Evidence map›Paper›PMID 23213241›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Direct and immune mediated antibody targeting of ERBB receptors in a colorectal cancer cell-line panel.

Shazad Q Ashraf, Angela M Nicholls, Jennifer L Wilding, Triantafyllia G Ntouroupi, Neil J Mortensen, Walter F Bodmer

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Spheroids and organoids derived from colorectal cancer as tools forExploration of targeted anti-tumor therapy · 2024
    Review
  4. Review
  5. PI3Kα Translocation Mediates Nuclear PtdIns(3,4,5)PMolecular & cellular proteomics : MCP · 2023
    Article
  6. Article
  7. Predictive and Therapeutic Implications of a Novel PLCγ1/SHP2-Driven Mechanism of Cetuximab Resistance in Metastatic Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  8. Review
  9. Review
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  12. Article
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  15. Article
  16. Article
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  18. Article
  19. Endocytosis in gene therapy with non-viral vectors.Wiener medizinische Wochenschrift (1946) · 2016
    Review
  20. 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

6 authors at 2 institutions in 1 country.

Shazad Q AshrafCancer and Immunogenetics Laboratory, Department of Oncology, Weatherall Institute of Molecular Medicine, Oxford OX3 9DS, United Kingdom.
Angela M Nicholls
Jennifer L Wilding
Triantafyllia G Ntouroupi
Neil J Mortensen
Walter F Bodmer
MRC Weatherall Institute of Molecular Medicine · GBJohn Radcliffe Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A significant proportion of colorectal cancer (CRC) patients are resistant to anti-ERBB1 [avian erythroblastic leukemia viral (v-erb-b) oncogene homolog, receptor for EGF] monoclonal antibodies (Mabs). We evaluated both immune and nonimmune effects of cetuximab (anti-ERBB1 Mab), trastuzumab (anti-ERBB2 Mab), pertuzumab (anti-ERBB2 Mab), and lapatinib (dual ERBB1 and ERBB2 tyrosine kinase inhibitor) in a large well-characterized panel of 64 CRC cell lines to find response predictive tumor characteristics. There was a significant correlation between the direct effects of cetuximab and lapatinib. Both agents were associated (P = 0.0004) with "triple' wild-type status in KRAS, BRAF, and PIK3CA exon 20. Most cell lines were resistant to the direct effects of anti-ERBB2 Mabs, suggesting that the effects of lapatinib might mainly be through ERBB1. Microarray mRNA expression profiles of sensitive and resistant cell lines showed that although ERBB1 receptor or ligand levels did not associate with cetuximab sensitivity, high levels of ERBB2 (P = 0.036) and amphiregulin (P = 0.026) predicted sensitivity to lapatinib. However, higher ERBB1 expression predicted susceptibility to cetuximab-induced antibody-dependent cellular cytotoxicity and occurred independently of KRAS/BRAF/PIK3CA mutations (P = 0.69). Lapatinib may be an effective alternative therapy to cetuximab in triple wild-type tumors. Microarray analysis provides suggestive biomarkers for resistance. ERBB1 levels, independent of mutation status, predict immune killing. Therefore, anti-ERBB1 antibodies may be considered in CRC tumors with higher ERBB1 expression and favorable FcγR polymorphisms.

Indexed as

Gene Expression Regulation, NeoplasticAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCell Line, TumorCetuximabColorectal NeoplasmsErbB ReceptorsGenes, rasHumansImmune SystemLapatinibModels, GeneticOligonucleotide Array Sequence AnalysisPolymorphism, GeneticQuinazolinesAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabEGFR protein, humanErbB ReceptorsLapatinibpertuzumabQuinazolinesTrastuzumab

Identifiers

PMID23213241
PMCPMC3529069
OpenAlexW1966067305

What OpenQuestion holds

Textmetadata
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.