Evidence map›Paper›PMID 17255336›Full record

ArticleThe American journal of pathology2007

Tumor signaling to the bone marrow changes the phenotype of monocytes and pulmonary macrophages during urethane-induced primary lung tumorigenesis in A/J mice.

Elizabeth F Redente, David J Orlicky, Ronald J Bouchard, Alvin M Malkinson

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Intranasal Iloprost Prevents Tumors in a Murine Lung Carcinogenesis Model.Cancer prevention research (Philadelphia, Pa.) · 2022
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  12. Expression of Chemokine XCL2 and CX3CL1 in Lung Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2016
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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

4 authors at 3 institutions in 1 country.

Elizabeth F RedenteUniversity of Colorado at Denver and Health Sciences Center, Department of Pharmaceutical Sciences, Box C238, East Ninth Ave., Denver, CO 80262, USA.
David J Orlicky
Ronald J Bouchard
Alvin M Malkinson
University of Colorado Denver · USUnited States Department of Veterans Affairs · USUniversity of Colorado Health · US

Funding

PROMOTION OF LUNG TUMORS BY BHT AND GLUCOCORTICOIDSR01CA033497 · NCI · UNIVERSITY OF COLORADO DENVER · PI MALKINSON, ALVIN M · 1985 to 2008
$3.2M
Chemoprevention of Early Pulmonary Lesions in MiceR01CA096133 · NCI · UNIVERSITY OF COLORADO DENVER · PI MALKINSON, ALVIN M · 2002 to 2004
$1.6M
NCI NIH HHS CA33497NCI NIH HHS CA96133NCI NIH HHS R01 CA033497NCI NIH HHS R01 CA096133
6 · The paper itself

Abstract

Little is known about how the composition of stromal cells within the lung cancer microenvironment varies during tumor progression. We examined by immunohistochemistry each of six different stromal cell populations during the development of chemically induced primary lung cancer in mice. Blood vessels were seen even in microscopic lesions, and their numbers increased with tumor size. Neutrophils infiltrated the alveoli of tumor-bearing lungs and within the periphery of macroscopic adenomas and adenocarcinomas. The numbers of peritumoral lymphocytes and macrophages increased during oncogeny, but quantitative changes in mast cells and fibroblasts were not evident. Because macrophage depletion reduces tumor growth and these cells are thus important to tumorigenesis, we also investigated their phenotype. Pulmonary macrophages expressed arginase I (subtype M2) but not inducible nitric-oxide synthase in lungs with premalignant lesions, whereas macrophages in carcinoma-bearing lungs expressed inducible nitric-oxide synthase (subtype M1) but not arginase I. Local pulmonary stimuli did not seem responsible for this shift in macrophage activation state because monocytes still residing within the bone marrow adopted these expression patterns before entering the circulation, presumably in response to tumor-derived signals. These biochemical markers of macrophage activation states would have diagnostic and/or therapeutic value if analogous systemic shifts occur in humans.

Indexed as

AdenocarcinomaAdenomaBone MarrowCell Transformation, NeoplasticLung NeoplasmsMacrophages, AlveolarAnimalsBiomarkers, TumorCarcinogensFibroblastsLungMacrophage ActivationMaleMast CellsMiceMonocytesBiomarkers, TumorCarcinogensNitric Oxide Synthase Type IINos2 protein, mouseUrethane

Identifiers

PMID17255336
PMCPMC1851863
OpenAlexW2025274960

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.