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  • 1
    In: International Journal of Hematology, Springer Science and Business Media LLC, Vol. 116, No. 3 ( 2022-09), p. 434-441
    Type of Medium: Online Resource
    ISSN: 0925-5710 , 1865-3774
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2028991-1
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  • 2
  • 3
    In: Haematologica, Ferrata Storti Foundation (Haematologica), Vol. 107, No. 3 ( 2021-03-18), p. 583-592
    Abstract: RAS pathway alterations have been implicated in the pathogenesis of various hematological malignancies. However, their clinical relevance in pediatric acute myeloid leukemia (AML) is not well characterized. We analyzed the frequency, clinical significance, and prognostic relevance of RAS pathway alterations in 328 pediatric patients with de novo AML. RAS pathway alterations were detected in 80 (24.4%) of 328 patients: NF1 (n=7, 2.1%), PTPN11 (n=15, 4.6%), CBL (n=6, 1.8%), NRAS (n=44, 13.4%), KRAS (n=12, 3.7%). Most of these alterations in the RAS pathway were mutually exclusive also together with other aberrations of signal transduction pathways such as FLT3-ITD (P=0.001) and KIT mutation (P=0.004). NF1 alterations were frequently detected in patients with complex karyotype (P=0.031) and were found to be independent predictors of poor overall survival (OS) in multivariate analysis (P=0.007). At least four of seven patients with NF1 alterations had biallelic inactivation. NRAS mutations were frequently observed in patients with CBFB-MYH11 and were independent predictors of favorable outcomes in multivariate analysis (OS, P=0.023; event-free survival [EFS] , P=0.037). Patients with PTPN11 mutations more frequently received stem cell transplantation (P=0.035) and showed poor EFS than patients without PTPN11 mutations (P=0.013). Detailed analysis of RAS pathway alterations may enable a more accurate prognostic stratification of pediatric AML and may provide novel therapeutic molecular targets related to this signal transduction pathway.
    Type of Medium: Online Resource
    ISSN: 1592-8721 , 0390-6078
    Language: Unknown
    Publisher: Ferrata Storti Foundation (Haematologica)
    Publication Date: 2021
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    detail.hit.zdb_id: 2030158-3
    detail.hit.zdb_id: 2805244-4
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  • 4
    In: Leukemia, Springer Science and Business Media LLC, Vol. 35, No. 5 ( 2021-05), p. 1480-1484
    Type of Medium: Online Resource
    ISSN: 0887-6924 , 1476-5551
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2008023-2
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  • 5
    In: Genes, Chromosomes and Cancer, Wiley, Vol. 56, No. 5 ( 2017-05), p. 382-393
    Abstract: ASXL2 is an epigenetic regulator involved in polycomb repressive complex regulation or recruitment. Clinical features of pediatric acute myeloid leukemia (AML) patients with ASXL2 mutations remain unclear. Thus, we investigated frequencies of ASXL1 and ASXL2 mutations, clinical features of patients with these mutations, correlations of these mutations with other genetic alterations including BCOR/BCORL1 and cohesin complex component genes, and prognostic impact of these mutations in 369 pediatric patients with de novo AML (0–17 years). We identified 9 (2.4%) ASXL1 and 17 (4.6%) ASXL2 mutations in 25 patients. These mutations were more common in patients with t(8;21)(q22;q22)/ RUNX1‐RUNX1T1 ( ASXL1 , 6/9, 67%, P  = 0.02; ASXL2, 10/17, 59%, P  = 0.01). Among these 25 patients, 4 (27%) of 15 patients with t(8;21) and 6 (60%) of 10 patients without t(8;21) relapsed. However, most patients with relapse were rescued using stem cell transplantation irrespective of t(8;21). The overall survival (OS) and event‐free survival (EFS) rates showed no differences among pediatric AML patients with t(8;21) and ASXL1 or ASXL2 mutations and ASXL wild‐type (5‐year OS, 75% vs. 100% vs. 91% and 5‐year EFS, 67% vs. 80% vs. 67%). In 106 patients with t(8;21) AML, the coexistence of mutations in tyrosine kinase pathways and chromatin modifiers and/or cohesin complex component genes had no effect on prognosis. These results suggest that ASXL1 and ASXL2 mutations play key roles as cooperating mutations that induce leukemogenesis, particularly in pediatric AML patients with t(8;21), and these mutations might be associated with a better prognosis than that reported previously.
