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References in periodicals archive ?
Loss of imprinting of a paternally expressed transcript, with antisense orientation to KVLQT1, occurs frequently in Beckwith-Wiedemann syndrome and is independent of insulin-like growth factor II imprinting.
Calcifying nested stromal-epithelial tumor (CNSET) of the liver in Beckwith-Wiedemann syndrome. Eur J Med Genet.
Marangi et al., "A case of Beckwith-Wiedemann syndrome caused by a cryptic 11p15 deletion encompassing the centromeric imprinted domain of the BWS locus," Journal of Medical Genetics, vol.
Successful laparoscopic operation of bilateral pheochromocytoma in a patient with Beckwith-Wiedemann syndrome. J Hum Hypertens 2002;16:281-4.
[1,8,10,11,13] In this series, there were 37.6% of patients with Beckwith-Wiedemann syndrome. This is often a clinical diagnosis that is easily missed, hence the low reports in the literature.
Twenty-one years to the right diagnosis--clinical overlap of Simpson-Golabi-Behmel and Beckwith-Wiedemann syndrome. Am J Med Genet 2015; 167A(1):151-155.
Longini et al., "Beckwith-Wiedemann syndrome: potassium ascorbate with ribose therapy in a syndrome with high neoplastic risk," Anticancer Research, vol.
Patients with Beckwith-Wiedemann syndrome and familial adenomatous polyposis have an increased risk for congenital pancreatoblastomas and should be screened regularly.
Weksberg, "Beckwith-Wiedemann syndrome," American Journal of Medical Genetics C: Seminars in Medical Genetics, vol.
[2] proposed a classification of overgrowth syndromes by ordering them according to their typical timing of clinical presentation as follows: (a) syndromes exhibiting overgrowth in the neonatal period, including Beckwith-Wiedemann syndrome, Sotos syndrome, Weaver syndrome, and Perlman syndrome and (b) overgrowth syndromes usually identified in childhood, including Klinefelter syndrome and Proteus syndrome.
This means that subtle variations of methylation in ICRs could represent a drastic deregulation of the expression of imprinted genes, leading to important phenotypic consequences, as observed in the Beckwith-Wiedemann syndrome (6).
Igf2, an important growth factor, is highly active during fetal development and its misregulation leads to overgrowth disorders such as Beckwith-Wiedemann Syndrome. It exerts its growth promoting effects through the Igfl receptor, which induces an intracellular signaling cascade that stimulates cell proliferation.