Evidence map›Paper›PMID 22028620›Full record

ArticleNeoplasia (New York, N.Y.)2011

B cells are critical to T-cell-mediated antitumor immunity induced by a combined immune-stimulatory/conditionally cytotoxic therapy for glioblastoma.

Marianela Candolfi, James F Curtin, Kader Yagiz, Hikmat Assi, Mia K Wibowo, Gabrielle E Alzadeh, David Foulad, A K M G Muhammad, Sofia Salehi, Naomi Keech and 8 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

82 citing papers in PubMed, 118 citations in OpenAlex.

  1. Trial
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  11. Immune Checkpoints in B Cells: Unlocking New Potentials in Cancer Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  12. Article
  13. Article
  14. Article
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  16. Radiation Therapy and Myeloid-Derived Suppressor Cells: Breaking Down Their Cancerous Partnership.International journal of radiation oncology, biology, physics · 2024
    Review
  17. Review
  18. Article
  19. Review
  20. Review

22 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

18 authors at 3 institutions in 1 country.

Marianela CandolfiGene Therapeutics Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
James F Curtin
Kader Yagiz
Hikmat Assi
Mia K Wibowo
Gabrielle E Alzadeh
David Foulad
A K M G Muhammad
Sofia Salehi
Naomi Keech
Mariana Puntel
Chunyan Liu
Nicholas R Sanderson
Kurt M Kroeger
Robert Dunn
Gislaine Martins
Pedro R Lowenstein
Maria G Castro
University of California, Los Angeles · USCedars-Sinai Medical Center · USBiogen (United States) · US

Funding

Gutless Adenovirus Mediated Gene Therapy for GliomaU01NS052465 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2007 to 2011
$3.1M
Engineering the Brain Immune System for Tumor TherapyR01NS057711 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2009 to 2013
$2.0M
Crosstalk between glioma cells & immune cells in the tumor microenvironment: TherR01NS074387 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CASTRO, MARIA G · 2011 to 2015
$1.9M
Brain immune responses:Cellular & Molecular MechanismsR01NS061107 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOWENSTEIN, PEDRO R. · 2008 to 2012
$1.7M
Gene Therapy and the Brain: Neuroimmune InteractionsR01NS054193 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LOWENSTEIN, PEDRO R. · 2007 to 2011
$1.6M
Regulation of effector T cell function by Blimp-1 in a murine model of colitisR21AI083948 · NIAID · CEDARS-SINAI MEDICAL CENTER · PI MARTINS, GISLAINE A · 2009 to 2010
$447k
Targeted Toxin for Brain Cancer Gene TherapyR21NS054143 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI CASTRO, MARIA G · 2007 to 2008
$383k
Gutless Adenovirus Mediated Targeted Therapeutics for GliomaF32NS058156 · NINDS · CEDARS-SINAI MEDICAL CENTER · PI CANDOLFI, MARIANELA · 2007 to 2009
$154k
NIAID NIH HHS 1R21-AI83948-01NIAID NIH HHS R21 AI083948NINDS NIH HHS 1F32 NS058156NINDS NIH HHS 1R01-NS 054193NINDS NIH HHS 1R01-NS057711NINDS NIH HHS 1R01-NS061107NINDS NIH HHS 1R21-NS054143NINDS NIH HHS 1UO1 NS052465NINDS NIH HHS F32 NS058156NINDS NIH HHS R01 NS054193NINDS NIH HHS R01 NS057711NINDS NIH HHS R01 NS061107NINDS NIH HHS R01 NS074387NINDS NIH HHS R21 NS054143NINDS NIH HHS U01 NS052465
6 · The paper itself

Abstract

We have demonstrated that modifying the tumor microenvironment through intratumoral administration of adenoviral vectors (Ad) encoding the conditional cytotoxic molecule, i.e., HSV1-TK and the immune-stimulatory cytokine, i.e., fms-like tyrosine kinase 3 ligand (Flt3L) leads to T-cell-dependent tumor regression in rodent models of glioblastoma. We investigated the role of B cells during immune-mediated glioblastoma multiforme regression. Although treatment with Ad-TK+Ad-Flt3L induced tumor regression in 60% of wild-type (WT) mice, it completely failed in B-cell-deficient Igh6(-/-) mice. Tumor-specific T-cell precursors were detected in Ad-TK+Ad-Flt3L-treated WT mice but not in Igh6(-/-) mice. The treatment also failed in WT mice depleted of total B cells or marginal zone B cells. Because we could not detect circulating antibodies against tumor cells and the treatment was equally efficient in WT mice and in mice with B-cell-specific deletion of Prdm 1 (encoding Blimp-1), in which B cells are present but unable to fully differentiate into antibody-secreting plasma cells, tumor regression in this model is not dependent on B cells' production of tumor antigen-specific immunoglobulins. Instead, B cells seem to play a role as antigen-presenting cells (APCs). Treatment with Ad-TK+Ad-Flt3L led to an increase in the number of B cells in the cervical lymph nodes, which stimulated the proliferation of syngeneic T cells and induced clonal expansion of antitumor T cells. Our data show that B cells act as APCs, playing a critical role in clonal expansion of tumor antigen-specific T cells and brain tumor regression.

Indexed as

AnimalsAntigen-Presenting CellsB-LymphocytesBrain NeoplasmsCytotoxicity, ImmunologicFemaleGenetic TherapyGlioblastomaHerpesvirus 1, HumanMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMicroscopy, Confocalflt3 ligand proteinMembrane ProteinsPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseThymidine KinaseTranscription Factors

Identifiers

PMID22028620
PMCPMC3201571
OpenAlexW2101335891

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.