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PU.1 downregulation in murine radiation-induced acute myeloid leukaemia (AML): from molecular mechanism to human AML

Verbiest, Tom, Bouffler, Simon, Nutt, Stephen L., Badie, Christophe·2015·Carcinogenesis
DOI 10.1093/carcin/bgv016PMC PMC4392607
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Figure 1. Involvement of PU.1 in murine rAML and human primary AML. In mice, exposure to ionising radiation induces a first mutational hit in haematopoietic cells (interstitial deletion of one Sfpi1 gene on chromosome 2), creating pre-leukaemic cells that have a growth advantage but which are not fully malignant. Subsequently, these cells acquire a second mutational hit (point mutation in the remaining Sfpi1 copy), resulting in the formation of a leukaemic cell which undergoes further clonal expansion and eventually leads to the development of rAML. In humans, no data is currently available on the involvement of PU.1 in tAML. However, various epigenetic (A) and genetic (B) modifications, contributing towards the formation of pre-leukaemic cells, have been linked with downregulation of PU.1 in human primary AML. These pre-leukaemic cells harbour some, but not all, of the mutations found in leukaemic cells (60). Numerous pre-leukaemic and leukaemic mutations contribute towards PU.1 downregulation in human primary AML, including the top three genes found mutated in human primary AML [NPM1, FLT3, and DNMT3A (17)]. Although the molecular targets seem to differ between species, it appears that a common PU.1 downregulation pathway is affected in murine rAML and human primary AML. Future studies investigating tAML patients receiving radiotherapy alone should confirm whether PU.1 is also commonly downregulated in human tAML. Blue intensity indicates PU.1 expression/activity levels (dark equals high levels).
Figure 1. Involvement of PU.1 in murine rAML and human primary AML. In mice, exposure to ionising radiation induces a first mutational hit in haematopoietic cells (interstitial deletion of one Sfpi1 gene on chromosome 2), creating pre-leukaemic cells that have a growth advantage but which are not fully malignant. Subsequently, these cells acquire a second mutational hit (point mutation in the remaining Sfpi1 copy), resulting in the formation of a leukaemic cell which undergoes further clonal expansion and eventually leads to the development of rAML. In humans, no data is currently available on the involvement of PU.1 in tAML. However, various epigenetic (A) and genetic (B) modifications, contributing towards the formation of pre-leukaemic cells, have been linked with downregulation of PU.1 in human primary AML. These pre-leukaemic cells harbour some, but not all, of the mutations found in leukaemic cells (60). Numerous pre-leukaemic and leukaemic mutations contribute towards PU.1 downregulation in human primary AML, including the top three genes found mutated in human primary AML [NPM1, FLT3, and DNMT3A (17)]. Although the molecular targets seem to differ between species, it appears that a common PU.1 downregulation pathway is affected in murine rAML and human primary AML. Future studies investigating tAML patients receiving radiotherapy alone should confirm whether PU.1 is also commonly downregulated in human tAML. Blue intensity indicates PU.1 expression/activity levels (dark equals high levels).CC BY-NC · PubMed Central

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Metadata

Authors
Verbiest, T., Bouffler, S., Nutt, S. L., & Badie, C.
Venue
Carcinogenesis
Publisher
Oxford University Press (OUP)
Published
2015-03-06
Volume
36
Issue
4
Pages
413-419
ISSN
  • 1460-2180
  • 0143-3334
DOI
10.1093/carcin/bgv016
PMC
PMC4392607
Cited by
46
References
16
Language
en

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