ライフサイエンスコーパス: biallelic inactivation

1 ntly, and this epigenetic mechanism leads to biallelic inactivation.

2 g BAP1 in familial mesotheliomas, indicating biallelic inactivation.

3 ergo tumor-specific mutation consistent with biallelic inactivation.

4 ost significantly mutated CMG is DNAAF1 with biallelic inactivation and loss of DNAAF1 expression sho

5 Additional biallelic inactivation and/or missense p53 mutation in t

6 were found in tumors from five patients, and biallelic inactivation as a result of a mutation and los

7 ith approximately 30% of patients displaying biallelic inactivation by mutations and/or deletions.

8 loma driver genes and the critical nature of biallelic inactivation events affecting tumor suppressor

9 In many recurrent deletions, however, such biallelic inactivation has not been found.

10 he unmethylated form was present, confirming biallelic inactivation in methylated lines.

11 the genome-wide identification of genes with biallelic inactivation involving nonsense mutations and

12 RCs and also confers the "second hit" in the biallelic inactivation mechanism for some proportion of

13 r ACVR2 mutation and expression to assess if biallelic inactivation occurs.

14 ssity for earlier genetic alterations before biallelic inactivation of a recessive tumor susceptibili

15 ising in Arf (+/-) mice consistently exhibit biallelic inactivation of Arf, but, unexpectedly, do not

16 In contrast to biallelic inactivation of autosomal tumor-suppressor gen

17 esothelioma cells from Bap1(+/-) mice showed biallelic inactivation of Bap1, consistent with its prop

18 Biallelic inactivation of BRCA1 or BRCA2 is associated w

19 We investigated the prevalence of biallelic inactivation of BRCA2 in the presumed precurso

20 Although biallelic inactivation of BRG1 could not initiate tumor

21 that a loss of cell viability underlies why biallelic inactivation of BRG1 does not increase tumorig

22 Biallelic inactivation of cancer susceptibility gene BRC

23 Biallelic inactivation of CDKN2A emerged exclusively in

24 known TSGs are not homozygously deleted, and biallelic inactivation of CDKN2A may contribute to tumor

25 Biallelic inactivation of DPC4 has been reported in half

26 tumors arising in a double heterozygote show biallelic inactivation of either BRCA1 or BRCA2, but not

27 ly, TSC is said to occur through a classical biallelic inactivation of either TSC genes (TSC1, hamart

28 diator complex subunit 12 (MED12) mutations, biallelic inactivation of fumarate hydratase (FH), and c

29 We demonstrate that biallelic inactivation of Lkb1 and Pten in the mouse lun

30 Biallelic inactivation of LKB1, a serine/threonine kinas

31 lial carcinoma, we generated mice containing biallelic inactivation of Pten in the urogenital epithel

32 Eleven tumor tissues showed biallelic inactivation of RIZ.

33 Thus, biallelic inactivation of SMAD4 occurs in both the epith

34 One case of apparent biallelic inactivation of Smad4 was found in our study o

35 In one of the two tumors, biallelic inactivation of the APC gene was found.

36 Biallelic inactivation of the Apc tumor suppressor gene

37 These results suggest that biallelic inactivation of the BRCA2 gene is a relatively

38 aggressive pediatric cancer characterized by biallelic inactivation of the core BAF complex subunit S

39 C) is an inherited cancer syndrome linked to biallelic inactivation of the gene encoding the tricarbo

40 When reintroduced in cell lines carrying biallelic inactivation of the gene, A20 induced apoptosi

41 s cause loss of ACVR2 expression, indicating biallelic inactivation of the gene.

42 RTs are characterized by biallelic inactivation of the INI1 tumor suppressor gene

43 bility that gliomagenesis requires more than biallelic inactivation of the NF1 tumor suppressor gene

44 g may result in the functional equivalent of biallelic inactivation of the NF1 tumor suppressor.

45 Biallelic inactivation of the NF2 gene occurs in the maj

46 is an inherited autosomal disorder caused by biallelic inactivation of the NF2 tumor suppressor gene.

47 n malignancies, but the demonstrated rate of biallelic inactivation of the PTEN gene by mutation or h

48 ma is a pediatric retinal tumor initiated by biallelic inactivation of the retinoblastoma gene (RB1).

49 In ccRCC the biallelic inactivation of the VHL gene leads to stabiliz

50 for more than 80% of cases, are typified by biallelic inactivation of the von Hippel-Lindau (VHL) tu

51 f kidney cancer and frequently are linked to biallelic inactivation of the von Hippel-Lindau (VHL) tu

52 Biallelic inactivation of the von Hippel-Lindau tumor su

53 Biallelic inactivation of the von Hippel-Lindau tumor su

54 r in sporadic colorectal cancers (CRCs), but biallelic inactivation of this site has not been frequen

55 number of copy number aberration changes and biallelic inactivation of tumor suppressor genes was inc

56 es that are much more similar to tumors with biallelic inactivation of VHL.

57 In addition, biallelic inactivations of BRG1 were observed in four ot

58 This biallelic inactivation resulted in loss of expression of

59 However, the low frequency of biallelic inactivation suggests that either PTEN/MMAC1 i

60 Overall, evidence of biallelic inactivation was found in 74.2% of patients wi

61 Loss of the WT Nf2 allele, leading to biallelic inactivation, was observed in all nine asbesto