Clinical features and biological implications of different U2AF1 mutation types in myelodysplastic syndromes
U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Ei...
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Published in | Genes chromosomes & cancer Vol. 57; no. 2; pp. 80 - 88 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Wiley Subscription Services, Inc
01.02.2018
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ISSN | 1045-2257 1098-2264 1098-2264 |
DOI | 10.1002/gcc.22510 |
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Abstract | U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty‐six patients (17%) were found to have U2AF1MT, which occurred more common in younger patients (P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1MT and isolated +8 were significantly enriched in U2AF1MT‐positive cases, whereas TP53MT, SF3B1MT, and complex karyotypes were inversely associated with U2AF1MT. U2AFS34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower‐risk and higher‐risk MDS. U2AF1S34 subjects had more frequently platelet levels of <50 × 109/L (P = .043) and U2AF1Q157/U2AF1R156 subjects had more frequently hemoglobin concentrations at <80 g/L (P = .008) and more often overt fibrosis (P = .049). In conclusion, our study indicates that U2AF1MT is one of the earliest genetic events in MDS patients and that different types of U2AF1MT have distinct clinical and biological characteristics. |
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AbstractList | U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty‐six patients (17%) were found to have U2AF1MT, which occurred more common in younger patients (P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1MT and isolated +8 were significantly enriched in U2AF1MT‐positive cases, whereas TP53MT, SF3B1MT, and complex karyotypes were inversely associated with U2AF1MT. U2AFS34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower‐risk and higher‐risk MDS. U2AF1S34 subjects had more frequently platelet levels of <50 × 109/L (P = .043) and U2AF1Q157/U2AF1R156 subjects had more frequently hemoglobin concentrations at <80 g/L (P = .008) and more often overt fibrosis (P = .049). In conclusion, our study indicates that U2AF1MT is one of the earliest genetic events in MDS patients and that different types of U2AF1MT have distinct clinical and biological characteristics. U2AF1 mutations ( U2AF1 MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty‐six patients (17%) were found to have U2AF1 MT, which occurred more common in younger patients ( P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1 MT and isolated +8 were significantly enriched in U2AF1 MT‐positive cases, whereas TP53 MT, SF3B1 MT, and complex karyotypes were inversely associated with U2AF1 MT. U2AF S34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1 MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower‐risk and higher‐risk MDS. U2AF1 S34 subjects had more frequently platelet levels of <50 × 10 9 /L ( P = .043) and U2AF1 Q157 / U2AF1 R156 subjects had more frequently hemoglobin concentrations at <80 g/L ( P = .008) and more often overt fibrosis ( P = .049). In conclusion, our study indicates that U2AF1 MT is one of the earliest genetic events in MDS patients and that different types of U2AF1 MT have distinct clinical and biological characteristics. U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty-six patients (17%) were found to have U2AF1MT, which occurred more common in younger patients (P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1MT and isolated +8 were significantly enriched in U2AF1MT-positive cases, whereas TP53MT, SF3B1MT, and complex karyotypes were inversely associated with U2AF1MT. U2AF subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower-risk and higher-risk MDS. U2AF1 subjects had more frequently platelet levels of <50 × 10 /L (P = .043) and U2AF1 /U2AF1 subjects had more frequently hemoglobin concentrations at <80 g/L (P = .008) and more