    Type of Medium: Online Resource
    ISSN: 1045-2257 , 1098-2264
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 1018988-9
    detail.hit.zdb_id: 1492641-6
    SSG: 12
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  • 6
    In: Genes, Chromosomes and Cancer, Wiley, Vol. 62, No. 7 ( 2023-07), p. 412-422
    Abstract: Pediatric acute myeloid leukemia (AML) is a poor prognostic subtype of pediatric leukemia. However, the detailed characteristics of many genetic abnormalities are yet to be established in this disease. Although TP53 and RB1 are established as representative tumor suppressor genes in various cancers, alterations of these two genes, especially RB1 , have not been characterized in pediatric AML. We performed next‐generation sequencing in 328 pediatric AML patients from the Japanese AML‐05 trial to ascertain TP53 and RB1 alterations, and their prognostic implications. We identified seven patients with TP53 alterations (2.1%) and six patients with RB1 alterations (1.8%). These alterations were found in only patients without RUNX1::RUNX1T1 , CBFB::MYH11 , or KMT2A rearrangements. TP53 and RB1 were frequently co‐deleted with their neighboring genes PRPF8 and ELF1 , respectively. Patients with TP53 alterations had significantly lower 5‐year overall survival (OS; 14.3% vs. 71.4%, p   〈  0.001) and lower 5‐year event‐free survival (EFS; 0% vs. 56.3%, p   〈  0.001); similarly, patients with RB1 had significantly lower 5‐year OS (0% vs. 71.8%, p   〈  0.001) and lower 5‐year EFS (0% vs. 56.0%, p   〈  0.001) when compared to patients without these alterations. In gene expression analyses, oxidative phosphorylation, glycolysis, and protein secretion were upregulated in patients with TP53 and/or RB1 alterations. Additionally, Kaplan–Meier analysis revealed that high expressions of SLC2A5 , KCNAB2 , and CD300LF were related to poor OS of non‐core‐binding factor AML patients ( p   〈  0.001, p  = 0.001, and p  = 0.021, respectively). This study will contribute to the development of risk‐stratified therapy and precision medicine in pediatric AML.
    Type of Medium: Online Resource
    ISSN: 1045-2257 , 1098-2264
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 1018988-9
    detail.hit.zdb_id: 1492641-6
    SSG: 12
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  • 7
    In: Blood, American Society of Hematology, Vol. 134, No. Supplement_1 ( 2019-11-13), p. 3833-3833
    Abstract: Introduction: Transient abnormal myelopoiesis (TAM) in neonates with Down syndrome (DS) is characterized by the transient appearance of blast cells that harbor somatic GATA1 gene mutation. Although most patients show spontaneously resolution without therapeutic interventions, approximately 20% of TAM cases result in early deaths within 9 months and 20% of survivors develop acute megakaryoblastic leukemia (AMKL) within 4 years. Although the risk factors associated with early deaths are known, the definite clinical predictive indicators of AMKL onset in patients with TAM remain unclear. Therefore, we analyzed 167 TAM patients with DS enrolled in the TAM-10 prospective observational study conducted by the Japan Pediatric Leukemia/Lymphoma Study Group (JPLSG) to determine the clinical characteristics of TAM and predictive factors of leukemia development. Patients and Methods: Between May 2011 and February 2014, 167 neonates (89 boys and 78 girls) diagnosed with TAM were prospectively registered in the TAM-10 study. Somatic GATA1 gene mutations were confirmed in 163 (98%) patients using Sanger and/or next-generation sequencing. Minimal residual disease using flow cytometry (FCM-MRD; cut-off level, ≥0.1%) was monitored at 1 (n = 133) and 3 months (n = 104). Results: Median (range) gestational age, birth body weight, white blood cell (WBC) count, and percentage of blasts at diagnosis were 37 (29-40) weeks, 2,612 (1,066-3714) g, 38.3 (2.4-478.7) × 109 cells/L, and 37% (0.5%-95.5%), respectively. Systemic edema and organ hemorrhage was observed in 31/167 (19%) and 14/167 (8%) patients, respectively; 68/167 (41%) patients received some therapeutic interventions, including low-dose cytarabine (LDCA; n = 52), exchange