| Autor: |
Swierczek SI; University of Utah School of Medicine and VAH, Salt Lake City, UT, USA., Yoon D, Bellanné-Chantelot C, Kim SJ, Saint-Martin C, Delhommeau F, Najman A, Prchal JT |
| Jazyk: |
angličtina |
| Zdroj: |
Haematologica [Haematologica] 2011 May; Vol. 96 (5), pp. 775-8. Date of Electronic Publication: 2011 Jan 27. |
| DOI: |
10.3324/haematol.2010.029678 |
| Abstrakt: |
TET2 mutations are found in polycythemia vera and it was initially reported that there is a greater TET2 mutational burden than JAK2(V617F) in polycythemia vera stem cells and that TET2 mutations precede JAK2(V617F). We quantified the proportion of TET2, JAK2(V617F) mutations and X-chromosome allelic usage in polycythemia vera cells, BFU-Es and in vitro expanded erythroid progenitors and found clonal reticulocytes, granulocytes, platelets and CD34(+) cells. We found that TET2 mutations may also follow rather than precede JAK2(V617F) as recently reported by others. Only a fraction of clonal early hematopoietic precursors and largely polyclonal T cells carry the TET2 mutation. We showed that in vitro the concomitant presence of JAK2(V617F) and TET2 mutations favors clonal polycythemia vera erythroid progenitors in contrast with non-TET2 mutated progenitors. We conclude that loss-of-function TET2 mutations are not the polycythemia vera initiating events and that the acquisition of TET2 somatic mutations may increase the aggressivity of the polycythemia vera clone. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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