
Beckwith-Wiedemann syndrome(BWS) is one of the most common overgrowth syndrome and is believed that imprinted genes contribute to the phenotypes of syndrome. Embryonic tumors are observed in 7.5%-10.0% of BWS, so BWS could be classified in one of the familial cancer syndrome. We describe here the causative mechanisms of BWS, mechanisms of tumorigenesis related to the BWS, and what to be uncovered in the next step.
Genomic Imprinting, Beckwith-Wiedemann Syndrome, Potassium Channels, KCNQ Potassium Channels, Potassium Channels, Voltage-Gated, Chromosomes, Human, Pair 11, KCNQ1 Potassium Channel, Humans, Loss of Heterozygosity, Genes, Suppressor, Genes, Dominant
Genomic Imprinting, Beckwith-Wiedemann Syndrome, Potassium Channels, KCNQ Potassium Channels, Potassium Channels, Voltage-Gated, Chromosomes, Human, Pair 11, KCNQ1 Potassium Channel, Humans, Loss of Heterozygosity, Genes, Suppressor, Genes, Dominant
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