ReviewInternational journal of clinical oncology2008
Novel therapeutic strategy for uterine endometrial cancers.
Review in International journal of clinical oncology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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.
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.
Who cites it
0 citing papers in PubMed, 6 citations in OpenAlex.
No citing paper in PubMed yet.
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Authors and funding
1 author at 1 institution in 1 country.
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Abstract
In general, tumors induce angiogenic factors specific to them, which leads to angiogenesis with tumor progression. However, angiogenesis in uterine endometrial cancers is complicated because the hormone dependency in their growth also modifies the angiogenic potential. Therefore, angiogenic potential in uterine endometrial cancers must be thoroughly analyzed. The upstream of the vascular endothelial growth factor (VEGF) gene conserves estrogen-responsive elements. Progesterone primed with estrogen induces thymidine phosphorylase (TP) in the uterine endometrium. Sex steroid-dependent VEGF and TP are highly expressed in early-stage and well-differentiated uterine endometrial cancers, and basic fibroblast growth factor (bFGF) is highly expressed in advanced and poorly differentiated uterine endometrial cancers. A transcriptional factor for angiogenesis, E26 transformation specific (ETS-1), is linked to VEGF in well-differentiated uterine endometrial cancers, and to bFGF in poorly differentiated uterine endometrial cancers. Therefore, even if dedifferentiation and angiogenic switching occur due to tumor progression and long-term hormone therapy, the inhibition of ETS-1, along with inhibition of the main angiogenic factors, may be an effective strategy to suppress uterine endometrial cancers as a novel antiangiogenic therapy.
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