Thrombopoietin receptor is required for the oncogenic function of CALR mutants

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F65269705%3A_____%2F16%3A00065931" target="_blank" >RIV/65269705:_____/16:00065931 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216224:14110/16:00091729

Výsledek na webu

<a href="http://www.nature.com/leu/journal/v30/n8/full/leu201632a.html" target="_blank" >http://www.nature.com/leu/journal/v30/n8/full/leu201632a.html</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1038/leu.2016.32" target="_blank" >10.1038/leu.2016.32</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Thrombopoietin receptor is required for the oncogenic function of CALR mutants

Popis výsledku v původním jazyce

Myeloproliferative neoplasms (MPNs) are diseases characterized by the pathologic expansion of myeloid cells of the hematopoietic lineage. The three 'classical' MPNs include polycythemia vera (PV, increase in erythrocytes), essential thrombocythemia (ET, increase in platelets) and primary myelofibrosis (PMF, usually elevated platelet counts associated with fibrotic deposition in the bone marrow).1 MPNs are essentially clonal diseases driven by somatic mutations in hematopoietic stem and progenitor cells. So far, three genes have been identified that can drive the disease phenotype when mutated.2 Activating mutations in Janus Kinase 2 (JAK2) and the thrombopoietin receptor (MPL) have been known for close to a decade and their mechanism of action has been extensively studied.3-8 Recently, we and others identified somatic mutations in the CALR gene in 25-35% of ET and PMF patients.9,10

Název v anglickém jazyce

Thrombopoietin receptor is required for the oncogenic function of CALR mutants

Popis výsledku anglicky

Myeloproliferative neoplasms (MPNs) are diseases characterized by the pathologic expansion of myeloid cells of the hematopoietic lineage. The three 'classical' MPNs include polycythemia vera (PV, increase in erythrocytes), essential thrombocythemia (ET, increase in platelets) and primary myelofibrosis (PMF, usually elevated platelet counts associated with fibrotic deposition in the bone marrow).1 MPNs are essentially clonal diseases driven by somatic mutations in hematopoietic stem and progenitor cells. So far, three genes have been identified that can drive the disease phenotype when mutated.2 Activating mutations in Janus Kinase 2 (JAK2) and the thrombopoietin receptor (MPL) have been known for close to a decade and their mechanism of action has been extensively studied.3-8 Recently, we and others identified somatic mutations in the CALR gene in 25-35% of ET and PMF patients.9,10

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FD - Onkologie a hematologie

OECD FORD obor

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Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2016

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Leukemia

ISSN

0887-6924

e-ISSN

—

Svazek periodika

30

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

5

Strana od-do

1759-1763

Kód UT WoS článku

000380826400018

EID výsledku v databázi Scopus

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