ArticleJournal of neuro-oncology1994
TM-1 cells from an established human malignant glioma cell line produce PDGF, TGF-alpha, and TGF-beta which cooperatively play a stimulatory role for an autocrine growth promotion.
Article in Journal of neuro-oncology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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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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.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Hypoxia and the hypoxia-inducible-factor pathway in glioma growth and angiogenesis.Neuro-oncology · 2005Review
- Interaction of transforming growth factor-beta (TGF-beta) and epidermal growth factor (EGF) in human glioma cells.Journal of neuro-oncology · 2003Article
- Modulation of tissue-type plasminogen activator expression by platelet activating factor in human glioma cells.Journal of neuro-oncology · 2002Article
- Tissue factor and cancer procoagulant expressed by glioma cells participate in their thrombin-mediated proliferation.Journal of neuro-oncology · 2000Article
- Plasma platelet-derived growth factor-B chain is elevated in patients with extensively large brain tumour.Acta neurochirurgica · 1995Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have previously established a human malignant glioma cell line, TM-1. TM-1 cells could proliferate in the serum-free medium. In the present study, immunochemical analysis demonstrated that platelet-derived growth factor (PDGF), transforming growth factor (TGF)-alpha, and TGF-beta are present in the serum-free medium conditioned by growing TM-1 cells. While the cells appeared to possess a single type of binding sites for epidermal growth factor (EGF) with properties comparable to those determined for other tumor cells, the conditioned medium did not contain EGF.PDGF, TGF-alpha, and EGF added exogenously to serum-free media stimulated thymidine incorporation into DNA of TM-1 cells. In addition, antibodies specific for PDGF and TGF-alpha suppressed this activity. These results indicate autocrine and stimulatory roles of PDGF and TGF-alpha for the proliferation of TM-1 cells. As observed for other tumor cells, TGF-beta by itself weakly suppressed thymidine incorporation by TM-1 cells. However, TGF-beta employed in combination with TGF-alpha or EGF appeared to stimulate thymidine incorporation, suggesting that a cooperative action of TGF-beta with different growth factors may be involved in the stimulatory growth regulation at least for TM-1 cells.
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