often overt fibrosis (P = .049). In conclusion, our study indicates that U2AF1MT is one of the earliest genetic events in MDS patients and that different types of U2AF1MT have distinct clinical and biological characteristics. U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty-six patients (17%) were found to have U2AF1MT, which occurred more common in younger patients (P=.001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1MT and isolated +8 were significantly enriched in U2AF1MT-positive cases, whereas TP53MT, SF3B1MT, and complex karyotypes were inversely associated with U2AF1MT. U2AFS34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower-risk and higher-risk MDS. U2AF1S34 subjects had more frequently platelet levels of <50×109/L (P=.043) and U2AF1Q157/U2AF1R156 subjects had more frequently hemoglobin concentrations at <80g/L (P=.008) and more often overt fibrosis (P=.049). In conclusion, our study indicates that U2AF1MT is one of the earliest genetic events in MDS patients and that different types of U2AF1MT have distinct clinical and biological characteristics. U2AF1 mutations ( U2AF1 MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty-six patients (17%) were found to have U2AF1 MT, which occurred more common in younger patients ( P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1 MT and isolated +8 were significantly enriched in U2AF1 MT-positive cases, whereas TP53 MT, SF3B1 MT, and complex karyotypes were inversely associated with U2AF1 MT. U2AF S34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1 MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower-risk and higher-risk MDS. U2AF1 S34 subjects had more frequently platelet levels of <50 × 10 9 /L ( P = .043) and U2AF1 Q157 / U2AF1 R156 subjects had more frequently hemoglobin concentrations at <80g/L ( P = .008) and more often overt fibrosis ( P = .049). In conclusion, our study indicates that U2AF1 MT is one of the earliest genetic events in MDS patients and that different types of U2AF1 MT have distinct clinical and biological characteristics. U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty-six patients (17%) were found to have U2AF1MT, which occurred more common in younger patients (P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1MT and isolated +8 were significantly enriched in U2AF1MT-positive cases, whereas TP53MT, SF3B1MT, and complex karyotypes were inversely associated with U2AF1MT. U2AFS34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower-risk and higher-risk MDS. U2AF1S34 subjects had more frequently platelet levels of <50 × 109 /L (P = .043) and U2AF1Q157 /U2AF1R156 subjects had more frequently hemoglobin concentrations at <80 g/L (P = .008) and more often overt fibrosis (P = .049). In conclusion, our study indicates that U2AF1MT is one of the earliest genetic events in MDS patients and that different types of U2AF1MT have distinct clinical and biological characteristics.U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical and biological implications of different U2AF1 mutation types in MDS. We performed targeted gene sequencing in a cohort of 511 MDS patients. Eighty-six patients (17%) were found to have U2AF1MT, which occurred more common in younger patients (P = .001) and represented ancestral lesions in a substantial proportion (71%) of cases. ASXL1MT and isolated +8 were significantly enriched in U2AF1MT-positive cases, whereas TP53MT, SF3B1MT, and complex karyotypes were inversely associated with U2AF1MT. U2AFS34 subjects were enriched for isolated +8 and were inversely associated with complex karyotypes. U2AF1MT was significantly associated with anemia, thrombocytopenia, and poor survival in both lower-risk and higher-risk MDS. U2AF1S34 subjects had more frequently platelet levels of <50 × 109 /L (P = .043) and U2AF1Q157 /U2AF1R156 subjects had more frequently hemoglobin concentrations at <80 g/L (P = .008) and more often overt fibrosis (P = .049). In conclusion, our study indicates that U2AF1MT is one of the earliest genetic events in MDS patients and that different types of U2AF1MT have distinct clinical and biological characteristics. |
