Evidence map›Paper›PMID 11583982›Full record

ArticleThe American journal of pathology2001

Tumor progression of skin carcinoma cells in vivo promoted by clonal selection, mutagenesis, and autocrine growth regulation by granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor.

M M Mueller, W Peter, M Mappes, A Huelsen, H Steinbauer, P Boukamp, M Vaccariello, J Garlick, N E Fusenig

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed, 139 citations in OpenAlex.

  1. Article
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  14. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
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  16. Depletion of langerinImmunology · 2020
    Article
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  19. Review
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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 2 countries.

M M MuellerDivision of Carcinogenesis and Differentiation, German Cancer Research Center (Deutsches Krebsforschungszentrum), Heidelberg, Germany.
W Peter
M Mappes
A Huelsen
H Steinbauer
P Boukamp
M Vaccariello
J Garlick
N E Fusenig
German Cancer Research Center · DEDKFZ-ZMBH Alliance · DEHeidelberg University · DEState University of New York · USStony Brook University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor microenvironment is crucial for cancer growth and progression as evidenced by reports on the significance of tumor angiogenesis and stromal cells. Using the HaCaT/HaCaT-ras human skin carcinogenesis model, we studied tumor progression from benign tumors to highly malignant squamous cell carcinomas. Progression of tumorigenic HaCaT-ras clones to more aggressive and eventually metastatic phenotypes was reproducibly achieved by their in vivo growth as subcutaneous tumors in nude mice. Their enhanced malignant phenotype was stably maintained in recultured tumor cells that represented, identified by chromosomal analysis, a distinct subpopulation of the parental line. Additional mutagenic effects were apparent in genetic alterations involving chromosomes 11 and 2, and in amplification and overexpression of the H-ras oncogene. Importantly, in vitro clonal selection of benign and malignant cell lines never resulted in late-stage malignant clones, indicating the importance of the in vivo environment in promoting an enhanced malignant phenotype. Independently of their H-ras status, all in vivo-progressed tumor cell lines (five of five) exhibited a constitutive and stable expression of the hematopoietic growth factors granulocyte colony-stimulating factor and granulocyte-macrophage colony-stimulating factor, which may function as autocrine/paracrine mediators of tumor progression in vivo. Thus, malignant progression favored by the in vivo microenvironment requires both clonal selection of subpopulations adapted to in vivo growth and mutational events leading to stable functional alterations.

Indexed as

Autocrine CommunicationCarcinomaClone CellsCytogenetic AnalysisDisease ProgressionGene AmplificationGene ExpressionGenes, rasGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating FactorHumansMutagenesisOncogenesPhenotypeSelection, GeneticSkin NeoplasmsGranulocyte Colony-Stimulating FactorGranulocyte-Macrophage Colony-Stimulating Factor

Identifiers

PMID11583982
PMCPMC1850484
OpenAlexW2063751527

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.