blood transfusion (n = 20), and systemic steroid therapy (n = 31). Early death ( 〈 9 months of age) occurred in 22/167 (13%) patients. In multivariate analysis, early death was significantly associated with a high WBC count [≥100 × 109 cells/L; HR (95% CI) = 5.329 (2.194-12.945), P 〈 0.001] and systemic edema [HR (95% CI) = 8.073 (3.130-20.823), P 〈 0.001]. Subgroup analysis in patients with such high WBC count (n = 36) showed that LDCA therapy significantly improved survival [1-year OS (95% CI) = 78.3% (55.4-90.3; n = 23) vs. 38.5% (14.1-62.8; n = 13); P = 0.009] . Among 145/167 patients without early death, 28 (19%) developed AMKL. FCM-MRD positivity at 1 month [positive, n = 107; negative, n = 26; cumulative incidence ratio (CIR) (95% CI) = 25.2% (17.3-33.9%) vs 3.8% (0.3%-16.8%), P = 0.022] and 3 months (positive, n = 20; negative, n = 84; CIR (95% CI), 45.0% (22.3%-65.4%) vs. 16.0% (9.0%-24.8%), P = 0.002] was significantly associated with leukemia development. However, other clinical covariates, including sex, birth weight, gestational age, WBC count, blast percentage, and GATA1 gene mutational types, could not predict AMKL development. Considering their severe clinical conditions, 13/31 (42%) patients who received systemic steroid therapy died before AMKL development; interestingly, none of the remaining 18 patients developed AMKL but they showed significantly lower CIR than those who did not receive this therapy [CIR (95% CI), 0% vs. 19.4% (10.9%-29.6%), P = 0.010]. Other therapeutic interventions, including LDCA and exchange blood transfusion, were not associated with AMKL development. Conclusion: FCM-MRD positivity at 1 month and 3 months might be a useful marker to predict leukemia development in patients with TAM. Although LDCA therapy significantly decreased the rate of early deaths, it did not suppress leukemia development. Interestingly, systemic steroid therapy might suppress leukemia development. These results pave the way to design clinical trials for developing MRD-directed leukemia prevention therapy for patients with TAM. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2019
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 8
    In: Blood, American Society of Hematology, Vol. 134, No. Supplement_1 ( 2019-11-13), p. 2739-2739
    Abstract: Introduction Acute myeloid leukemia (AML) is a clinically and biologically heterogeneous hematologic malignancy characterized by various genetic alterations. Currently, DNA methylation patterns were reported to be associated with molecular subtypes, chromosomal abnormalities, gene fusion, and prognosis in AML. Furthermore, previous study reported that aberrant cancer-associated DNA hypermethylation targets CpG islands characterized by bivalent chromatin in human embryonic stem cells (hESCs), and the bivalent chromatin signature in hESCs was a key determinant of the instructive program for aberrant DNA methylation. Thus, we analyzed genome-wide DNA methylation in 64 pediatric patients with AML to reveal its association with clinical features, genetic alterations, and prognostic impact. Methods Between 2006 and 2010, 443 pediatric patients with de novo AML (0-17 years) participated in the Japanese AML-05 trial conducted by the Japanese Pediatric Leukemia/Lymphoma Study Group. Of these, 64 patients were enrolled in this study. The cytogenetic features of 64 patients were as follows: normal karyotype, 28; RUNX1-RUNX1T1, 8; KMT2A rearrangement, 15; complex karyotype, 6; and other cytogenetics, 7. This cohort included 15 patients with FLT3-internal tandem duplication (ITD), 8 with CEBPA biallelic mutations, 5 with high MECOM (EVI1) expression, and 17 with high PRDM16 (MEL1) expression. We performed genome-wide DNA methylation analysis using Infinium MethylationEPIC BeadChip (Illumina) in 64 pediatric patients. Results and Discussion 824,848 methylation sites per sample were analyzed in 64 pediatric patients with AML. To capture DNA methylation differences across samples, we selected 567 CpG sites which showed most variable methylation values between 64 individuals such as standard deviations across samples were more than 0.3. The unsupervised