ライフサイエンスコーパス: Beckwith

1 Beckwith-Wiedemann syndrome (BWS) is a clinically variab

2 Beckwith-Wiedemann syndrome (BWS) is a congenital cancer

3 Beckwith-Wiedemann syndrome (BWS) is a fetal overgrowth

4 Beckwith-Wiedemann syndrome (BWS) is a hereditary human

5 Beckwith-Wiedemann syndrome (BWS) is a human stem cell d

6 Beckwith-Wiedemann syndrome (BWS) is a model human impri

7 Beckwith-Wiedemann syndrome (BWS) is an autosomal domina

8 Beckwith-Wiedemann syndrome (BWS), which causes prenatal

9 Beckwith-Wiedemann syndrome (BWS), which predisposes to

10 ing guidelines for neurofibromatosis type 1, Beckwith-Wiedemann syndrome/ hemihypertrophy, and PTEN h

11 ted with the Prader-Willi Syndrome (PWS) and Beckwith-Wiedemann Syndrome (BWS) where imprinting is kn

12 line balanced chromosomal rearrangements and Beckwith-Wiedemann syndrome.

13 This locus is of specific interest, as Beckwith-Wiedemann syndrome and various childhood and ad

14 associated with imprinting disorders such as Beckwith-Wiedemann syndrome (BWS).

15 s region to growth-related disorders such as Beckwith-Wiedemann syndrome and a variety of human cance

16 to develop rare epigenetic disorders such as Beckwith-Wiedemann Syndrome or Angelman Syndrome, both o

17 diseases associated with imprinting such as Beckwith-Wiedemann syndrome.

18 them from the mutations of CDKN1C that cause Beckwith-Wiedemann syndrome, an overgrowth syndrome.

19 ergrowth and cancer predisposition condition Beckwith-Wiedemann syndrome (BWS).

20 1 that are associated with the human disease Beckwith-Wiedemann syndrome (BWS) may disrupt CDKN1C exp

21 nd genotypes characterize the human disease, Beckwith--Wiedemann syndrome (BWS).

22 s associated with the developmental disorder Beckwith Wiedemann Syndrome (BWS) and with several cance

23 ) we have found that the hereditary disorder Beckwith-Wiedemann syndrome, which predisposes to cancer

24 mprinting-related fetal overgrowth disorder, Beckwith-Wiedemann syndrome.

25 gene is associated with the growth disorders Beckwith-Wiedemann and Silver-Russell syndromes and many

26 sociated with the human imprinting disorders Beckwith-Wiedemann syndrome (BWS) and Silver-Russell syn

27 on and the two contrasting growth disorders, Beckwith-Wiedemann syndrome (BWS) and Silver-Russell syn

28 l group migration, similar to that in a Dowd-Beckwith ring expansion.

29 In these cases a fully equilibrated Beckwith-Houk-type transition state provides a satisfact

30 developing human brains and fibroblasts from Beckwith-Wiedemann syndrome patients.

31 lead to serious imprinting disorders (e.g., Beckwith-Wiedemann syndrome) and is described in some ca

32 mosome 11p15.1, centromeric to the imprinted Beckwith-Wiedemann syndrome (BWS) locus at 11p15.5.

33 of several pediatric and adult tumors and in Beckwith-Wiedemann syndrome (BWS).

34 ryonal tumors, including Wilms tumor, and in Beckwith-Wiedemann syndrome.

35 ome 11 at band p15.5, a region implicated in Beckwith-Wiedemann syndrome and a region of frequent los

36 s in human p57(Kip2) have been implicated in Beckwith-Wiedemann syndrome, a disease that has also bee

37 ed expression of IGF2 has been implicated in Beckwith-Wiedemann syndrome, a human fetal overgrowth sy

38 man chromosome 11p15.5, a region involved in Beckwith-Wiedemann syndrome, Wilms' tumor, and ovarian,

39 tes, a situation similar to that observed in Beckwith-Wiedemann syndrome, another imprinted disorder.

