Genetic and molecular characterization of myelodysplastic syndromes and related myeloid neoplasms

被引:0
作者
Bhumika Patel
Cassandra Hirsch
Michael Clemente
Mikkael Sekeres
Hideki Makishima
Jaroslaw P. Maciejewski
机构
[1] Taussig Cancer Institute,Department of Translational Hematology and Oncology Research
[2] Cleveland Clinic,Leukemia Program
[3] Cleveland Clinic Taussig Cancer Institute,undefined
[4] Taussig Cancer Institute/R40,undefined
来源
International Journal of Hematology | 2015年 / 101卷
关键词
MDS; Somatic mutations; NGS; Clonal architecture; AML;
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学科分类号
摘要
Whole exome next generation sequencing systematically applied as a discovery tool in myelodysplastic syndromes (MDS) has led to the identification of a large number of novel mutations. Despite hundreds of patients studied, mutational saturation has not been reached and it is expected that new driver mutations will be discovered in this very heterogeneous condition. Serial samples and deep sequencing of the identified alterations has allowed for a dynamic/chronologic analysis of clonal architecture and identification of a subset of ancestral and secondary molecular lesions. Chromosomal gains and losses have been incorporated into the mutational analyses because they can either cooperate with mutations or produce a functional phenocopy. In addition to the search for somatic defects in MDS, similar discovery studies have been also performed to identify germ line mutations/alterations. Clinical analysis showed applicability of multiplexed somatic mutational panels that would complement current pathomorphologic diagnosis, allow for subclassification of nosologic entities, and enhance predictive power of current prognostic algorithms. Overall, comprehensive genomic analysis in MDS has revealed a tremendous heterogeneity of somatic lesions and their combinations further enhanced by the heterogeneity of clonal architecture and chromosomal lesions.
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页码:213 / 218
页数:5
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  • [1] Makishima H(2013)Clinical MUTATOME of myelodysplastic syndrome; comparison to primary acute myelogenous leukemia Blood (ASH Annual Meeting Abstracts). 122 518-3627
  • [2] LaFramboise T(2013)Clinical and biological implications of driver mutations in myelodysplastic syndromes Blood 122 3616-247
  • [3] Przychodzen BP(2014)Landscape of genetic lesions in 944 patients with myelodysplastic syndromes Leukemia 28 241-501
  • [4] Yoshida K(2014)Discovery and saturation analysis of cancer genes across 21 tumour types Nature 505 495-2301
  • [5] Ruffalo M(2009)Mutation in TET2 in myeloid cancers N Engl J Med 360 2289-6410
  • [6] Ines Gomez-Segui I(2009)Loss of heterozygosity 4q24 and TET2 mutations associated with myelodysplastic/myeloproliferative neoplasms Blood 113 6403-3941
  • [7] Papaemmanuil E(2011)Mutational spectrum analysis of chronic myelomonocytic leukemia includes genes associated with epigenetic regulation: UTX, EZH2, and DNMT3A Blood 118 3932-290
  • [8] Gerstung M(2013)Genetic predispositions to childhood leukemia Ther Adv Hematol 4 270-4645
  • [9] Malcovati L(2008)Five new pedigrees with inherited RUNX1 mutations causing familial platelet disorder with propensity to myeloid malignancy Blood 112 4639-132
  • [10] Tauro S(2008)Familial myelodysplasia and acute myeloid leukaemia––a review Br J Haematol 140 123-1017