hierarchical clustering of DNA methylation data from 567 CpG sites generated 4 clusters (clusters 1-4) with distinct molecular and clinical characteristics. Cluster 1 or 2 was the lowest or highest methylation level, respectively. Clusters 3 and 4 showed intermediate methylation level. Cluster 1 was characterized by RUNX1-RUNX1T1 and KMT2A rearrangement with low MECOM expression, which are known as favorable prognostic factors. Clusters 2 and 4 were composed of patients with the molecular features showing adverse outcome such as FLT3-ITD, KMT2A-PTD and/or normal karyotype with high PRDM16 expression. Interestingly, KMT2A rearrangement with high MECOM expression, considered as the adverse prognostic factor, were included in clusters 2 or 4. As for KMT2A rearrangement, nine of 15 patients with KMT2A rearrangement harbored KMT2A-MLLT3. Of these, five of nine classified into the hypomethylation group, and all five patients had no event. On the other hand, remaining four patients with KMT2A-MLLT3 all relapsed. All patients with normal karyotype with CEBPA biallelic mutations considered as the favorable factor were found in cluster 3. When we focused on CpG sites with significant difference in their methylation values between patients with and without FLT3-ITD, 15 FLT3-ITD patients were divided into two clusters (clusters A and B) by the hierarchical clustering. Remarkably, 8 FLT3-ITD positive patients in cluster A showed significantly worse overall survival (OS) and event-free survival (EFS) when compared with those in cluster B (5-year OS, 13% vs. 100%, P = 0.002; 5-year EFS 0% vs. 86%, P 〈 0.001). Next, 244 CpG sites significantly associated with PRDM16 expression were extracted to investigate the relationship between PRDM16 expression and DNA methylation profiles. Interestingly, patients with high and low PRDM16 expression showed distinct methylation pattern, respectively. Furthermore, most of hypermethylated sites gene were PRDM16 gene body in patients with high PRDM16 expression and located at important regions which were the targets of repressed polycomb in reference cells. As for 567 CpG sites which were used for the unsupervised hierarchical clustering, 168 of 567 (30%) CpG sites colocalized at bivalent promoter regions in reference leukemic blast cells, and the hypermethylation of bivalent promoter regions tended to be related to worse outcome. These results indicate DNA methylation plays key role for leukemogenesis and is remarked as a novel biomarker to predict prognosis. Disclosures Ogawa: ChordiaTherapeutics, Inc.: Consultancy, Equity Ownership; RegCell Corporation: Equity Ownership; Kan Research Laboratory, Inc.: Consultancy; Asahi Genomics: Equity Ownership; Qiagen Corporation: Patents & Royalties; Dainippon-Sumitomo Pharmaceutical, Inc.: Research Funding.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2019
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 9
    In: Blood, American Society of Hematology, Vol. 134, No. Supplement_1 ( 2019-11-13), p. 1419-1419
    Abstract: Introduction Recent medical advances and development of comprehensive genetic understanding dramatically improve the clinical outcome of whole pediatric cancers, particularly in pediatric acute lymphoblastic lymphoma. However, approximately 50% of patients have disease relapse, and overall survival (OS) of pediatric acute myeloid leukemia (AML) is less than 70% as of the major therapeutic challenges. AML is caused by various chromosomal aberrations, gene mutations/epigenetic modifications, and deregulated/overregulated gene expressions, leading to increased proliferation and decreased hematopoietic progenitor cell differentiation. AML with RUNX1-RUNX1T1 gene fusions are generally classified as a low-risk group and resulted in favorable prognosis. However approximately 30% of the patients relapsed within 3 years. Conversely, KIT mutations were found in approximately 30% of AML cases with RUNX1-RUNX1T1 and thought to be a risk factor for relapse, particularly when occurring in D816V within KIT exon 17. Recently, droplet digital PCR (ddPCR), a method for measuring target nucleic acid sequence quantity, has been used