Evidence map›Paper›PMID 21760628›Full record

ArticleCancer gene therapy2011

Therapeutic effectiveness of intratumorally delivered dendritic cells engineered to express the pro-inflammatory cytokine, interleukin (IL)-32.

Y Qu, J L Taylor, A Bose, W J Storkus

Open access · bronzeAbstract read
In one paragraph

Article in Cancer gene therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

12 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Interleukin 32 expression in human melanoma.Journal of translational medicine · 2019
    Article
  6. Review
  7. Review
  8. Article
  9. The role of IL-32 in cutaneous T-cell lymphoma.The Journal of investigative dermatology · 2014
    Article
  10. Article
  11. Novel insights into the biology of interleukin-32.Cellular and molecular life sciences : CMLS · 2013
    Review
  12. Article
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

4 authors at 1 institution in 1 country.

Y QuDepartment of Dermatology, University of Pittsburgh School of Medicine, PA, USA.
J L Taylor
A Bose
W J Storkus
University of Pittsburgh · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
UNIVERSITY OF PITTSBURGH CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE: BPCAUL1RR024153 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2006 to 2011
$73.9M
University of Pittsburgh Clinical and Translational Science InstituteUL1TR000005 · NCATS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2012 to 2015
$50.8M
VECTOR COREP01CA100327 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STORKUS, WALTER J. · 2005 to 2009
$4.5M
Vaccines to promote Tc-1-based targeting of tumor stromaR01CA140375 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STORKUS, WALTER J. · 2010 to 2014
$1.5M
NCATS NIH HHS UL1 TR000005NCI NIH HHS P01 CA100327NCI NIH HHS P01 CA100327-05NCI NIH HHS P30 CA047904NCI NIH HHS R01 CA140375NCI NIH HHS R01 CA140375-01NCRR NIH HHS UL1 RR024153
6 · The paper itself

Abstract

Interleukin-32 (IL-32) is a pro-inflammatory cytokine conditionally produced by T cells, natural killer (NK) cells, monocytes, epithelial cells and keratinocytes, which has an important role in host resistance against infectious disease. Interestingly, elevated levels of IL-32 transcripts in fine needle aspirates of tumor tissue have also been correlated with objective clinical responses in cancer patients receiving immunotherapy. To evaluate the antitumor impact of IL-32 gene therapy, we treated BALB/c mice bearing established subcutaneous CMS4 sarcomas with intratumoral (i.t.) injections of syngenic dendritic cells (DCs) engineered to express human IL-32β complementary DNA (that is, DC.IL32). Although ectopic expression of IL-32β by DC resulted in only modest phenotypic changes in these antigen-presenting cells, DC.IL32 produced higher levels of IL-12p70 than control DC. DC.IL32 were more potent activators of type-1 T-cell responses in vitro and in vivo, with i.t. administration of DC.IL32 leading to the CD8(+) T-cell-dependent (but CD4(+) T-cell- and NK cell-independent) suppression of tumor growth. Effective DC.IL32-based therapy promoted infiltration of tumors by type-1 (that is, CXCR3(+)VLA-4(+)GrB(+)) CD8(+) T cells and CD11b(+)CD11c(+) host myeloid DC, but led to reductions in the prevalence of CD11b(+)Gr1(+) myeloid-derived suppressor cells and CD31(+) blood vessels.

Indexed as

AnimalsCD8-Positive T-LymphocytesCell Line, TumorCells, CulturedDendritic CellsEnzyme-Linked Immunosorbent AssayFemaleHumansImmunotherapy, AdoptiveInterleukinsMiceMice, Inbred BALB CSarcomainterleukin-32, mouseInterleukins

Identifiers

PMID21760628
PMCPMC3348582
OpenAlexW1997080388

What OpenQuestion holds

Textmetadata
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.