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Effect of Mutation Order on Myeloproliferative Neoplasms

by Guglielmelli, Paola , Silber, Yvonne , Döhner, Konstanze , Harrison, Claire N , Papaemmanuil, Elli , Menon, Suraj , Kent, David G , Massie, Charles E , Bellosillo, Beatriz , Vassiliou, George S , Grinfeld, Jacob , Godfrey, Anna L , Baxter, E. Joanna , Dimitropoulou, Danai , Campbell, Peter J , Ortmann, Christina A , Wedge, David C , Besses, Carles , Nangalia, Jyoti , Vannucchi, Alessandro , Green, Anthony R

in Age of Onset / Blood cancer / Cancer / Cell Proliferation - genetics / Cloning / Colonies / Colony-forming cells / Dioxygenases / Disease / DNA Mutational Analysis / DNA-Binding Proteins - genetics / Epigenetics / Gene Expression / Genotyping / Hematopoietic stem cells / Hematopoietic Stem Cells - physiology / Homozygote / Humans / Influence / Janus kinase / Janus kinase 2 / Janus Kinase 2 - genetics / Kinases / Leukemia / Lymphoma / Medical research / Mutation / Myeloproliferative Disorders - genetics / Next-generation sequencing / Polycythemia / Polycythemia vera / Polycythemia Vera - genetics / Progenitor cells / Proto-Oncogene Proteins - genetics / Scholarships & fellowships / Software / Stem cells / Thrombocythemia, Essential - genetics / Thrombosis / Thrombosis - genetics / Transcription / Transcription, Genetic / Tumors / Up-Regulation

2015

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Effect of Mutation Order on Myeloproliferative Neoplasms

2015

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2015

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Journal Article

Effect of Mutation Order on Myeloproliferative Neoplasms

Guglielmelli, Paola,

Silber, Yvonne,

Döhner, Konstanze,

Harrison, Claire N,

Papaemmanuil, Elli,

Menon, Suraj,

Kent, David G,

Massie, Charles E,

Bellosillo, Beatriz,

Vassiliou, George S,

Grinfeld, Jacob,

Godfrey, Anna L,

Baxter, E. Joanna,

Dimitropoulou, Danai,

Campbell, Peter J,

Ortmann, Christina A,

Wedge, David C,

Besses, Carles,

Nangalia, Jyoti,

Vannucchi, Alessandro,

Green, Anthony R

2015

Overview

About 10% of myeloproliferative neoplasms carry mutations in both TET2 and JAK2 . Clinical presentation, risk of thrombosis, and rates of tumor progression are affected by which gene mutation is acquired first. Cancers evolve as a consequence of the stepwise accumulation of somatic lesions, with competition between subclones and sequential subclonal evolution. 1 , 2 Darwinian selection of variant subclones results in acquisition of biologic attributes required for tumor formation. 3 Genetic interaction is central to this process, but it is unclear how mutated genes interact to generate the phenotypic hallmarks of cancer, and the influence, if any, of the order in which mutations are acquired is unknown. 4 Cooperation between different genetic lesions has been observed in cell-line models of transformation 5 and in mouse models of several cancers. 6 , 7 Moreover, the consequences of an early . . .

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Publisher

Massachusetts Medical Society

Subject

Age of Onset

/ Blood cancer

/ Cancer

/ Cell Proliferation - genetics

/ Cloning

/ Colonies

/ Colony-forming cells