Evidence map›Paper›PMID 23460534›Full record

ArticleClinical cancer research : an official journal of the American Association for Cancer Research2013

Agonistic CD40 antibodies and cancer therapy.

Robert H Vonderheide, Martin J Glennie

Abstract read
In one paragraph

Article in Clinical cancer research : an official journal of the American Association for Cancer Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers.

0numbers the graph read from it
0cells of the map it votes in
274citing papers in PubMed
29.4field-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

274 citing papers in PubMed, 411 citations in OpenAlex.

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  19. Harnessing chimeric antigen receptor macrophages against solid tumors.Cancer communications (London, England) · 2025
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214 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

2 authors at 1 institution in 1 country.

Robert H VonderheideAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. rhv@exchange.upenn.edu
Martin J Glennie
University of Pennsylvania · US

Funding

UNIVERSITY OF PENNSYLVANIA CAN CTR SUPPORT GRANTP30CA016520 · NCI · UNIVERSITY OF PENNSYLVANIA · PI SHELLEY L BERGER · 1985 to 2026
$222.3M
Immunobiology and immunotherapy of pancreatic cancerR01CA169123 · NCI · UNIVERSITY OF PENNSYLVANIA · PI STANGER, BEN Z, VONDERHEIDE, ROBERT H · 2012 to 2016
$3.1M
Combined CD40 activation and CTLA4 blockade in melanomaR01CA158186 · NCI · UNIVERSITY OF PENNSYLVANIA · PI VONDERHEIDE, ROBERT H · 2011 to 2015
$1.6M
Cancer Research UK 10834NCI NIH HHS P30 CA016520NCI NIH HHS R01 CA158186NCI NIH HHS R01 CA169123
6 · The paper itself

Abstract

Recent success in cancer immunotherapy has reinvigorated the hypothesis that the immune system can control many if not most cancers, in some cases producing durable responses in a way not seen with many small-molecule drugs. Agonistic CD40 monoclonal antibodies (mAb) offer a new therapeutic option which has the potential to generate anticancer immunity by various mechanisms. CD40 is a TNF receptor superfamily member expressed broadly on antigen-presenting cells (APC) such as dendritic cells, B cells, and monocytes as well as many nonimmune cells and a range of tumors. Agonistic CD40 mAb have been shown to activate APC and promote antitumor T-cell responses and to foster cytotoxic myeloid cells with the potential to control cancer in the absence of T-cell immunity. Thus, agonistic CD40 mAb are fundamentally different from mAb which block negative immune checkpoint such as anti-CTLA-4 or anti-PD-1. Initial clinical trials of agonistic CD40 mAb have shown highly promising results in the absence of disabling toxicity, both in single-agent studies and in combination with chemotherapy; however, numerous questions remain about dose, schedule, route of administration, and formulation. Recent findings about the role played by the IgG isotype and the Fc gamma receptor (FcγR) in mAb cross-linking, together with insights into mechanisms of action, particularly with regard to the role of myeloid cells, are predicted to help design next-generation CD40 agonistic reagents with greater efficacy. Here, we will review the preclinical and clinical data and discuss the major issues facing the field.

Indexed as

ImmunotherapyT-Lymphocytes, CytotoxicAnimalsAntibodies, MonoclonalCD40 AntigensHumansNeoplasmsAntibodies, MonoclonalCD40 Antigens

Identifiers

PMID23460534
PMCPMC3590838
OpenAlexW2168302786

What OpenQuestion holds

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LicenceTDM
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.