ライフサイエンスコーパス: trisomy 8

1 sed patients (71%) with cytogenetic data had trisomy 8.

2 g increased Fas susceptibility of cells with trisomy 8.

3 osomal aberrations were trisomy 22 (18%) and trisomy 8 (16%).

4 M5 morphology, and frequently had additional trisomy 8 (39.6%; P < .001).

5 ing abnormalities included trisomy 15 (49%), trisomy 8 (46%), and -X/-Y (54%).

6 constitutes the single largest group, while trisomy 8 (+8) as a sole abnormality is the most frequen

7 55, 11.5%), inv(16)/t(16;16) (n = 28, 5.9%), trisomy 8 alone (n = 10, 2.1%), monosomy 7 (n = 9, 1.9%)

8 The prognostic impact of trisomy 8, alone or with other clonal aberrations, was e

9 cohort, TERT mutations were associated with trisomy 8 and inversion 16.

10 es maintained the ring chromosome 4, but the trisomy 8 and trisomy 18 segregated into BLIN-4E and BLI

11 Our findings demonstrate that trisomy 8 and trisomy 20 are also nonrandom aberrations

12 Trisomy 8 and trisomy 20 are nonrandom aberrations in de

13 Trisomy 8 and trisomy 20 were detected by molecular cyto

14 normalities associated with MDS (monosomy 7, trisomy 8, and 5q-) for evidence of apoptosis.

15 ar abnormalities, such as t(11q23), isolated trisomy 8, and FLT3-ITD mutations.

16 ment of APL differs in each group: FLT3-ITD, trisomy 8, and other genomic changes.

17 Cells with trisomy 8 appear to be more susceptible to Fas-mediated

18 percent of patients who had de novo MDS with trisomy 8 as the sole karyotypic abnormality responded t

19 e, with stable increase in the proportion of trisomy 8 bone marrow cells and normalization of the T-c

20 ng CD34 cells was increased in patients with trisomy 8, but decreased in monosomy 7, as compared with

21 YC protooncogene is of central importance in trisomy 8, but the experimental data to support this are

22 low levels of DNA degradation in annexin(+) trisomy 8 CD34 cells, which were comparable with annexin

23 ed comparable colony formation by annexin(+) trisomy 8(-) CD34(+) and annexin(-) CD34 cells.

24 not of the remaining subfamilies, inhibited trisomy 8 cell growth in short-term hematopoietic cultur

25 Fas expression was increased in the trisomy 8 cells and decreased in the monosomy 7 cells wh

26 ber of T cells with apparent specificity for trisomy 8 cells is consistent with an autoimmune pathoph

27 These results suggest that trisomy 8 cells undergo incomplete apoptosis and are non

28 Trisomy 8 cells were more likely to express activated ca

29 Trisomy 8 cells were resistant to apoptosis induced by g

30 in by siRNA resulted in preferential loss of trisomy 8 cells.

31 Paradoxically, trisomy 8 clones can persist in patients with bone marro

32 In contrast, trisomy 8 developed in patients with good hematologic re

33 e genomic abnormalities: 8 samples (17%) had trisomy 8 either with or without an additional duplicati

34 Thus, the trisomy 8 group as a whole had poor survival, which was

35 Patients with monosomy 7 and trisomy 8 have distinctly different clinical courses, re

36 , we found that human myeloid leukemias with trisomy 8 have increased MYC.

37 ilms tumor 1 (WT1) gene was overexpressed by trisomy 8 hematopoietic progenitor (CD34(+)) cells compa

38 P = .006), trisomy 22 (HR = 0.45; P = .07), trisomy 8 (HR = 2.26; P = .02), age (difference of 10 ye

39 llular marrow and, unexpectedly, evidence of trisomy 8 in 21.6% of cells.

40 0%); the most common were -Y in 25 (43%) and trisomy 8 in 7 patients (12%).

41 similar prognosis to those with primary MDS, trisomy 8 in AA appears to have a more favorable prognos

42 We studied 34 patients with trisomy 8 in bone marrow cells, some of whom were underg

43 Traditional cytogenetic analysis revealed trisomy 8 in two cases of osteofibrous dysplasia.

44 Trisomy 8 is a frequent cytogenetic abnormality in bone

45 Aneuploidy, especially monosomy 7 and trisomy 8, is a frequent cytogenetic abnormality in the

46 inct molecular mechanisms for monosomy 7 and trisomy 8 MDS and implicate specific pathogenic pathways

47 Previously, we showed that trisomy 8 MDS patients had clonally expanded CD8(+) T-ce

48 istent with an autoimmune pathophysiology in trisomy 8 MDS.

49 gulated in CD34 cells of both monosomy 7 and trisomy 8 MDS.

50 isomy 8 relative to healthy controls and non-trisomy 8 MDS; WT1 protein levels were also significantl

51 Trisomy 8 mosaicism (T8M) was subsequently diagnosed by

52 CD34 cells from patients with trisomy 8 myelodysplastic syndrome (MDS) are distinguish

53 by way of complex karyotype (n = 41) or sole trisomy 8 (n = 21).

54 duplication of the BCR-ABL1 gene (n = 8) and trisomy 8 (n = 3), recurrent submicroscopic alterations,

55 14q11 breakpoints, 15 with del(9p), 11 with trisomy 8, nine with 11q23 breakpoints, nine with 14q32

56 nist facilitated the expansion of cells with trisomy 8 only.

57 Moreover, trisomy 8 or amplification of 8q24 (MYC) was almost excl

58 Interphase BM cells with trisomy 8 or monosomy 7 increased in 6 of 6 patients wit

59 Trisomy 8 or monosomy 7 was shown by fluorescence in sit

60 a low percentage of cells also having either trisomy 8 or trisomy 18.

61 ples (23%) had genomic abnormalities without trisomy 8 (other abnormalities group).

62 arrow mononuclear cells of MDS patients with trisomy 8 relative to healthy controls and non-trisomy 8

63 mplex karyotype without monosomies, and sole trisomy 8, respectively (P < .0001).

64 7 accounted for 40% of all cases followed by trisomy 8, structural and numerical abnormalities of chr

65 ing the responsiveness of some patients with trisomy 8 to anti-thymocyte globulin (ATG) and cyclospor

66 In trisomy 8, up-regulated genes were primarily involved in

67 tained from MDS patients with monosomy 7 and trisomy 8 using Affymetrix GeneChips.

68 le to worsened outcomes among patients whose trisomy 8 was associated with other unfavorable cytogene

69 Fas antagonist, the percentage of cells with trisomy 8 was significantly decreased in most cases afte

70 1 with a relatively good prognosis including trisomy 8, -Y, and an extra copy of Philadelphia chromos