Author | Xu, Zefeng Song, Zhen Shi, Zhongxun Peng, Shuailing Wu, Jian Xiao, Zhijian Huang, Huijun Wang, Jingya Hu, Naibo Ru, Kun Li, Bing Qu, Shiqiang Qin, Tiejun Zhang, Yue Liu, Na Jia, Yujiao Huang, Gang Liu, Jinqin Fang, Liwei Pan, Lijuan Zhang, Hongli |
AuthorAffiliation | 6 Divisions of Pathology and Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 3 Department of Pathology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China 5 MyGenostic Inc, Beijing, China 1 MDS and MPN Centre, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China 2 State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China 4 Medical Service Division, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China |
AuthorAffiliation_xml | – name: 1 MDS and MPN Centre, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China – name: 2 State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China – name: 6 Divisions of Pathology and Experimental Hematology and Cancer Biology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH – name: 5 MyGenostic Inc, Beijing, China – name: 3 Department of Pathology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China – name: 4 Medical Service Division, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China |
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Cites_doi | 10.1016/j.molcel.2016.04.011 10.1038/onc.2013.520 10.1038/nm.3733 10.1038/ncomms14060 10.1007/s11912-015-0489-2 10.1172/JCI91363 10.1056/NEJMoa1103283 10.1016/j.tig.2017.03.001 10.1056/NEJMoa1408617 10.1038/leu.2015.91 10.1016/j.ccell.2015.04.008 10.1038/nrc.2016.51 10.1182/blood-2015-03-633537 10.1016/j.leukres.2010.06.004 10.1056/NEJMoa1409405 10.1038/nature10496 10.1101/gad.278424.116 10.1038/ng.3742 10.1016/j.leukres.2012.08.015 10.1038/leu.2013.336 10.1182/blood-2017-02-692715 10.1016/j.cell.2012.04.023 10.1182/blood.V89.6.2079 10.14694/EDBK_175397 10.1016/j.celrep.2015.02.005 10.1182/blood-2013-08-518886 10.1146/annurev-biochem-060614-034316 10.1158/2159-8290.CD-13-0253 10.1182/blood-2016-03-643544 10.1038/ng.1031 10.1200/JCO.2016.67.3616 10.1182/blood-2011-12-399337 10.1101/gr.181016.114 10.1002/ajh.23541 10.1038/sj.leu.2403688 10.1056/NEJMoa1013343 10.3324/haematol.2016.159772 10.1038/leu.2017.109 10.3109/10428190903515200 10.1038/nm.4097 10.1038/leu.2015.337 |
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Notes | Funding information Bing Li, Jinqin Liu, and Yujiao Jia contributed equally to this study. National Natural Science Funds, Grant Number: 81530008, 81370611, 81600098, 81270585, and 81470295; Program for Peking Union Scholars and Innovative Research Team; PUMC Youth Fund & Fundamental Research Funds for the Central Universities, Grant Number: 3332016089; Science and technology project of Tianjin, Grant Number: 15ZXLCSY00010 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
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References | 2011; 478 2017; 8 2013; 3 2015; 126 2013; 88 2017; 49 1997; 89 2015; 10 2013; 122 2016; 30 2011; 32 2011; 35 2016; 127 2014; 371 2014; 28 2016; 18 2012; 36 2016; 16 2012; 149 2016; 34 2014; 20 2017; 31 2015; 25 2005; 19 2015; 27 2015; 29 2017; 37 2013; 2013 2015; 84 2017; 33 2000; 96 2011; 44 2016; 62 2017; 102 2011; 365 2011; 364 2014; 33 2012; 119 2010; 51 2017; 127 2017; 129 2016; 22 e_1_2_5_28_1 e_1_2_5_25_1 e_1_2_5_26_1 e_1_2_5_23_1 e_1_2_5_24_1 e_1_2_5_45_1 e_1_2_5_21_1 e_1_2_5_44_1 e_1_2_5_22_1 e_1_2_5_43_1 Ley TJ (e_1_2_5_36_1) 2013; 2013 e_1_2_5_29_1 e_1_2_5_42_1 e_1_2_5_20_1 e_1_2_5_41_1 e_1_2_5_40_1 Qu SQ (e_1_2_5_30_1) 2011; 32 e_1_2_5_15_1 e_1_2_5_38_1 e_1_2_5_14_1 e_1_2_5_39_1 e_1_2_5_17_1 Cheson BD (e_1_2_5_27_1) 2000; 96 e_1_2_5_9_1 e_1_2_5_16_1 e_1_2_5_37_1 e_1_2_5_8_1 e_1_2_5_11_1 e_1_2_5_34_1 e_1_2_5_7_1 e_1_2_5_10_1 e_1_2_5_35_1 e_1_2_5_6_1 e_1_2_5_13_1 e_1_2_5_32_1 e_1_2_5_5_1 e_1_2_5_12_1 e_1_2_5_33_1 e_1_2_5_4_1 e_1_2_5_3_1 e_1_2_5_2_1 e_1_2_5_19_1 e_1_2_5_18_1 e_1_2_5_31_1 |
