- Nov 2017
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Genetic studies have also suggested that Sox10and Ednrb do not interact during murine melanocyte development (Hakami et al., 2006).
Sox10 is expressed in melanoblasts, which are the precursors of melanocytes, that do not contain Ednrb. Ednrb is expressed in embryos that do not contain Sox10. Therefore, Sox10 expression does not depend on the expression of Ednrb. (DB)
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Recent studies using the Ednrb antagonist bonsentan suggest that the use of Ednrb antagonists may prove useful for the treatment of melanoma.
Ednrb antagonists could potentially be used for the treatment of melanoma. Read more: www.theoncologist.alphamedpress.org/content/20/10/1121.full.pdf (DB)
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High VEGF levels are in turn associated with poor prognosis in human melanoma tumors (Giatromanolaki et al., 2003).
Studies show that there is a high expression of VEGF in human melanoma tumors, indicating that VEGF can serve as a marker for melanoma prognosis. Moreover, tumors with a high vascular density (VD) were also associated with poor prognosis. (DB)
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Moreover, in situ melanomas appeared in adult skin grafts, while invasive melanomas developed in newborn skin grafts indicating that the susceptibility of skin to environmental tumor promoters is dependent on age (Berking et al., 2004).
Exposure to ultraviolet (UV) radiation is a risk factor for the development of melanoma. Researchers have shown that people who sunburned in childhood are at a greater risk of developing melanoma than are people who sunburned in adulthood. This study suggests that age is associated with the susceptibility of skin to environmental carcinogens. (DB)
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Moreover, in situ melanomas appeared in adult skin grafts, while invasive melanomas developed in newborn skin grafts indicating that the susceptibility of skin to environmental tumor promoters is dependent on age (Berking et al., 2004).
Exposure to UV radiation increases the risk of melanoma development. Read more: www.skincancer.org/media-and-press/press-release-2013/kids (DB)
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Although Ednrb downregulation has been reported in some human melanoma cell lines (Eberle et al., 1999), other studies found Ednrb to be upregulated in most melanoma cell lines (Bittner et al., 2000; Ross et al., 2000).
There is an increase in the amount of Ednrb in most cell lines. This is significant because Ednrb expression is increased in melanoma metastases. (DB)
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Cancer progression exhibits many of the characteristics seen during development.
The progression of cancer is characterized by features that can be seen during development. Read more: https://www.cancerquest.org/cancer-biology/cancer-development (DB)
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This suggests that Ednrb may function to activate tyrosinase production indirectly by inducing the production or secretion of Kitl (Hou et al., 2004).
Ednrb encodes a G-protein-coupled receptor that is necessary for the development of melanocytes. Studies have shown that Ednrb is not necessary for the development of early melanoblasts but is essential for the expression of the differentiation marker tyrosinase. Ednrb wild-type cultures must be able to generate the KIT ligand. Moreover, a soluble KIT ligand allows tyrosinase to be expressed in cultures that do not contain sufficient amounts of Ednrb. (DB)
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This increase in cell numbers in the treated cultures could not be accounted for solely by a proliferative effect, pointing to a possible role for Edn3 in the survival of melanoblasts from the NC (Opdecamp et al., 1998).
Mutations in genes that code for Edn3 result in deficiencies in melanocytes. Edn3 serves as a stimulator of melanoblast proliferation and differentiation. When melanoblasts differentiate, they become melanocytes. (DB)
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Edn3 was most effective in promoting the long-term propagation of glia-melanocyte precursor cells as opposed to the other precursors (Real et al., 2006).
Researchers have shown that individual melanocytes produce multipotent cells that are able to regenerate during consecutive subcloning. This indicates that the multipotent cells display stem cell qualities. Edn3 encourages the maintenance of the multipotent cells. Moreover, Edn3 stimulates the proliferation of melanoblasts, which are the precursors of melanocytes. (DB)
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In the absence of contact inhibition, cells treated with Edn3 were found to proliferate for two weeks without producing pigment (Lahav et al., 1996).
Cells proliferate in the presence of Edn3. The cells that are produced are melanoblasts, which subsequently become melanocytes. (DB)
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It was first identified as a potent vasopressor derived from vascular endothelial cells (Yanagisawa et al., 1988).
Researchers isolated Edn1 to determine its function. Edn1 was shown to be responsible for an increase in blood pressure. Expression of the gene was controlled by factors that affect blood vessels, suggesting that there is a cardiovascular control system. (DB)
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A possible migratory function is supported by the observation that some of the remaining melanoblasts appear to accumulate in the MSA (Lee et al., 2003).
Melanoblasts are cells that become melanocytes. They proliferate and pile up in the migrating stage area. Then they become part of developing hair follicles, where they differentiate into melanocytes. (DB)
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