Evidence map›Paper›PMID 22422663›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012

Activation state of stromal inflammatory cells in murine metastatic pancreatic adenocarcinoma.

Douglas D Benson, Xianzhong Meng, David A Fullerton, Ernest E Moore, Joon H Lee, Lihua Ao, Christopher C Silliman, Carlton C Barnett

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Innate Immunity in Cancer Biology and Therapy.International journal of molecular sciences · 2023
    Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Hepatic thermal injury promotes colorectal cancer engraftment in C57/black 6 mice.American journal of physiology. Cell physiology · 2021
    Article
  12. Emerging roles for the IL-6 family of cytokines in pancreatic cancer.Clinical science (London, England : 1979) · 2020
    Review
  13. Article
  14. Neutrophils in the Tumor Microenvironment.Advances in experimental medicine and biology · 2020
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Immunologic and Metabolic Features of Pancreatic Ductal Adenocarcinoma Define Prognostic Subtypes of Disease.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016
    Article
  20. Review
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

8 authors at 2 institutions in 1 country.

Douglas D BensonDenver Health Medical Center, Denver, CO 80204-0206, USA.
Xianzhong Meng
David A Fullerton
Ernest E Moore
Joon H Lee
Lihua Ao
Christopher C Silliman
Carlton C Barnett
Denver Health Medical Center · USUniversity of Colorado Denver · US

Funding

Trauma Reprograms CellsP50GM049222 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI BANERJEE, ANIRBAN · 1993 to 2017
$26.1M
NIGMS NIH HHS P50 GM049222
6 · The paper itself

Abstract

The histologic presence of macrophages (tumor-associated macrophages, TAMs) and neutrophils (tumor-associated neutrophils, TANs) has been linked to poor clinical outcomes for solid tumors. The exact mechanism for this association with worsened prognosis is unclear. It has been theorized that TAMs are immunomodulated to an alternatively activated state and promote tumor progression. Similarly, TANs have been shown to promote angiogenesis and tumor detachment. TAMs and TANs were characterized for activation state and production of prometastatic mediators in an immunocompetent murine model of pancreatic adenocarcinoma. Specimens from liver metastases were evaluated by immunofluorescence and immunoblotting. TAMS have upregulated expression of CD206 and CD163 markers of alternative activation, (4.14 ± 0.55-fold and 7.36 ± 1.13-fold over control, respectively, P < 0.001) but do not have increased expression of classically activated macrophage markers CCR2 and CCR5. TAMs also express oncostatin M (OSM). We found that TANs, not TAMs, predominantly produce matrix metalloproteinase-9 (MMP-9) in this metastatic tumor microenvironment, while MMP-2 production is pan-tumoral. Moreover, increased expression of VEGF colocalized with TAMs as opposed to TANs. TAMs and TANs may act as distinct effector cells, with TAMs phenotypically exhibiting alternative activation and releasing OSM and VEGF. TANs are localized at the invasive front of the metastasis, where they colocalize with MMP-9. Improved understanding of these interactions may lead to targeted therapies for pancreas adenocarcinoma.

Indexed as

AdenocarcinomaAnimalsCell Line, TumorCytokinesLiver NeoplasmsMacrophage ActivationMacrophagesMiceMice, Inbred C57BLPancreatic NeoplasmsStromal CellsCytokines

Identifiers

PMID22422663
PMCPMC4073963
OpenAlexW2123132717

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.