Evidence map›Paper›PMID 24063894›Full record

ArticleCancer research2013

Cetuximab response of lung cancer-derived EGF receptor mutants is associated with asymmetric dimerization.

Jeonghee Cho, Liang Chen, Naveen Sangji, Takafumi Okabe, Kimio Yonesaka, Joshua M Francis, Richard J Flavin, William Johnson, Jihyun Kwon, Soyoung Yu and 6 more

Abstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
–field-weighted citation impact
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

75 citing papers in PubMed.

  1. Randomized Trial of Afatinib Plus Cetuximab Versus Afatinib Alone for First-Line Treatment ofJournal of clinical oncology : official journal of the American Society of Clinical Oncology · 2020
    Trial
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Article
  7. Precision medicine in the first-line treatment ofTranslational lung cancer research · 2026
    Article
  8. The role of kinase domain dimerization in EGFR activation.Structure (London, England : 1993) · 2026
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. [EGFR Exon 20 Insertion Mutation: Research Status and New Treatment Strategies].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2024
    Review
  20. Article

15 more citing papers are in PubMed but not listed here.

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

16 authors.

Jeonghee ChoAuthors' Affiliations: Departments of Medical Oncology and Cancer Biology; Center for Cancer Genome Discovery, Lowe Center for Thoracic Oncology, and Center for Molecular Oncologic Pathology, Dana-Farber Cancer Institute; Departments of Medicine, Brigham and Women's Hospital; Departments of Biological Chemistry and Molecular Pharmacology and Pathology, Harvard Medical School, Boston, Massachusetts; Samsung Genome Institute, Samsung Medical Center, Seoul, Republic of Korea; and The Broad Institute of Harvard and MIT, Cambridge, Massachusetts.
Liang Chen
Naveen Sangji
Takafumi Okabe
Kimio Yonesaka
Joshua M Francis
Richard J Flavin
William Johnson
Jihyun Kwon
Soyoung Yu
Heidi Greulich
Bruce E Johnson
Michael J Eck
Pasi A Jänne
Kwok-Kin Wong
Matthew Meyerson

Funding

StructureP01CA154303 · NCI · DANA-FARBER CANCER INST · PI JANNE, PASI A · 2012 to 2021
$17.8M
Inhibitor-sensitive and -resistant EGFR mutants from lung cancer and glioblastomaR01CA116020 · NCI · DANA-FARBER CANCER INST · PI ECK, MICHAEL J, MEYERSON, MATTHEW L. · 2006 to 2022
$5.1M
NCI NIH HHS P01 CA154303NCI NIH HHS R01 CA116020
6 · The paper itself

Abstract

Kinase domain mutations of the EGF receptor (EGFR) are common oncogenic events in lung adenocarcinoma. Here, we explore the dependency upon asymmetric dimerization of the kinase domain for activation of lung cancer-derived EGFR mutants. We show that whereas wild-type EGFR and the L858R mutant require dimerization for activation and oncogenic transformation, the exon 19 deletion, exon 20 insertion, and L858R/T790M EGFR mutants do not require dimerization. In addition, treatment with the monoclonal antibody, cetuximab, shrinks mouse lung tumors induced by the dimerization-dependent L858R mutant, but exerts only a modest effect on tumors driven by dimerization-independent EGFR mutants. These data imply that different EGFR mutants show differential requirements for dimerization and that disruption of dimerization may be among the antitumor mechanisms of cetuximab.

Indexed as

AdenocarcinomaAmino Acid SubstitutionAnimalsAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCells, CulturedCell Transformation, NeoplasticCetuximabErbB ReceptorsHumansLung NeoplasmsMiceNIH 3T3 CellsProtein ConformationProtein MultimerizationAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabErbB Receptors

Identifiers

PMID24063894
PMCPMC3903789

What OpenQuestion holds

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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.