References_xml | – volume: 28 start-page: 241 year: 2014 end-page: 247 article-title: Landscape of genetic lesions in 944 patients with myelodysplastic syndromes publication-title: Leukemia. – volume: 371 start-page: 2488 year: 2014 end-page: 2498 article-title: Age related clonal hematopoiesis associated with adverse outcomes publication-title: N Engl J Med. – volume: 364 start-page: 2496 year: 2011 end-page: 2506 article-title: Clinical effect of point mutations in myelodysplastic syndromes publication-title: N Engl J Med. – volume: 31 start-page: 1640 year: 2017 end-page: 1644 article-title: Acute myeloid leukemia in the elderly is characterized by a distinct genetic landscape publication-title: Leukemia. – volume: 89 start-page: 2079 year: 1997 end-page: 2088 article-title: International scoring system for evaluating prognosis in myelodysplastic syndromes publication-title: Blood. – volume: 96 start-page: 3671 year: 2000 end-page: 3674 article-title: Report of an international working group to standardize response criteria for myelodysplastic syndromes publication-title: Blood. – volume: 19 start-page: 767 year: 2005 end-page: 775 article-title: Clinical and cytogenetic features of 508 Chinese patients with myelodysplastic syndrome and comparison with those in Western countries publication-title: Leukemia. – volume: 371 start-page: 2477 year: 2014 end-page: 2487 article-title: Clonal hematopoiesis and blood‐cancer risk inferred from blood DNA sequence publication-title: N Engl J Med. – volume: 62 start-page: 479 year: 2016 end-page: 490 article-title: U2AF35 (S34F) promotes transformation by directing aberrant ATG7 pre‐mRNA 3′ end formation publication-title: Mol Cell. – volume: 30 start-page: 906 year: 2016 end-page: 913 article-title: Age‐related mutations and chronic myelomonocytic leukemia publication-title: Leukemia. – volume: 88 start-page: E277 year: 2013 end-page: E282 article-title: Clinical implications of U2AF1 mutations in patients with myelodysplastic syndrome and its stability during disease progression publication-title: Am J Hematol. – volume: 149 start-page: 994 year: 2012 end-page: 1007 article-title: The life history of 21 breast cancers publication-title: Cell. – volume: 10 start-page: 1239 year: 2015 end-page: 1245 article-title: Leukemia‐associated somatic mutations drive distinct patterns of age‐related clonal hemopoiesis publication-title: Cell Rep. – volume: 49 start-page: 204 year: 2017 end-page: 212 article-title: Dynamics of clonal evolution in myelodysplastic syndromes publication-title: Nat Genet. – volume: 478 start-page: 64 year: 2011 end-page: 69 article-title: Frequent pathway mutations of splicing machinery in myelodysplasia publication-title: Nature. – volume: 34 start-page: 3627 year: 2016 end-page: 3637 article-title: Clinical effects of driver somatic mutations on the outcomes of patients with myelodysplastic syndromes treated with allogenetic hematopoietic stem‐cell transplantation publication-title: J Clin Oncol. – volume: 37 start-page: 480 year: 2017 end-page: 494 article-title: New insight into the biology, risk stratification, and targeted treatment of myelodysplastic syndromes publication-title: AM Soc Clin Oncol Educ Book. – volume: 365 start-page: 1384 year: 2011 end-page: 1395 article-title: Somatic SF3B1 mutation in myelodysplasia with ring sideroblasts publication-title: N Engl J Med. – volume: 119 start-page: 2578 year: 2012 end-page: 2584 article-title: Frequency and prognostic impact of mutations in SRSF2, U2AF1, and ZRSR2 in patients with myelodysplastic syndromes publication-title: Blood. – volume: 22 start-page: 672 year: 2016 end-page: 678 article-title: Modulation of splicing catalysis for therapeutic targeting of leukemia with mutations in genes encoding spliceosomal proteins publication-title: Nat Med. – volume: 33 start-page: 336 year: 2017 end-page: 348 article-title: Splicing factor mutations in myelodysplasia: