ライフサイエンスコーパス: hyperdiploid

1 s in nearly 40% of tumors, most of which are hyperdiploid.

2 showed that more than 95% of the cells were hyperdiploid.

3 lonal proteins and is much less likely to be hyperdiploid.

4 NA content, whereas the remaining cases were hyperdiploid.

5 an intervening mitosis) and the cells become hyperdiploid.

6 Despite high-hyperdiploid acute lymphoblastic leukaemia (HD-ALL) bein

7 basis for the excellent clinical outcome of hyperdiploid acute lymphoblastic leukemia (ALL), defined

8 cer and revealed minimal residual disease in hyperdiploid acute lymphocytic leukemia, providing "proo

9 reatest effect on MTXPG(1-7) accumulation in hyperdiploid ALL (median: 3,919 v 2,417 pmol/10(9) cells

10 association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78).

11 cumulation of MTX polyglutamates (MTX-PG) in hyperdiploid ALL and lower accumulation in T-lineage ALL

12 r (P =.0013), with the highest expression in hyperdiploid ALL blasts with 4 copies of chromosome 21.

13 T3 occur in 18% of MLL-rearranged and 28% of hyperdiploid ALL cases.

14 10(-9), OR = 1.62) but also distinguished B-hyperdiploid ALL from other subtypes (rs10821936, P = 1.

15 These ARID5B SNPs also distinguished B-hyperdiploid ALL from other subtypes in an independent v

16 All 6 patients with hyperdiploid ALL had detectable "leukemic" clones on the

17 ith monosomy 7/5q- were associated with high hyperdiploid ALL karyotypes, whereas 11q23/MLL-rearrange

18 Because hyperdiploid ALL samples also show high-level expression

19 ata show that approximately 25% (6 of 25) of hyperdiploid ALL samples possess FLT3 mutations, whereas

20 A cohort of children with hyperdiploid ALL without gain of chromosomes 17 and 18 h

21 was shown to be specifically associated with hyperdiploid ALL, whereas the rs3824662-associated risk

22 The remaining tumors are hyperdiploid and contain multiple trisomies involving ch

23 gnificant expression differences between the hyperdiploid and diploid groups on other chromosomes (mo

24 d by subtype, with a lower frequency in high-hyperdiploid and higher frequency in ETV6-RUNX1 fusion A

25 with high-dose therapy if their tumors were hyperdiploid and lacked MYCN amplification.

26 lls entirely deficient in p53 protein become hyperdiploid, and display 8N to 16N DNA content.

27 ted with a shorter survival), pseudodiploid, hyperdiploid, and near-tetraploid MM.

28 ineteen patients were pseudodiploid, 10 were hyperdiploid, and seven were hypodiploid.

29 Hyperdiploid B-cell ALLs were 23-fold more likely to be

30 ren, with significantly higher expression in hyperdiploid B-lineage ALL (median, 11.3) compared with

31 a mechanism for greater MTX accumulation in hyperdiploid B-lineage ALL and indicate that lineage dif

32 er LDMTX, MTX-PG accumulation was highest in hyperdiploid B-lineage ALL with 4 copies of chromosome 2

33 2A-PBX1 fusion, and were less likely to have hyperdiploid blast cells, a favorable prognostic factor

34 ALL cells, failed to improve the survival of hyperdiploid blasts.

35 strikingly, patients were less likely to be hyperdiploid by DNA content analysis (n = 251, 14% vs 62

36 Among the 25 hyperdiploid cases, only two had cell recoveries above t

37 The demise of hyperdiploid cells on stroma was not due to failure to a

38 potential explanation for the prevalence of hyperdiploid chromosome number and centrosome amplificat

39 The hyperdiploid D1 group is virtually absent in extramedull

40 these genetic abnormalities or compared with hyperdiploid (fewer than 50 chromosomes) ALL.

41 a, and breast cancers, and two ALL subtypes: Hyperdiploid > 50 and TEL-AML1.

42 By G-banding, most cases showed complex hyperdiploid karyotypes and diverse cytogenetic abnormal

43 , TEL-AML1, MLL rearrangements, BCR-ABL, and hyperdiploid karyotypes with more than 50 chromosomes.

44 condensation chromosomes frequently display hyperdiploid karyotypes, indicating that delay in replic

45 ciated with age over 10 years (p=0.003), non-hyperdiploid leukaemia (p=0.031), and T-cell immunopheno

46 The hyperdiploid leukaemia karyotype was highly over-represe

47 The CD5(+), IgM(+), B220(dim), hyperdiploid LPD was linked to 3 loci on chromosomes 14,

48 Hyperdiploid MM (48 to 74 chromosomes, median 53 chromos

49 reported in the literature, suggesting that hyperdiploid MM may originate early during disease evolu

50 ) is remarkably similar to the percentage of hyperdiploid MM reported in the literature, suggesting t

51 Hyperdiploid multiple myeloma (H-MM) is the most common

52 e trisomies from a 3-chromosome combination, hyperdiploid myeloma can be detected with high specifici

53 These data suggest that patients with hyperdiploid or relapsed ALL might be considered candida

54 c leukemia (ALL) histology (P = 0.008), high hyperdiploid (P < 0.0001), and translocation-negative (P

55 high prevalence of IgH translocations and a hyperdiploid pathway associated with multiple trisomies

56 increased frequencies in T-cell acute LL and hyperdiploid precursor B-cell acute LL.

57 cantly higher for patients whose tumors were hyperdiploid rather than diploid (EFS, 82% +/- 20% v 37%

58 Two groups of hyperdiploid samples were identified, on the basis of un

59 MGUS) who had normal karyotype, 11 cases of hyperdiploid SMM/MGUS were detected.

60 quent reduplication of DNA and the resulting hyperdiploid state.

61 th a balanced t(1;19) were less likely to be hyperdiploid than patients with an unbalanced der(19)t(1

62 ses in the 12- to 18-month-old subgroup with hyperdiploid tumors (4-year EFS, 92.9% +/- 7.2%) compare

63 d 87% +/- 9%, respectively for patients with hyperdiploid tumors and 25% +/- 11% and 38% +/- 12% for

64 with stage D NB (P <.001); and patients with hyperdiploid tumors had better outcome than those with d

65 The remaining hyperdiploid tumors have multiple trisomies involving ch

66 utcomes for patients with MYCN-nonamplified, hyperdiploid tumors were excellent.

67 ied neuroblastoma, outcomes of patients with hyperdiploid tumors were statistically, significantly be

68 an SE of 10%; patients with MYCN-amplified, hyperdiploid tumors, 46% with an SE of 15%; and patients

69 arm B were patients with MYCN nonamplified, hyperdiploid tumors, 86% with an SE of 3%; patients with

70 bi-allelically dysregulated in a majority of hyperdiploid tumors.

71 oward improved EFS was seen in children with hyperdiploid versus diploid tumors.

72 lusion of t(1;19)+ patients whose cells were hyperdiploid with more than 50 chromosomes.