Evidence map›Paper›PMID 19155514›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Myeloid-specific expression of Api6/AIM/Sp alpha induces systemic inflammation and adenocarcinoma in the lung.

Peng Qu, Hong Du, Yuan Li, Cong Yan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Interaction of AIM with insulin-like growth factor-binding protein-4.International journal of molecular medicine · 2015
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Tumor microenvironment and myeloid-derived suppressor cells.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2013
    Article
  19. Article
  20. 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 2 institutions in 1 country.

Peng QuCenter for Immunobiology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Hong Du
Yuan Li
Cong Yan
Cincinnati Children's Hospital Medical Center · USIndiana University School of Medicine

Funding

RETINOIC ACID RECEPTOR AND SP-B GENE REGULATIONR01HL061803 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI YAN, CONG · 1999 to 2006
$1.9M
Pathophysiology of PPARgamma in the lungR01HL087001 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI DU, HONG · 2008 to 2012
$1.9M
Nuclear Receptor Co-Activators in the LungR01HL067862 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI YAN, CONG · 2003 to 2006
$1.5M
NHLBI NIH HHS HL-061803NHLBI NIH HHS HL-067862NHLBI NIH HHS HL087001NHLBI NIH HHS R01 HL061803NHLBI NIH HHS R01 HL067862NHLBI NIH HHS R01 HL087001
6 · The paper itself

Abstract

To study the functional role of apoptosis inhibition of myeloid lineage cells in tumor formation, apoptosis inhibitor 6 (Api6/AIM/Sp alpha) was overexpressed in a myeloid-specific c-fms-rtTA/(TetO)(7)-CMV-Api6 bitransgenic mouse model under the control of the c-fms promoter/intron 2. In this bitransgenic system, the Api6-Flag fusion protein was expressed in myeloid lineage cells after doxycycline treatment. Induction of Api6 abnormally elevated levels of macrophages, neutrophils, and dendritic cells in the bone marrow, blood, and lung in vivo. BrdU incorporation and annexin V binding studies showed systemically increased cell proliferation and inhibition of apoptosis in myeloid lineage cells. Api6 overexpression activated oncogenic signaling pathways, including Stat3, Erk1/2, and p38 in myeloid lineage cells in multiple organs of the bitransgenic mice. In the lung, severe inflammation and massive tissue remodeling were observed in association with increased expression of procancer cytokines/chemokines, decreased expression of proapoptosis molecule genes, and increased expression of matrix metalloproteinase genes as a result of Api6 overexpression. Oncogenic CD11b(+)/Gr-1(+) myeloid-derived suppressor cells were systemically increased. After Api6 overexpression, lung adenocarcinoma was observed in bitransgenic mice with a 35% incidence rate. These studies suggest that dysregulation of myeloid cell populations by extracellular Api6 signaling leads to abnormal myelopoiesis and lung cancer.

Indexed as

AdenocarcinomaAnimalsApoptosis Regulatory ProteinsCell MovementCell ProliferationCells, CulturedCytokinesDown-RegulationExtracellular SpaceInflammation MediatorsLung NeoplasmsMiceMice, TransgenicMyeloid CellsMyeloproliferative DisordersReceptor, Macrophage Colony-Stimulating FactorApoptosis Regulatory ProteinsCd5l protein, mouseCytokinesInflammation MediatorsReceptor, Macrophage Colony-Stimulating FactorReceptors, ImmunologicReceptors, Scavenger

Identifiers

PMID19155514
PMCPMC2630116
OpenAlexW1479736751

What OpenQuestion holds

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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.