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Immunoediting is not a primary transformation event in a murine model of MLL-ENL AML

Dudenhöffer-Pfeifer, Monika LU and Bryder, David LU (2018) In Life Science Alliance 1(4).
Abstract

Although it is firmly established that endogenous immunity can prevent cancer outgrowth, with a range of immunomodulatory strategies reaching clinical use, most studies on the topic have been restricted to solid cancers. This applies in particular to cancer initiation, where model constraints have precluded investigations of immunosurveillance and immunoediting during the multistep progression into acute myeloid leukemia (AML). Here, we used a mouse model where the chimeric transcription factor MLL-ENL can be conditionally activated in vivo as a leukemic “first-hit,” which is followed by spontaneous transformation into AML. We observed similar disease kinetics regardless of whether AML developed in WT or immunocompromised hosts, despite... (More)

Although it is firmly established that endogenous immunity can prevent cancer outgrowth, with a range of immunomodulatory strategies reaching clinical use, most studies on the topic have been restricted to solid cancers. This applies in particular to cancer initiation, where model constraints have precluded investigations of immunosurveillance and immunoediting during the multistep progression into acute myeloid leukemia (AML). Here, we used a mouse model where the chimeric transcription factor MLL-ENL can be conditionally activated in vivo as a leukemic “first-hit,” which is followed by spontaneous transformation into AML. We observed similar disease kinetics regardless of whether AML developed in WT or immunocompromised hosts, despite more permissive preleukemic environments in the latter. When assessing transformed AML cells from either primary immunocompetent or immunocompromised hosts, AML cells from all sources could be targets of endogenous immunity. Our data argue against immunoediting in response to selective pressure from endogenous immunity as a universal primary transformation event in AML.

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author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Life Science Alliance
volume
1
issue
4
article number
e201800079
publisher
Rockefeller University Press
external identifiers
  • pmid:30456365
  • scopus:85057021231
ISSN
2575-1077
DOI
10.26508/lsa.201800079
language
English
LU publication?
yes
id
3c6af303-cb8d-4422-a4c5-6600584449db
date added to LUP
2018-12-04 13:37:47
date last changed
2024-04-15 18:08:36
@article{3c6af303-cb8d-4422-a4c5-6600584449db,
  abstract     = {{<p>Although it is firmly established that endogenous immunity can prevent cancer outgrowth, with a range of immunomodulatory strategies reaching clinical use, most studies on the topic have been restricted to solid cancers. This applies in particular to cancer initiation, where model constraints have precluded investigations of immunosurveillance and immunoediting during the multistep progression into acute myeloid leukemia (AML). Here, we used a mouse model where the chimeric transcription factor MLL-ENL can be conditionally activated in vivo as a leukemic “first-hit,” which is followed by spontaneous transformation into AML. We observed similar disease kinetics regardless of whether AML developed in WT or immunocompromised hosts, despite more permissive preleukemic environments in the latter. When assessing transformed AML cells from either primary immunocompetent or immunocompromised hosts, AML cells from all sources could be targets of endogenous immunity. Our data argue against immunoediting in response to selective pressure from endogenous immunity as a universal primary transformation event in AML.</p>}},
  author       = {{Dudenhöffer-Pfeifer, Monika and Bryder, David}},
  issn         = {{2575-1077}},
  language     = {{eng}},
  number       = {{4}},
  publisher    = {{Rockefeller University Press}},
  series       = {{Life Science Alliance}},
  title        = {{Immunoediting is not a primary transformation event in a murine model of MLL-ENL AML}},
  url          = {{http://dx.doi.org/10.26508/lsa.201800079}},
  doi          = {{10.26508/lsa.201800079}},
  volume       = {{1}},
  year         = {{2018}},
}