Risk- and response-based classification of childhood B-precursor acute lymphoblastic leukemia: a combined analysis of prognostic markers from the Pediatric Oncology Group (POG) and Children's Cancer Group (CCG)

Schultz, Kirk R.; Pullen, DJ; Sather, Harland N.; Shuster, Jonathan J.; Devidas, Meenakshi; Borowitz, Michael J.; Carroll, Andrew J.; Heerema, Nyla A.; Rubnitz, Jeffrey E.; Loh, Mignon L.; Raetz, Elizabeth A.; Winick, Naomi J.; Hunger, Stephen P.; Carroll, William L.; Gaynon, Paul S.; Camitta, Bruce M.

doi:10.1182/blood-2006-01-024729

Cited by 420 publications

(328 citation statements)

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“…Despite the fact that simultaneous occurrence of þ 4, þ 10 and þ 17 in childhood ALL has been associated with low-risk pediatric ALL, 10 we nevertheless found these triple trisomies in the majority (7 of 11; 64%) of the patients who later relapsed (Table 1), a frequency on a par with the incidence of 55% of these triple trisomies in close to 60 high hyperdiploid cases also analyzed by high-resolution arrays at the time of diagnosis. [18][19][20][21] Thus, it is clear that the triple trisomies are seen in a substantial proportion of relapses of high hyperdiploid ALLs, a finding that may question their favorable prognostic impact.…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, several investigators have identified 'favorable' aberrations, reporting a superior outcome for cases harboring certain trisomies, that is, þ 4, þ 10, þ 17 and þ 18; 2,3,8,9 findings that are now used for risk stratification, at least by the Children's Oncology Group with regard to triple trisomies þ 4, þ 10 and þ 17. 10 Another approach to identify genetic changes associated with relapse of high hyperdiploid ALL is to compare the genetic features of paired diagnostic and relapse samples. This would also provide valuable information with regard to the temporal order of the various chromosome abnormalities and gene mutations and thus enable identification of 'preleukemic' ancestral clones as well as secondary, progressionrelated changes.…”

Section: Introductionmentioning

confidence: 99%

“…Simultaneous trisomies of chromosomes 4, 10 and 17Fthe triple trisomies used for stratification of patients into a lower-risk group by the Children's Oncology Group 10 Fwere found in 7 of the 11 patients both at diagnosis and at relapse (Table 1). Abbreviations: D, sample from the time of diagnosis; F, female; M, male; R, sample from the time relapse; SNP, single nucleotide polymorphism; UPD, uniparental isodisomy.…”

Section: Patterns Of Gained Chromosomesmentioning

confidence: 99%

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Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations

et al. 2010

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Although childhood high hyperdiploid acute lymphoblastic leukemia is associated with a favorable outcome, 20% of patients still relapse. It is important to identify these patients already at diagnosis to ensure proper risk stratification. We have investigated 11 paired diagnostic and relapse samples with single nucleotide polymorphism array and mutation analyses of FLT3, KRAS, NRAS and PTPN11 in order to identify changes associated with relapse and to ascertain the genetic evolution patterns. Structural changes, mainly cryptic hemizygous deletions, were significantly more common at relapse (Po0.05). No single aberration was linked to relapse, but four deletions, involving IKZF1, PAX5, CDKN2A/B or AK3, were recurrent. On the basis of the genetic relationship between the paired samples, three groups were delineated: (1) identical genetic changes at diagnosis and relapse (2 of 11 cases), (2) clonal evolution with all changes at diagnosis being present at relapse (2 of 11) and (3) clonal evolution with some changes conserved, lost or gained (7 of 11), suggesting the presence of a preleukemic clone. This ancestral clone was characterized by numerical changes only, with structural changes and RTK-RAS mutations being secondary to the high hyperdiploid pattern.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Patterns Of Gained Chromosomesmentioning

confidence: 99%

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Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations

et al. 2010

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“…[1][2][3] Based on these results, MRD testing has become a part of the risk-group stratification procedure in several of the most progressive ALL treatment protocols. [4][5][6][7] In 2000, the International BerlinFrankfurt-Mü nster Study Group (I-BFM-SG) incorporated MRD testing into risk-group stratification in the AIEOP-BFM ALL 2000 trial. Almost all 'classical' risk features (except prednisone response, t(4;11), t(9;22) and induction failure) were omitted in this risk-group stratification.…”

