Kinase-associated gene mutation pattern and clinical relevance in 205 patients with core binding factor leukemias

Ys, Chen; Wang, PP; Hu, Yifei; Zhu, Yuelin; Chen, B; Jy, Huang; Jm, Li; Xq, Weng; Yu, Yonghao; Shen, Yang

doi:10.1038/bcj.2016.107

Cited by 4 publications

(3 citation statements)

References 15 publications

(14 reference statements)

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“…Notably, patients with bi CEBPA in this study presented a lower platelet count at diagnosis compared with those without (median, 24 × 10 9 /L vs. 49 × 10 9 /L, P < 0.001; Supplementary Table 4 ), which was also observed by Taskesen et al 11 These results suggest that CEBPA mutations may exert adverse impact on hematopoietic differentiation and recovery of blood count after chemotherapy. In contrast, although we 12 and others 13 have reported that C-KIT mutations were adverse events in core binding factor leukemias, they were less common in CRi patients compared with those who achieved CR, which needs to be verified in large population.…”

mentioning

confidence: 57%

Impact of blood count recovery on outcomes of acute myeloid leukemia patients achieving morphologic leukemia-free state

Cheng

Zhu

Liu

et al. 2018

Blood Cancer Journal

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confidence: 57%

Impact of blood count recovery on outcomes of acute myeloid leukemia patients achieving morphologic leukemia-free state

Cheng

Zhu

Liu

et al. 2018

Blood Cancer Journal

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“…Gene mutations associated with epigenetic modification are also considered as poor factors, such as MLL , DNMT3A , TET2 , and ASXL1 mutations [ 12 , 17 , 18 ], while mutant NPM1 is regarded as a favorable one [ 12 , 19 , 20 ]. In addition, numerous clinical studies have proven the role of tumor suppressor genes such as TP53 and WT1 in cytogenetic normal AML (CN-AML) [ 21 – 24 ] and C - KIT in core binding factor AML (CBF-AML) [ 25 ]. Metallothionein III (MT3) may also act as a tumor suppressor gene of which the promoter hypermethylation can inactivate the gene and downregulate its expression level in pediatric AML [ 26 ].…”

Section: Introductionmentioning

confidence: 99%

Gene mutational pattern and expression level in 560 acute myeloid leukemia patients and their clinical relevance

et al. 2017

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BackgroundCytogenetic aberrations and gene mutations have long been regarded as independent prognostic markers in AML, both of which can lead to misexpression of some key genes related to hematopoiesis. It is believed that the expression level of the key genes is associated with the treatment outcome of AML.MethodsIn this study, we analyzed the clinical features and molecular aberrations of 560 newly diagnosed non-M3 AML patients, including mutational status of CEBPA, NPM1, FLT3, C-KIT, NRAS, WT1, DNMT3A, MLL-PTD and IDH1/2, as well as expression levels of MECOM, ERG, GATA2, WT1, BAALC, MEIS1 and SPI1.ResultsCertain gene expression levels were associated with the cytogenetic aberration of the disease, especially for MECOM, MEIS1 and BAALC. FLT3, C-KIT and NRAS mutations contained conversed expression profile regarding MEIS1, WT1, GATA2 and BAALC expression, respectively. FLT3, DNMT3A, NPM1 and biallelic CEBPA represented the mutations associated with the prognosis of AML in our group. Higher MECOM and MEIS1 gene expression levels showed a significant impact on complete remission (CR) rate, disease free survival (DFS) and overall survival (OS) both in univariate and multivariate analysis, respectively; and an additive effect could be observed. By systematically integrating gene mutational status results and gene expression profile, we could establish a more refined system to precisely subdivide AML patients into distinct prognostic groups.ConclusionsGene expression abnormalities contained important biological and clinical informations, and could be integrated into current AML stratification system.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-017-1279-4) contains supplementary material, which is available to authorized users.

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“…However, several lines of evidence suggest that CBFB::MYH11 and RUNX1:: RUNX1T1 may act by different mechanisms. AMLs with these fusions have distinct DNA methylation patterns (43)(44)(45), distinct gene expression profiles (43,46), distinct proteomic signatures (47), different common cooperating mutations (43,(48)(49)(50)(51)(52), and different clinical phenotypes (53)(54)(55)(56)(57)(58)(59). Other proposed models of CBFB::MYH11 AML initiation take some of these differences into account.…”

Section: Introductionmentioning

confidence: 99%

Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia–initiating CBFB::MYH11 oncofusion protein

Day,

Hickman,

et al. 2023

Journal of Clinical Investigation

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Kinase-associated gene mutation pattern and clinical relevance in 205 patients with core binding factor leukemias

Cited by 4 publications

References 15 publications

Impact of blood count recovery on outcomes of acute myeloid leukemia patients achieving morphologic leukemia-free state

Impact of blood count recovery on outcomes of acute myeloid leukemia patients achieving morphologic leukemia-free state

Gene mutational pattern and expression level in 560 acute myeloid leukemia patients and their clinical relevance

Proteogenomic analysis reveals cytoplasmic sequestration of RUNX1 by the acute myeloid leukemia–initiating CBFB::MYH11 oncofusion protein

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