Evidence map›Paper›PMID 20431028›Full record

ArticleThe American journal of pathology2010

Tumor progression stage and anatomical site regulate tumor-associated macrophage and bone marrow-derived monocyte polarization.

Elizabeth F Redente, Lori D Dwyer-Nield, Daniel T Merrick, Komal Raina, Rajesh Agarwal, William Pao, Pamela L Rice, Kenneth R Shroyer, Alvin M Malkinson

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

59 citing papers in PubMed, 93 citations in OpenAlex.

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  11. Live or Heat-KilledInternational journal of molecular sciences · 2022
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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

9 authors at 5 institutions in 1 country.

Elizabeth F RedenteDepartment of Pharmaceutical Sciences, University of Colorado Denver, 12700 East 19th Avenue, Aurora, CO 80045, USA.
Lori D Dwyer-Nield
Daniel T Merrick
Komal Raina
Rajesh Agarwal
William Pao
Pamela L Rice
Kenneth R Shroyer
Alvin M Malkinson
University of Colorado Denver · USMemorial Sloan Kettering Cancer Center · USStony Brook University · USUniversity of Colorado Anschutz Medical Campus · USVeterans Health Administration · US

Funding

Tissue Bank and Biomarkers CoreP50CA058187 · NCI · UNIVERSITY OF COLORADO DENVER · PI MILLER, YORK E · 1992 to 2018
$43.8M
Overcoming acquired resistance to EGFR inhibitors in lung cancerR01CA121210 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LOVLY, CHRISTINE M. · 2007 to 2016
$2.9M
Angioprevention of Lung Tumorigenesis by SilibininR01CA113876 · NCI · UNIVERSITY OF COLORADO DENVER · PI AGARWAL, RAJESH · 2005 to 2009
$1.5M
NCI NIH HHS CA113876NCI NIH HHS P50 CA058187NCI NIH HHS PA50CA058187NCI NIH HHS R01 CA113876NCI NIH HHS R01 CA121210PHS HHS NCI 033497PHS HHS NCI 132552
6 · The paper itself

Abstract

Tumor-associated macrophages (TAMs) encourage and coordinate neoplastic growth. In late stage human lung adenocarcinoma, TAMs exhibited mixed M1 (classical; argI(low)iNOS(high)) and M2 (alternative; argI(high)iNOS(low)) polarization based on arginine metabolism. In several murine cancer models including chemically and genetically-induced primary lung tumors, prostate tumors, colon xenografts, and lung metastases, TAMs expressed argI(high)iNOS(low) early during tumor formation; argI(low)iNOS(high) polarization also occurred during malignancy in some models. In a chemically-induced lung tumor model, macrophages expressed argI(high)iNOS(low) within one week after carcinogen treatment, followed by similar polarization of bone marrow-derived monocytes (BDMCs) a few days later. TAMs surrounding murine prostate tumors also expressed argI(high)iNOS(low) early during tumorigenesis, indicating that this polarization is not unique to neoplastic lungs. In a human colon cancer xenograft model, the primary tumor was surrounded by argI(high)iNOS(low)-expressing TAMs, and BDMCs also expressed argI(high)iNOS(low), but pulmonary macrophages adopted argI(high)iNOS(low) polarization only after tumors metastasized to the lungs. Persistence of tumors is required to maintain TAM polarization. Indeed, in both conditional mutant Kras- and FGF10-driven models of lung cancer, mice expressing the transgene develop lung tumors that regress rapidly when the transgene is silenced. Furthermore, pulmonary macrophages expressed argI(high)iNOS(low) on tumor induction, but then returned to argI(low) iNOS(low) (no polarization) after tumors regressed. Manipulating TAM function or depleting TAMs may provide novel therapeutic strategies for preventing and treating many types of cancer.

Indexed as

Cell PolarityDisease ProgressionMacrophages, AlveolarMonocytesAnimalsBronchoalveolar Lavage FluidDisease Models, AnimalFemaleHumansInterferon-gammaInterleukin-4MaleMiceMice, Inbred StrainsNeoplasmsInterferon-gammaInterleukin-4

Identifiers

PMID20431028
PMCPMC2877857
OpenAlexW2158813742

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.