to determine low-prevalence somatic mutations that were not detectable using Sanger sequencing. It shows the possibility that there are some of Pediatric AML cases which were not detected minor clones with somatic KIT mutation by using ordinary PCR. In this study, we explored KIT D816V mutations including the cases which are not detected by Sanger sequencing and found the prognosis of them by using Japanese pediatric AML cases. Methods We reanalyzed somatic KIT mutations (p.D816V) in the DNA extracted from 335 pediatric AML patients with RUNX1-RUNX1T1 who participated in the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG) AML-05 trial using ddPCR . In this trial, we conducted the tests as follows,: PCR mixture containing 10 μL 2x ddPCR Supermix for probes, 900 nM target-specific PCR primers, and 250 nM mutant-specific (FAM) and wild-type-specific (HEX) probes.20 µL of PCR mixture and 70 μL Droplet generation oil were mixed, and droplet generation was performed using a Bio-Rad QX100 Droplet Generator. The droplet emulsion was thermally cycled in the following conditions: denaturing at 95 °C for 10 min, 40 cycles of PCR at 94 °C for 30 s and at 57 °C for 2 min, and a final extension at 98 °C for 10 min. PCR amplification in the droplets was confirmed using Bio-Rad QX200 Droplet Reader. ThresholdThe threshold was determined by comparing the non-template ddPCR results. All the data were evaluated above the threshold. We also performed targeted gene mutation analysis of KIT in all patients using Sanger sequencing. Results We identified 24 KIT D816V mutations (7.2%) in the 335 pediatric AML. Variant allele frequency (VAF) was 0.1%-46.9%.It is noteworthy that 12 out of 24 KIT D816V mutations were undetected in our previous study using Sanger sequencing. Fourteen out of these 24 patients were AML with RUNX1-RUNX1T1, 5 cases with inv(16), and 5 cases with other alterations. Ten of the 14 RUNX1-RUNX1T1 (71%) patients were newly identified using ddPCR. Six of these 14 RUNX1-RUNX1T1 patients had relapsed, and D816V mutations were only detected using ddPCR in 4 of these 6 relapsed cases. The mean VAF of KIT D816V was 3.8% (0.1%-13.4%) in the 10 undetected patients with RUNX1-RUNX1T1. Two of the 5 patients with inv(16) were newly identified, and 1 had relapsed. All 5 cases with other alterations were already identified using Sanger sequencing. The mean VAF of KIT D816V in the 3 patients with inv(16) was 44.8% (42.7%-46.9%), detected using Sanger sequencing, whereas the mean VAF of KIT D816V was 8.6% (6.5% and 10.7%) in the undetected patients with inv(16). The mean VAF of KIT D816V with other alterations was 28.1% (16.2%-42.9%). Conclusion We identified 12 KIT D816V mutations using ddPCR that were undetected using Sanger sequencing. ddPCR may be useful for detecting accurate frequencies of mutations that were undetected using Sanger sequencing. Potential co-existing gene mutations may contribute different significance of leukemogenesis and relapse. Disclosures Ito: Asahi Kasei Pharma: Consultancy, Other: Grants; Astellas Pharma: Consultancy, Other: Grants; Teijin: Other: Grants; Novartis Pharma: Consultancy; Zenyaku Kogyo Co. Ltd: Consultancy; Chugai Pharma: Consultancy, Other: Grants; Japan Blood Products Organization: Other: Grants; Pfizer inc.: Other: Grants.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
    RVK:
    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2019
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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  • 10
    In: Blood, American Society of Hematology, Vol. 126, No. 23 ( 2015-12-03), p. 1380-1380