40 ncer and some hereditary diseases, including Beckwith-Wiedemann syndrome (BWS), a disorder of prenata

41 A related developmental disorder is Beckwith-Wiedemann syndrome (BWS), which increases risk

42 ted with a human overgrowth syndrome-namely, Beckwith-Wiedemann syndrome (BWS).

43 Igf2 overexpression as a key determinant of Beckwith-Wiedemann syndrome.

44 all report an unexpectedly high incidence of Beckwith-Wiedemann syndrome (BWS) in children conceived

45 he mouse which will lead to animal models of Beckwith-Wiedemann syndrome and childhood tumours.

46 , are both implicated in the pathogenesis of Beckwith-Wiedemann syndrome.

47 , with six patients not showing phenotype of Beckwith-Wiedemann syndrome.

48 n of Igf2 results in most of the symptoms of Beckwith-Wiedemann syndrome, including prenatal overgrow

49 umor suppression and the cancer-predisposing Beckwith-Wiedemann syndrome (BWS).

50 implicated in the development of tumor-prone Beckwith-Wiedemann syndrome, is an effector molecule of

51 imprinted status of the genes in the region, Beckwith-Wiedemann syndrome (BWS) and Wilms tumor are ea

52 during childhood, including retinoblastoma, Beckwith-Wiedemann syndrome/idiopathic hemihypertrophy a

53 roblasts derived from patients with sporadic Beckwith-Wiedemann syndrome (BWS), a fetal overgrowth sy

54 ype often associated with the human syndrome Beckwith-Wiedemann.

55 re likely to develop the overgrowth syndrome Beckwith-Wiedemann (BWS).

56 loss-of-imprinting (LOI) overgrowth syndrome Beckwith-Wiedemann (BWS).

57 und in the human foetal overgrowth syndrome, Beckwith-Wiedemann syndrome (BWS).

58 The Beckwith-Wiedemann syndrome (BWS) is genetically linked

59 The Beckwith-Wiedemann syndrome (BWS) is marked by fetal org

60 The Beckwith-Wiedemann syndrome is associated with the failu

61 ed groups, consistent with prediction by the Beckwith-Houk model for stereocontrol in 5-hexenyl radic

62 nkage analysis to harbor the gene(s) for the Beckwith-Wiedemann syndrome.

63 e p57(Kip2) locus has been implicated in the Beckwith-Wiedemann syndrome and in the development of sp

64 enal defects, which are also features of the Beckwith-Wiedemann syndrome (BWS), a genetically complex

65 ons affecting the WT1 gene or linkage to the Beckwith-Weidemann syndrome of the BWS region on the sho

66 ilms' tumors, and tumors associated with the Beckwith-Wiedemann syndrome.

67 H analysis to map the breakpoints from three Beckwith-Wiedemann syndrome patients and a rhabdoid tumo

68 Disruption of imprinting leads to Beckwith-Wiedemann syndrome (BWS), an overgrowth and can

69 p57(Kip2) has been linked to Beckwith-Wiedemann syndrome and IMAGe syndrome in humans

70 imprinting region at 11p15.5 associated with Beckwith-Wiedemann syndrome.

71 Children with Beckwith-Wiedemann syndrome (BWS) are at increased risk

72 uency of ART conceptions among children with Beckwith-Wiedemann syndrome or Angelman syndrome caused

73 ART was found in registries of children with Beckwith-Wiedemann syndrome, Angelman syndrome, and reti

74 n of human chromosome 11p15.5 is linked with Beckwith-Wiedemann syndrome that is associated with susc

75 rearrangement breakpoints from patients with Beckwith-Wiedemann syndrome (BWS) have been mapped to 11

76 rearrangement breakpoints from patients with Beckwith-Wiedemann syndrome (BWS), a condition character

77 chromosomal rearrangements in patients with Beckwith-Wiedemann syndrome (BWS), which causes prenatal

78 he normal kidney and tongue of patients with Beckwith-Wiedemann syndrome (BWS), which predisposes to

79 their occasional occurrence in patients with Beckwith-Wiedemann syndrome and the case presented here

80 se phenotypes are also seen in patients with Beckwith-Wiedemann syndrome, a pleiotropic hereditary di