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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 %], TCF3-PBX1 [6.9%], PAX5 P80R [4.1%], high-hyperdiploid [6.9%]); 50.2% had high-risk genotypes with
7                                 Despite high-hyperdiploid acute lymphoblastic leukaemia (HD-ALL) bein
8 enetic risk factors among patients with high hyperdiploid acute lymphoblastic leukaemia treated on UK
9  basis for the excellent clinical outcome of hyperdiploid acute lymphoblastic leukemia (ALL), defined
10 cer and revealed minimal residual disease in hyperdiploid acute lymphocytic leukemia, providing "proo
11  When stratified by subtype characteristics, hyperdiploid ALL (74 cases) was associated with 6.26 tim
12 reatest effect on MTXPG(1-7) accumulation in hyperdiploid ALL (median: 3,919 v 2,417 pmol/10(9) cells
13  association with DP1, particularly for high-hyperdiploid ALL (OR = 1.83; 95% CI, 1.20-2.78).
14 n ETV6::RUNX1 ALL, IKZF1, and CREBBP in high-hyperdiploid ALL and FHIT in BCR::ABL1-like ALL.
15 cumulation of MTX polyglutamates (MTX-PG) in hyperdiploid ALL and lower accumulation in T-lineage ALL
16 31 (rs76925697, P = 2.11 x 10(-8)), for high-hyperdiploid ALL at 5q31.1 (rs886285, P = 1.56 x 10(-8))
17 r (P =.0013), with the highest expression in hyperdiploid ALL blasts with 4 copies of chromosome 21.
18 T3 occur in 18% of MLL-rearranged and 28% of hyperdiploid ALL cases.
19                                              Hyperdiploid ALL exhibited particular sensitivities to a
20  10(-9), OR = 1.62) but also distinguished B-hyperdiploid ALL from other subtypes (rs10821936, P = 1.
21       These ARID5B SNPs also distinguished B-hyperdiploid ALL from other subtypes in an independent v
22                          All 6 patients with hyperdiploid ALL had detectable "leukemic" clones on the
23 ith monosomy 7/5q- were associated with high hyperdiploid ALL karyotypes, whereas 11q23/MLL-rearrange
24                                      Because hyperdiploid ALL samples also show high-level expression
25 ata show that approximately 25% (6 of 25) of hyperdiploid ALL samples possess FLT3 mutations, whereas
26                    A cohort of children with hyperdiploid ALL without gain of chromosomes 17 and 18 h
27               Among different definitions of hyperdiploid ALL, DI is optimal based on independent pro
28                                  Within high-hyperdiploid ALL, gain of chromosome 10 with disomy of c
29 was shown to be specifically associated with hyperdiploid ALL, whereas the rs3824662-associated risk
30 , cCMV was associated with increased risk of hyperdiploid ALL.
31 atin architecture, display low expression in hyperdiploid ALL.
32 l disease, including NRAS and CREBBP in high-hyperdiploid ALL.
33 ns), and 2 subtypes had higher MTXPG levels (hyperdiploid and BCR-ABL like).
34                     The remaining tumors are hyperdiploid and contain multiple trisomies involving ch
35 gnificant expression differences between the hyperdiploid and diploid groups on other chromosomes (mo
36 well as Hi-C of primary patient samples from hyperdiploid and ETV6/RUNX1-positive pediatric ALL.
37 d by subtype, with a lower frequency in high-hyperdiploid and higher frequency in ETV6-RUNX1 fusion A
38  with high-dose therapy if their tumors were hyperdiploid and lacked MYCN amplification.
39 ically, MM is categorized into two subtypes: hyperdiploid and non-hyperdiploid tumors, with distinct
40 lls entirely deficient in p53 protein become hyperdiploid, and display 8N to 16N DNA content.
41 ted with a shorter survival), pseudodiploid, hyperdiploid, and near-tetraploid MM.
42 onging to the BCR::ABL1+, ETV6::RUNX1+, high hyperdiploid, and recently discovered DUX4-rearranged (D
43 ineteen patients were pseudodiploid, 10 were hyperdiploid, and seven were hypodiploid.
44 found depletion of transplanted E2A-PBX1 and hyperdiploid B-ALL cells in wild-type recipients and in
45 ents, 93% with ETV6::RUNX1 and 54% with high-hyperdiploid B-ALL experienced excellent outcomes with a
46                                Collectively, hyperdiploid B-ALL is associated with a defective conden
47 lent outcomes, except for NCI high-risk high-hyperdiploid B-ALL patients with slow MRD response, who
48  high-risk patients with ETV6::RUNX1 or high-hyperdiploid B-ALL who received SJ low-risk therapy had
49                                           In hyperdiploid B-ALL, chromosomal gains are acquired early
50                                     For high-hyperdiploid B-ALL, NCI high-risk patients had worse EFS
51            Children with ETV6::RUNX1 or high-hyperdiploid B-cell acute lymphoblastic leukemia (B-ALL)
52                                              Hyperdiploid B-cell ALLs were 23-fold more likely to be
53 ren, with significantly higher expression in hyperdiploid B-lineage ALL (median, 11.3) compared with
54  a mechanism for greater MTX accumulation in hyperdiploid B-lineage ALL and indicate that lineage dif
55 er LDMTX, MTX-PG accumulation was highest in hyperdiploid B-lineage ALL with 4 copies of chromosome 2
56 .2 deletions are highly enriched in the high-hyperdiploid BCP ALL subtype (frequency 3.9% vs 0.5% in
57 2A-PBX1 fusion, and were less likely to have hyperdiploid blast cells, a favorable prognostic factor
58 ALL cells, failed to improve the survival of hyperdiploid blasts.
59  strikingly, patients were less likely to be hyperdiploid by DNA content analysis (n = 251, 14% vs 62
60 er was associated with inferior DFS, whereas hyperdiploid cases showed a superior outcome.
