Evidence map›Paper›PMID 20697078›Full record

ReviewJournal of clinical oncology : official journal of the American Society of Clinical Oncology2010

Tumor antigen-targeted, monoclonal antibody-based immunotherapy: clinical response, cellular immunity, and immunoescape.

Robert L Ferris, Elizabeth M Jaffee, Soldano Ferrone

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical oncology : official journal of the American Society of Clinical Oncology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed, 2 pooled it
10.1field-weighted citation impact, top 1% 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

168 citing papers in PubMed, 2 syntheses or guidelines pooled it, 322 citations in OpenAlex.

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  4. PD-L1 Mediates Dysfunction in Activated PD-1Cancer immunology research · 2018
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108 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

3 authors at 1 institution in 1 country.

Robert L FerrisThe Hillman Cancer Center Research Pavilion, 5117 Centre Ave, Room 2.26b, Pittsburgh, PA 15213, USA. ferrisrl@upmc.edu
Elizabeth M Jaffee
Soldano Ferrone
UPMC Hillman Cancer Center · US

Funding

WILD TYPE P53-BASED ADJUVANT IMMUNOTHERAPY FOR SCCHNP50CA097190 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHRISTOPHER J. BAKKENIST · 2004 to 2026
$49.6M
Immune activation by cetuximab in head and neck cancer patientsR01DE019727 · NIDCR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FERRIS, ROBERT L. · 2010 to 2014
$2.0M
NCI NIH HHS 1P50 CA097190NCI NIH HHS P50 CA097190NIDCR NIH HHS R01 DE019727NIDCR NIH HHS R01 DE19727
6 · The paper itself

Abstract

purposeTumor antigen (TA) -targeted monoclonal antibodies (mAb), rituximab, trastuzumab, and cetuximab, are clinically effective for some advanced malignancies, especially in conjunction with chemotherapy and/or radiotherapy. However, these results are only seen in a subset (20% to 30%) of patients. We discuss the immunologic mechanism(s) underlying these clinical findings and their potential role in the variability in patients' clinical response.

methodsWe reviewed the evidence indicating that the effects of TA-targeted mAb-based immunotherapy are mediated not only by inhibition of signaling pathways, but also by cell-mediated cytotoxicity triggered by the infused TA-targeted mAb. We analyzed the immunologic variables that can influence the outcome of antibody-dependent cell-mediated cytotoxicity (ADCC) in vitro and in animal model systems. We also analyzed the correlation reported between these variables and the clinical response to mAb-based immunotherapy.

resultsOf the variables that influence ADCC mediated by TA-targeted mAb, only polymorphisms of Fcγ receptors (FcγR) expressed by patients' lymphocytes were correlated with clinical efficacy. However, this correlation is not absolute and is not observed in all malignancies. Thus other variables may be responsible for the antitumor effects seen in mAb-treated patients. We discuss the evidence that triggering of TA-specific cellular immunity by TA-targeted mAb, in conjunction with immune escape mechanisms used by tumor cells, may contribute to the differential clinical responses to mAb-based immunotherapy.

conclusionIdentification of the mechanism(s) underlying the clinical response of patients with cancer treated with TA-targeted mAb is crucial to optimizing their application in the clinic and to selecting the patients most likely to benefit from their use.

Indexed as

Immunity, CellularAnimalsAntibodies, MonoclonalAntigens, NeoplasmDrug Resistance, NeoplasmHumansImmunotherapyNeoplasmsReceptors, FcSignal TransductionAntibodies, MonoclonalAntigens, NeoplasmReceptors, Fc

Identifiers

PMID20697078
PMCPMC2954137
OpenAlexW2112887207

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.