin B4 serine protease inhibitor was observed in both ALK fusion inducible and patient-derived cells. We show that Signal transducer and activator of transcription 3 (STAT3), Nuclear Factor Kappa B (NF-κB) and Activator protein 1 (AP1) are major transcriptional regulators of

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsSerpinsAnaplastic Lymphoma KinaseAntigens, NeoplasmHumansOncogene Proteins, FusionOncogenesProtein Kinase InhibitorsProtein-Tyrosine KinasesProteomicsRetrospective StudiesALK protein, humanAnaplastic Lymphoma KinaseAntigens, NeoplasmOncogene Proteins, FusionProtein Kinase InhibitorsProtein-Tyrosine KinasesSerpinssquamous cell carcinoma-related antigenALK fusionanaplastic lymphoma kinaseNGSnon-small cell lung cancerphosphoprofiling

Identifiers

PMID36791109
PMCPMC9974509
OpenAlexW4320857814

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.