ArticleOncogene2002
Absence of fibroblast growth factor 2 does not prevent tumor formation originating from the RPE.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- What Can We Learn from FGF-2 Isoform-Specific Mouse Mutants? Differential Insights into FGF-2 Physiology In Vivo.International journal of molecular sciences · 2020Review
- FGF2 promotes metastasis of uveal melanoma cells via store-operated calcium entry.OncoTargets and therapy · 2017Article
- Pax genes in embryogenesis and oncogenesis.Journal of cellular and molecular medicine · 2008Review
- Melanocytes and pigmentation are affected in dopachrome tautomerase knockout mice.Molecular and cellular biology · 2004Article
- Fibroblast growth factor 2.Differentiation; research in biological diversityReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have analysed the importance of fibroblast growth factor 2 (FGF2) in tumor development. In a transgenic mouse model (Tyrp1-Tag) tumors form in the retinal pigment epithelium (RPE), invade surrounding tissues, and metastasize to lymph node and spleen. To address whether RPE tumor formation is dependent on FGF2, we generated FGF2-deficient mice. Such mice appeared healthy and exhibited no impairment of growth or development. Tyrp1-Tag transgenic mice, which are lacking FGF2 (FGF2-/-) developed RPE tumors that metastasize to spleen and lymph nodes. Tumor growth and survival rate are identical to Tyrp1-Tag transgenic littermates expressing FGF2. Cell lines were isolated from RPE tumors of wild-type and FGF2-deficient mice. They grow in culture, are pigmented and form vascularized tumors, when injected subcutaneously into nude mice of either FGF2-/- or FGF2+/+ genetic background. Kinetics of tumor growth was identical and independent of presence of FGF2. Together, these results demonstrate that FGF2 is not essential for tumor formation of the RPE thus suggesting that tumor growth in general may not be dependent on FGF2.
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Registered trials
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