61                                 Among the 25 hyperdiploid cases, only two had cell recoveries above t
62                                The demise of hyperdiploid cells on stroma was not due to failure to a
63     Furthermore, Hi-C of a limited number of hyperdiploid childhood ALL cases revealed that 2/4 cases
64  potential explanation for the prevalence of hyperdiploid chromosome number and centrosome amplificat
65                                          The hyperdiploid D1 group is virtually absent in extramedull
66  78% of IgL-MYC translocations co-occur with hyperdiploid disease, a marker of standard risk, suggest
67 .6); United Kingdom ALL study group low-risk hyperdiploid, either trisomy of chromosomes 17 and 18 or
68 these genetic abnormalities or compared with hyperdiploid (fewer than 50 chromosomes) ALL.
69 he validation cohort, patients with the high hyperdiploid good risk profile had an improved response
70 iating domain (TAD) borders were seen in the hyperdiploid group.
71 a, and breast cancers, and two ALL subtypes: Hyperdiploid > 50 and TEL-AML1.
72                                              Hyperdiploid (HD) B-cell acute lymphoblastic leukemia (A
73                             Furthermore, our hyperdiploid HMCLs correlated better with hyperdiploid t
74                             Acquisition of a hyperdiploid (HY) karyotype or immunoglobulin heavy chai
75      By G-banding, most cases showed complex hyperdiploid karyotypes and diverse cytogenetic abnormal
76 , TEL-AML1, MLL rearrangements, BCR-ABL, and hyperdiploid karyotypes with more than 50 chromosomes.
77  condensation chromosomes frequently display hyperdiploid karyotypes, indicating that delay in replic
78 ciated with age over 10 years (p=0.003), non-hyperdiploid leukaemia (p=0.031), and T-cell immunopheno
79                                          The hyperdiploid leukaemia karyotype was highly over-represe
80               The CD5(+), IgM(+), B220(dim), hyperdiploid LPD was linked to 3 loci on chromosomes 14,
81                                              Hyperdiploid MM (48 to 74 chromosomes, median 53 chromos
82 distinguish patients with low- and high-risk hyperdiploid MM and identify patients with prolongation
83  reported in the literature, suggesting that hyperdiploid MM may originate early during disease evolu
84 ) is remarkably similar to the percentage of hyperdiploid MM reported in the literature, suggesting t
85                                              Hyperdiploid multiple myeloma (H-MM) is the most common
86 e trisomies from a 3-chromosome combination, hyperdiploid myeloma can be detected with high specifici
87  Patients with ETV6::RUNX1 (n = 222) or high-hyperdiploid (n = 296) B-ALL had 5-year event-free survi
88        These data suggest that patients with hyperdiploid or relapsed ALL might be considered candida
89 c leukemia (ALL) histology (P = 0.008), high hyperdiploid (P < 0.0001), and translocation-negative (P
90  high prevalence of IgH translocations and a hyperdiploid pathway associated with multiple trisomies
91 correlated better with hyperdiploid than non-hyperdiploid patient samples.
92                         The outcome for high hyperdiploid poor risk patients was similar to that of p
93 increased frequencies in T-cell acute LL and hyperdiploid precursor B-cell acute LL.
94      The prognostic effect of the UKALL high hyperdiploid profile was independent of minimal residual
95 e count to incorporate this novel UKALL high hyperdiploid profile.
96 cantly higher for patients whose tumors were hyperdiploid rather than diploid (EFS, 82% +/- 20% v 37%
97 ease and the profile outperformed other high hyperdiploid risk profiles.
98                                Two groups of hyperdiploid samples were identified, on the basis of un
99  clonal expansion in hyperdiploid versus non-hyperdiploid samples.
100  MGUS) who had normal karyotype, 11 cases of hyperdiploid SMM/MGUS were detected.
101 nger than 547 days with favorable histology, hyperdiploid stage 4, or unfavorable histology stage 3 t
102 quent reduplication of DNA and the resulting hyperdiploid state.
103 ur hyperdiploid HMCLs correlated better with hyperdiploid than non-hyperdiploid patient samples.
104 th a balanced t(1;19) were less likely to be hyperdiploid than patients with an unbalanced der(19)t(1
105 uroblastoma Pathology Classification (INPC), hyperdiploid tumors (12-18mo/Stage4/FavBiology), and 365
106 ses in the 12- to 18-month-old subgroup with hyperdiploid tumors (4-year EFS, 92.9% +/- 7.2%) compare
107 d 87% +/- 9%, respectively for patients with hyperdiploid tumors and 25% +/- 11% and 38% +/- 12% for
108 with stage D NB (P <.001); and patients with hyperdiploid tumors had better outcome than those with d
109                                The remaining hyperdiploid tumors have multiple trisomies involving ch
110 utcomes for patients with MYCN-nonamplified, hyperdiploid tumors were excellent.
111 ied neuroblastoma, outcomes of patients with hyperdiploid tumors were statistically, significantly be
112  an SE of 10%; patients with MYCN-amplified, hyperdiploid tumors, 46% with an SE of 15%; and patients
113  arm B were patients with MYCN nonamplified, hyperdiploid tumors, 86% with an SE of 3%; patients with
114 ized into two subtypes: hyperdiploid and non-hyperdiploid tumors, with distinct chromosomal character
115 bi-allelically dysregulated in a majority of hyperdiploid tumors.
116 oward improved EFS was seen in children with hyperdiploid versus diploid tumors.
117  features, and divergent clonal expansion in hyperdiploid versus non-hyperdiploid samples.
118 lusion of t(1;19)+ patients whose cells were hyperdiploid with more than 50 chromosomes.

 
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