Section: Introductionmentioning

confidence: 99%

Minimal residual disease (MRD) analysis in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: is it possible to avoid MRD testing?

et al. 2008

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The ALL IC-BFM 2002 protocol was created as an alternative to the MRD-based AIEOP-BFM ALL 2000 study, to integrate early response criteria into risk-group stratification in countries not performing routine PCR-based MRD testing. ALL IC stratification comprises the response to prednisone, bone marrow (BM) morphology at days 15 and 33, age, WBC and BCR/ABL or MLL/ AF4 presence. Here, we compared this stratification to the MRDbased criteria using MRD evaluation in 163 patients from four ALL IC member countries at days 8, 15 and 33 and week 12. MRD negativity at day 33 was associated with an age of 1-5 years, WBCo20 000 ll À1 , non-T immunophenotype, good prednisone response and non-M3 morphology at day 15. There were no significant associations with gender or hyperdiploidy in the study group, or with TEL/AML1 fusion within BCP-ALL. Patients with M1/2 BM at day 8 tended to be MRD negative at week 12. Patients stratified into the standard-risk group had a better response than intermediate-risk group patients. However, 34% of them were MRD positive at day 33 and/or week 12. Our findings revealed that morphology-based ALL IC risk-group stratification allows the identification of most MRD high-risk patients, but fails to discriminate the MRD low-risk group assigned to therapy reduction.

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“…13 Further, MRD detection overcomes the inherent disadvantage of morphology, namely the difficulty in distinguishing ALL cells from the lymphocytes and undifferentiated hematopoietic cells. Those patients achieving molecular remission with leukemic blasts less than 0.01% of nucleated cells in bone marrow at the end of remissioninduction therapy fare better than those who did not.…”

Section: Discussionmentioning

confidence: 99%

Flow cytometric detection of minimal residual disease in B-lineage acute lymphoblastic leukemia by using “MRD lite” panel

Chatterjee

Somasundaram

2017

Medical Journal Armed Forces India

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IntroductionMinimal residual disease (MRD) refers to the presence of recalcitrant leukemic blasts in the peripheral blood or bone marrow, which is beyond the lower limit of morphologic detection by light microscopy and can only be detected by highly sensitive assays, be it polymerase chain reaction based or flow cytometry based. 1 PCR-based and flow cytometric MRD technologies have been developed over the past two decades with their inherent advantages and disadvantages. 2-9 Detection of MRD would aid in the patient management by either intensifying therapy in MRD positive cases or de-intensifying and thereby reducing treatment-related mortality and morbidity in MRD negative cases. Prospective studies in large series of patients have demonstrated a strong correlation between MRD levels during clinical remission and treatment outcome. 10,11 For MRD studies, leukemia-associated immunophenotypes (LAIP)m e d i c a l j o u r n a l a r m e d f o r c e s i n d i a 7 3 ( 2 0 1 7 ) 5 4 -5 7

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Risk- and response-based classification of childhood B-precursor acute lymphoblastic leukemia: a combined analysis of prognostic markers from the Pediatric Oncology Group (POG) and Children's Cancer Group (CCG)

Cited by 420 publications

References 42 publications

Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations

Relapsed childhood high hyperdiploid acute lymphoblastic leukemia: presence of preleukemic ancestral clones and the secondary nature of microdeletions and RTK-RAS mutations

Minimal residual disease (MRD) analysis in the non-MRD-based ALL IC-BFM 2002 protocol for childhood ALL: is it possible to avoid MRD testing?

Flow cytometric detection of minimal residual disease in B-lineage acute lymphoblastic leukemia by using “MRD lite” panel

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