Evidence map›Paper›PMID 23296156›Full record

Trial reportThe pharmacogenomics journal2014

Role of immunoglobulin G fragment C receptor polymorphism-mediated antibody-dependant cellular cytotoxicity in colorectal cancer treated with cetuximab therapy.

F V Negri, A Musolino, N Naldi, B Bortesi, G Missale, D Laccabue, A Zerbini, R Camisa, N Chernyschova, G Bisagni and 4 more

Open access · greenAbstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in The pharmacogenomics journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  7. Review
  8. Role of Fcγ receptors in HER2-targeted breast cancer therapy.Journal for immunotherapy of cancer · 2022
    Review
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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 4 institutions in 1 country.

F V NegriMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
A MusolinoMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
N NaldiMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
B BortesiMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
G MissaleLaboratory of Viral Immunopathology, Department of Infectious Diseases and Hepatology, University Hospital of Parma, Parma, Italy.
D LaccabueLaboratory of Viral Immunopathology, Department of Infectious Diseases and Hepatology, University Hospital of Parma, Parma, Italy.
A ZerbiniClinical Microbiology Laboratory, Department of Laboratory Medicine, Santa Maria Nuova Hospital, Reggio Emilia, Italy.
R CamisaMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
N ChernyschovaDepartment of Radiology University Hospital of Parma, Parma, Italy.
G BisagniDepartment of Oncology, IRCCS, Santa Maria Nuova Hospital, Reggio Emilia, Italy.
F LoupakisDivision of Medical Oncology, Department of Oncology, Transplants and New Technologies in Medicine, University of Pisa, Pisa, Italy.
A RuzzoDepartment of Biomolecular Sciences, University of Urbino, Urbino, Italy.
T M NeriMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
A ArdizzoniMedical Oncology Unit and Medical Genetics Unit, University Hospital of Parma, Parma, Italy.
University of Parma · ITSanta Maria Nuova Hospital · ITUniversity of Pisa · ITUniversity of Urbino · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Antibody-dependent cellular cytotoxicity (ADCC), which is activated by effector cells via immunoglobulin G (IgG) fragment C receptors (FcRs), was proposed as a mechanism of cetuximab efficacy. Peripheral blood mononuclear cells (PBMCs) from 23 healthy donors and 13 patients with metastatic colorectal cancer (mCRC) treated with cetuximab were tested for FcγR polymorphisms and cetuximab-mediated ADCC. ADCC was measured by chromium-51 release on a epidermal growth factor receptor (EGFR)-positive human colon cancer cell line. Overall, 86 mCRC patients were genotyped for study purposes. PBMCs harbouring the FcγRIIIa 158 V/V genotype had a significantly higher cetuximab-mediated ADCC. No correlation was found between FcγR polymorphisms and response rate or time to progression after cetuximab-based therapy. Despite the in vitro analysis showing that the FcγRIIIa 158 V/V genotype is associated with higher ADCC, clinical data do not support a predictive role of FcγRIIIa polymorphisms in mCRC treated with cetuximab.

Indexed as

Polymorphism, GeneticAdultAgedAged, 80 and overAntibodies, Monoclonal, HumanizedAntibody-Dependent Cell CytotoxicityAntineoplastic AgentsAntineoplastic Combined Chemotherapy ProtocolsCetuximabColorectal NeoplasmsDisease-Free SurvivalFemaleGenotypeHumansLeukocytes, MononuclearMaleAntibodies, Monoclonal, HumanizedAntineoplastic AgentsCetuximabFc gamma receptor IIAFCGR3A protein, humanReceptors, IgG

Identifiers

PMID23296156
OpenAlexW2089103160

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.