    Abstract: Background Several molecular markers, such as FLT3-internal tandem duplication (ITD), NPM1, CEBPA are well known to correlate with mortality in patients with acute myeloid leukemia (AML). Recently, a number of gene mutations have been implicated in the pathogenesis of AML, including mutations of DNMT3A, IDH1/2, TET2 and EZH2 in addition to RAS, KIT and FLT3. However, DNMT3A, IDH1/2, and TET2 are rare in pediatric patients with AML, thus accurate risk evaluation remained challenging even after incorporating these molecular markers. On the other hand, overexpression of the EVI1 gene is reported to be associated with adverse outcome in pediatric AML. Moreover, we have previously reported that measuring of PRDM16 gene expression was a powerful tool to predict the prognosis of pediatric AML. PRDM16 gene is highly homologous to the MDS1/EVI1 gene, which is an alternatively spliced transcript of the EVI1 gene. In this study, we investigated EVI1 gene expression to verify the prognosis of EVI1 gene expression and the relationship between EVI1 and PRDM16 gene expression. Methods Between 2006 and 2010, 485 de novo pediatric AML patients participated in the Japanese AML-05 study conducted by the Japanese Pediatric Leukemia/Lymphoma Study Group (JPLSG). Among them, 116 patients were excluded from the study because of misdiagnosis and unavailability of their RNA samples. Therefore, 369 patients were analyzed. Quantitative RT-PCR analysis was performed in these patients using the 7900HT Fast Real Time PCR System with TaqMan Gene Expression Master Mix and TaqMan Gene Expression Assay. In addition to EVI1 and PRDM16, ABL1 was also evaluated as a control gene. We investigated the correlations between these gene expressions and other genetic alterations, and clarified the prognostic impact of EVI1 and association between EVI1 and PRDM16 genes. Results A total of 58 of 369 patients (15.7%) showed high expression of EVI1 gene. Overexpression of EVI1 gene was strongly associated with dismal prognosis; low risk (LR; 1 of 123 patients, or 0.8%); intermediate risk (IR; 38 of 147 patients, or 25.9%); high risk (HR; 6 of 50 patients, or 12%); and non-complete remission (Non-CR; 13 of 49 patients, or 26.5%), (P 〈 0.001). Overexpression of EVI1 correlated with the following characteristics: younger age at diagnosis; M4, M5, and M7 subtype; higher coincidence of MLL-rearrangement; and lower coincidence of t(8;21), and inv(16). EVI1 overexpression was very frequent among patients with de novo pediatric AML and IR/non-CR groups. Furthermore, more than half of patients in M6 (5 of 8 patients, or 62.5%) were EVI1 high expression. Interestingly, no patients with EVI1 high expression in M7 had a fusion of CBFA2T3-GLIS2. Patients with EVI1 overexpression also more frequently harbored a complex karyotype and monosomy 7. The frequencies of patients with high or low EVI1 expression differed widely with respect to each genetic alteration, as follows: t(8;21), 1% vs 99%, P 〈 0.001; inv(16), 0% vs 100%, P 〈 0.001; NUP98-JARID1A, 83% vs 17%, P 〈 0.001; OTT-MAL, 100% vs 0%, P = 0.02; and KIT, 5% vs 95%, P = 0.003. The overall survival (OS) and event-free survival (EFS) among patients with EVI1 high expressions were significantly lower than that among patients without such gene aberrant expression (3-year OS 54% vs. 77%, P=0.008G3-year EFS: 34% vs 58%, P 〈 0.001), respectively. On the other hand, a total of 84 of 369 patients (22.8%) showed high expression of PRDM16 gene. The OS and EFS among PRDM16 overexpressing patients were significantly worse than those among low expression group (3-year OS: 51% vs 81%, P 〈 0.001; 3-year EFS: 32% vs 64%, P 〈 0.001), respectively. Remarkably, concerning 125 patients with high EVI1 and/or PRDM16 expression, their prognosis was much worse than that of patients without these high expression (3-year OS: 54% vs 84%, P 〈 0.001; 3-year EFS: 32% vs 68%, P 〈 0.001) , respectively. Conclusions We investigated EVI1 and PRDM16 gene expression in de novo pediatric AML patients, and their high expression was associated with inferior survival, respectively. We suggest that high EVI1 and/or PRDM16 expression is useful marker for adverse outcome. On the other hand, low EVI1 and PRDM16 expressions are useful to elucidate low risk patients. Disclosures No relevant conflicts of interest to declare.
    Type of Medium: Online Resource
    ISSN: 0006-4971 , 1528-0020
    RVK:
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    Language: English
    Publisher: American Society of Hematology
    Publication Date: 2015
    detail.hit.zdb_id: 1468538-3
    detail.hit.zdb_id: 80069-7
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