Evidence map›Paper›PMID 23363817›Full record

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

Effective anti-neu-initiated antitumor responses require the complex role of CD4+ T cells.

Eric D Mortenson, SaeGwang Park, Zhujun Jiang, Shengdian Wang, Yang-Xin Fu

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
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 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.8field-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

43 citing papers in PubMed, 64 citations in OpenAlex.

  1. Determinants of Survival with Combined HER2 and PD-1 Blockade in Metastatic Esophagogastric Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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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

5 authors at 2 institutions in 3 countries.

Eric D MortensonInstitute of Biophysics and the University of Chicago Group for Immunotherapy, Chinese Academy of Science Key Laboratory for Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China.
SaeGwang Park
Zhujun Jiang
Shengdian Wang
Yang-Xin Fu
University of Chicago · USChinese Academy of Sciences · CN

Funding

Protein Expression and Peptide CoreP01CA097296 · NCI · UNIVERSITY OF CHICAGO · PI SCHREIBER, HANS · 2003 to 2012
$15.0M
Synergy of Radiation and Immunotherapy: New ApproachesR01CA134563 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MALTER, JAMES S · 2010 to 2019
$3.4M
TNF family members for lymph angiogenesis and lymph node hypertrophyR01CA141975 · NCI · UNIVERSITY OF CHICAGO · PI FU, YANG-XIN · 2010 to 2014
$1.6M
NCI NIH HHS CA141975NCI NIH HHS CA97296NCI NIH HHS P01 CA097296NCI NIH HHS R01 CA134563NCI NIH HHS R01 CA141975
6 · The paper itself

Abstract

purposeTargeting oncogenic receptors with antibodies has been thought to suppress tumor growth mainly by interrupting oncogenic signals. Recently, the essential role for adaptive immunity, and CD8(+) T cells in particular, has been established as a major factor for anti-HER2/neu-mediated tumor regression. However, the role of CD4(+) T cells is still being defined. The purpose of this study was to explore whether and to what extent CD4(+) T cells are involved in mediating the effects of anti-HER2/neu therapy. EXPERIMENTAL

designThe role of CD4(+) T cells was examined using a transplant model of the rat HER2/neu-overexpressing cell line TUBO. Tumor-bearing mice were treated with anti-neu therapy in conjunction with CD4 depletion or CD40L blockade. The effects of CD4 depletion on the antitumor response were examined by tumor growth analysis and enzyme-linked immunospot (ELISPOT).

resultsIn addition to CD8(+) T cells, CD4(+) T cells are also essential for anti-neu antibody-mediated tumor regression, but B cells are not required. The role for CD4(+) cells is necessary throughout anti-neu therapy and not limited to helping CD8(+) T cells. Expression of IFN-γ is necessary for anti-neu therapy and IFN-γ induces MHC-II expression in TUBO cells promoting direct recognition by CD4(+) T cells. Furthermore, intratumoral depletion of CD4(+) T cells or blockade of the activating cell-surface protein CD40L inhibits the antitumor response.

conclusionsThis study reveals the essential role of CD4(+) T cell for anti-neu-mediated tumor regression.

Indexed as

ImmunotherapyAnimalsAntibodiesB-LymphocytesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell Line, TumorErb-b2 Receptor Tyrosine KinasesHumansInterferon-gammaMammary Neoplasms, AnimalMiceRatsAntibodiesERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesInterferon-gamma

Identifiers

PMID23363817
PMCPMC3602165
OpenAlexW2113404235

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.