Journal
HAEMATOLOGICA-THE HEMATOLOGY JOURNAL
Volume 95, Issue 12, Pages 2153-2156Publisher
FERRATA STORTI FOUNDATION
DOI: 10.3324/haematol.2010.029306
Keywords
MPL; JAK2; TP53; TET2; myeloproliferative neoplasm; acute myeloid leukemia; essential thrombocythemia; primary myelofibrosis; hydroxycarbamide
Categories
Funding
- UK Medical Research Council
- Leukaemia and Lymphoma Research
- Kay Kendal Leukaemia Fund
- NIHR Cambridge Biomedical Research Centre
- Leukemia and Lymphoma Society of America
- MIUR
- Cancer Research UK [8961] Funding Source: researchfish
Ask authors/readers for more resources
Somatic activating mutations in MPL, the thrombopoietin receptor, occur in the myeloproliferative neoplasms, although virtually nothing is known about their role in evolution to acute myeloid leukemia. In this study, the MPL T487A mutation, identified in de novo acute myeloid leukemia, was not detected in 172 patients with a myeloproliferative neoplasm. In patients with a prior MPL W515L-mutant myeloproliferative neoplasm, leukemic transformation was accompanied by MPL-mutant leukemic blasts, was seen in the absence of prior cytoreductive therapy and often involved loss of wild-type MPL by mitotic recombination. Moreover, clonal analysis of progenitor colonies at the time of leukemic transformation revealed the presence of multiple genetically distinct but phylogenetically-related clones bearing different TP53 mutations, implying a mutator-phenotype and indicating that leukemic transformation may be preceded by the parallel expansion of diverse hematopoietic clones.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available