insights from spliceosome structures publication-title: Trends Genet. – volume: 33 start-page: 5139 year: 2014 end-page: 5150 article-title: Stem cell origin of myelodysplastic syndromes publication-title: Oncogene. – volume: 20 start-page: 1472 year: 2014 end-page: 1478 article-title: Age‐related mutations associated with clonal hematopoietic expansion and malignancies publication-title: Nat Med. – volume: 127 start-page: 2206 year: 2017 end-page: 2221 article-title: The U2AF1S34F mutation induces lineage‐specific splicing alterations in myelodysplastic syndromes publication-title: J Clin Invest. – volume: 25 start-page: 14 year: 2015 end-page: 26 article-title: U2AF1 mutations alter splice site recognition in hematological malignancies publication-title: Genome Res. – volume: 36 start-page: 1428 year: 2012 end-page: 1433 article-title: Clinical importance of SF3B1 mutations in Chinese with myelodysplastic syndromes with ring sideroblasts publication-title: Leuk Res. – volume: 51 start-page: 549 year: 2010 end-page: 551 article-title: Low‐dose melphalan in myelodysplastic syndromes: an effective treatment for elderly RAEB‐I or II patients? publication-title: Leuk Lymphoma. – volume: 2013 start-page: 2059 year: 2013 end-page: 2074 article-title: Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia publication-title: N Engl J Med. – volume: 32 start-page: 819 year: 2011 end-page: 824 article-title: Study on prognostic significances of different cytogenetic risk categories in patients with primary myelodysplastic syndromes publication-title: Zhonghua Xue Ye Xue Za Zhi. – volume: 29 start-page: 2134 year: 2015 end-page: 2142 article-title: Clinical and biological implications of ancestral and non‐ancestral IDH1 and IDH2 mutations in myeloid neoplasms publication-title: Leukemia. – volume: 126 start-page: 233 year: 2015 end-page: 241 article-title: SF3B1 mutation identifies a distinct subset of myelodysplastic syndrome with ring sideroblasts publication-title: Blood. – volume: 35 start-page: 61 year: 2011 end-page: 65 article-title: Cyclosporin A and thalidomide in patients with myelodysplastic syndromes: results of a pilot study publication-title: Leuk Res. – volume: 27 start-page: 631 year: 2015 end-page: 643 article-title: Mutant U2AF1 expression alters hematopoiesis and pre‐mRNA splicing in vivo publication-title: Cancer Cell. – volume: 122 start-page: 3616 year: 2013 end-page: 3627 article-title: Clinical and biological implications of driver mutations in myelodysplastic syndromes publication-title: Blood. – volume: 16 start-page: 413 year: 2016 end-page: 430 article-title: RNA splicing factors as oncoproteins and tumor suppressor publication-title: Nat Rev Cancer. – volume: 30 start-page: 989 year: 2016 end-page: 1001 article-title: Spliceosomal gene mutations in myelodysplasia: molecular links to clonal abnormalities of hematopoiesis publication-title: Genes Dev. – volume: 18 start-page: 4 year: 2016 article-title: Unraveling myelodysplastic syndromes: current knowledge and future directions publication-title: Curr Oncol Rep. – volume: 127 start-page: 2391 year: 2016 end-page: 2405 article-title: The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia publication-title: Blood. – volume: 102 start-page: 1028 year: 2017 end-page: 1034 article-title: Molecular features of early onset adult myelodysplastic syndrome publication-title: Haematologica. – volume: 84 start-page: 291 year: 2015 end-page: 323 article-title: Mechanisms and regulation of alternative pre‐mRNA splicing publication-title: Annu Rev Biochem. – volume: 3 start-page: 1228 year: 2013 end-page: 1237 article-title: Misregulation of pre‐mRNA alternative splicing in cancer publication-title: Cancer Discov. – volume: 8 start-page: 14060 year: 2017 article-title: Mutant U2AF1‐expressing cells are sensitive to pharmacological modulation of the spliceosome publication-title: Nat Commun. – volume: 129 start-page: 2465 year: 2017 end-page: 2470 article-title: How do messenger RNA splicing alterations drive myelodysplasia? publication-title: Blood. – volume: 44 start-page: 53 year: 2011 end-page: 57 article-title: Recurrent mutations in the U2AF1 splicing factor in myelodysplastic syndromes publication-title: Nat Genet. – ident: e_1_2_5_42_1 doi: 10.1016/j.molcel.2016.04.011 – ident: e_1_2_5_9_1 doi: 10.1038/onc.2013.520 – ident: e_1_2_5_37_1 doi: 10.1038/nm.3733 – ident: e_1_2_5_45_1 doi: 10.1038/ncomms14060 – ident: e_1_2_5_2_1 doi: 10.1007/s11912-015-0489-2 – ident: e_1_2_5_41_1 doi: 10.1172/JCI91363 – ident: e_1_2_5_10_1 doi: 10.1056/NEJMoa1103283 – ident: e_1_2_5_21_1 doi: 10.1016/j.tig.2017.03.001 – ident: e_1_2_5_38_1 doi: 10.1056/NEJMoa1408617 – ident: e_1_2_5_29_1 doi: 10.1038/leu.2015.91 – ident: e_1_2_5_40_1 doi: 10.1016/j.ccell.2015.04.008 – ident: e_1_2_5_13_1 doi: 10.1038/nrc.2016.51 – volume: 32 start-page: 819 year: 2011 ident: e_1_2_5_30_1 article-title: Study on prognostic significances of different cytogenetic risk categories in patients with primary myelodysplastic syndromes publication-title: Zhonghua Xue Ye Xue Za Zhi. – volume: 96 start-page: 3671 year: 2000 ident: e_1_2_5_27_1 article-title: Report of an international working group to standardize response criteria for myelodysplastic syndromes publication-title: Blood. – ident: e_1_2_5_16_1 doi: 10.1182/blood-2015-03-633537 – ident: e_1_2_5_25_1 doi: 10.1016/j.leukres.2010.06.004 – ident: e_1_2_5_39_1 doi: 10.1056/NEJMoa1409405 – ident: e_1_2_5_11_1 doi: 10.1038/nature10496 – ident: e_1_2_5_20_1 doi: 10.1101/gad.278424.116 – ident: e_1_2_5_8_1 doi: 10.1038/ng.3742 – ident: e_1_2_5_15_1 doi: 10.1016/j.leukres.2012.08.015 – ident: e_1_2_5_7_1 doi: 10.1038/leu.2013.336 – ident: e_1_2_5_22_1 doi: 10.1182/blood-2017-02-692715 – ident: e_1_2_5_28_1 doi: 10.1016/j.cell.2012.04.023 – ident: e_1_2_5_24_1 doi: 10.1182/blood.V89.6.2079 – ident: e_1_2_5_3_1 doi: 10.14694/EDBK_175397 – ident: e_1_2_5_35_1 doi: 10.1016/j.celrep.2015.02.005 – ident: e_1_2_5_6_1 doi: 10.1182/blood-2013-08-518886 – ident: e_1_2_5_12_1 doi: 10.1146/annurev-biochem-060614-034316 – ident: e_1_2_5_14_1 doi: 10.1158/2159-8290.CD-13-0253 – ident: e_1_2_5_23_1 doi: 10.1182/blood-2016-03-643544 – ident: e_1_2_5_17_1 doi: 10.1038/ng.1031 – ident: e_1_2_5_4_1 doi: 10.1200/JCO.2016.67.3616 – ident: e_1_2_5_18_1 doi: 10.1182/blood-2011-12-399337 – ident: e_1_2_5_43_1 doi: 10.1101/gr.181016.114 – ident: e_1_2_5_19_1 doi: 10.1002/ajh.23541 – volume: 2013 start-page: 2059 year: 2013 ident: e_1_2_5_36_1 article-title: Genomic and epigenomic landscapes of adult de novo acute myeloid leukemia publication-title: N Engl J Med. – ident: e_1_2_5_31_1 doi: 10.1038/sj.leu.2403688 – ident: e_1_2_5_5_1 doi: 10.1056/NEJMoa1013343 – ident: e_1_2_5_32_1 doi: 10.3324/haematol.2016.159772 – ident: e_1_2_5_34_1 doi: 10.1038/leu.2017.109 – ident: e_1_2_5_26_1 doi: 10.3109/10428190903515200 – ident: e_1_2_5_44_1 doi: 10.1038/nm.4097 – ident: e_1_2_5_33_1 doi: 10.1038/leu.2015.337 |
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Snippet | U2AF1 mutations (U2AF1MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical... U2AF1 mutations ( U2AF1 MT) occur commonly in myelodysplastic syndromes (MDS) without ring sideroblasts. The aim of this study was to investigate the clinical... |
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SubjectTerms | Adolescent Adult Aged Aged, 80 and over Cohort Studies DNA Mutational Analysis - methods Female Fibrosis Hemoglobin High-Throughput Nucleotide Sequencing - methods Humans Karyotypes Male Middle Aged Mutation Mutation - genetics Myelodysplastic syndrome Myelodysplastic syndromes Myelodysplastic Syndromes - genetics Myelodysplastic Syndromes - metabolism Prognosis Sequence Analysis, DNA - methods Sideroblasts Splicing Factor U2AF - genetics Splicing Factor U2AF - metabolism Thrombocytopenia |
Title | Clinical features and biological implications of different U2AF1 mutation types in myelodysplastic syndromes |
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