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The PML domain of PML-RARα blocks senescence to promote leukemia

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The PML domain of PML-RARα blocks senescence to promote leukemia. / Korf, Katharina; Wodrich, Harald; Haschke, Alexander; Ocampo, Corinne; Harder, Lena; Gieseke, Friederike; Pollmann, Annika; Dierck, Kevin; Prall, Sebastian; Staege, Hannah; Ma, Hui; Horstmann, Martin A; Evans, Ronald M; Sternsdorf, Thomas.

in: P NATL ACAD SCI USA, Jahrgang 111, Nr. 33, 19.08.2014, S. 12133-8.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Korf, K, Wodrich, H, Haschke, A, Ocampo, C, Harder, L, Gieseke, F, Pollmann, A, Dierck, K, Prall, S, Staege, H, Ma, H, Horstmann, MA, Evans, RM & Sternsdorf, T 2014, 'The PML domain of PML-RARα blocks senescence to promote leukemia', P NATL ACAD SCI USA, Jg. 111, Nr. 33, S. 12133-8. https://doi.org/10.1073/pnas.1412944111

APA

Korf, K., Wodrich, H., Haschke, A., Ocampo, C., Harder, L., Gieseke, F., Pollmann, A., Dierck, K., Prall, S., Staege, H., Ma, H., Horstmann, M. A., Evans, R. M., & Sternsdorf, T. (2014). The PML domain of PML-RARα blocks senescence to promote leukemia. P NATL ACAD SCI USA, 111(33), 12133-8. https://doi.org/10.1073/pnas.1412944111

Vancouver

Korf K, Wodrich H, Haschke A, Ocampo C, Harder L, Gieseke F et al. The PML domain of PML-RARα blocks senescence to promote leukemia. P NATL ACAD SCI USA. 2014 Aug 19;111(33):12133-8. https://doi.org/10.1073/pnas.1412944111

Bibtex

@article{61ec9dd0e3a047f5965f0e9769f6574e,
title = "The PML domain of PML-RARα blocks senescence to promote leukemia",
abstract = "In most acute promyelocytic leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor α (PML-RARα) fusion gene. Although expression of the human PML fusion in mice promotes leukemia, its efficiency is rather low. Unexpectedly, we find that simply replacing the human PML fusion with its mouse counterpart results in a murine PML-RARα (mPR) hybrid protein that is transformed into a significantly more leukemogenic oncoprotein. Using this more potent isoform, we show that mPR promotes immortalization by preventing cellular senescence, impeding up-regulation of both the p21 and p19(ARF) cell-cycle regulators. This induction coincides with a loss of the cancer-associated ATRX/Daxx-histone H3.3 predisposition complex and suggests inhibition of senescence as a targetable mechanism in APL therapy.",
keywords = "Animals, Bone Marrow Cells, Cell Aging, Cell Line, Cell Line, Tumor, Humans, Leukemia, Promyelocytic, Acute, Mice, Oncogene Proteins, Fusion, Tretinoin",
author = "Katharina Korf and Harald Wodrich and Alexander Haschke and Corinne Ocampo and Lena Harder and Friederike Gieseke and Annika Pollmann and Kevin Dierck and Sebastian Prall and Hannah Staege and Hui Ma and Horstmann, {Martin A} and Evans, {Ronald M} and Thomas Sternsdorf",
year = "2014",
month = aug,
day = "19",
doi = "10.1073/pnas.1412944111",
language = "English",
volume = "111",
pages = "12133--8",
journal = "P NATL ACAD SCI USA",
issn = "0027-8424",
publisher = "National Academy of Sciences",
number = "33",

}

RIS

TY - JOUR

T1 - The PML domain of PML-RARα blocks senescence to promote leukemia

AU - Korf, Katharina

AU - Wodrich, Harald

AU - Haschke, Alexander

AU - Ocampo, Corinne

AU - Harder, Lena

AU - Gieseke, Friederike

AU - Pollmann, Annika

AU - Dierck, Kevin

AU - Prall, Sebastian

AU - Staege, Hannah

AU - Ma, Hui

AU - Horstmann, Martin A

AU - Evans, Ronald M

AU - Sternsdorf, Thomas

PY - 2014/8/19

Y1 - 2014/8/19

N2 - In most acute promyelocytic leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor α (PML-RARα) fusion gene. Although expression of the human PML fusion in mice promotes leukemia, its efficiency is rather low. Unexpectedly, we find that simply replacing the human PML fusion with its mouse counterpart results in a murine PML-RARα (mPR) hybrid protein that is transformed into a significantly more leukemogenic oncoprotein. Using this more potent isoform, we show that mPR promotes immortalization by preventing cellular senescence, impeding up-regulation of both the p21 and p19(ARF) cell-cycle regulators. This induction coincides with a loss of the cancer-associated ATRX/Daxx-histone H3.3 predisposition complex and suggests inhibition of senescence as a targetable mechanism in APL therapy.

AB - In most acute promyelocytic leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor α (PML-RARα) fusion gene. Although expression of the human PML fusion in mice promotes leukemia, its efficiency is rather low. Unexpectedly, we find that simply replacing the human PML fusion with its mouse counterpart results in a murine PML-RARα (mPR) hybrid protein that is transformed into a significantly more leukemogenic oncoprotein. Using this more potent isoform, we show that mPR promotes immortalization by preventing cellular senescence, impeding up-regulation of both the p21 and p19(ARF) cell-cycle regulators. This induction coincides with a loss of the cancer-associated ATRX/Daxx-histone H3.3 predisposition complex and suggests inhibition of senescence as a targetable mechanism in APL therapy.

KW - Animals

KW - Bone Marrow Cells

KW - Cell Aging

KW - Cell Line

KW - Cell Line, Tumor

KW - Humans

KW - Leukemia, Promyelocytic, Acute

KW - Mice

KW - Oncogene Proteins, Fusion

KW - Tretinoin

U2 - 10.1073/pnas.1412944111

DO - 10.1073/pnas.1412944111

M3 - SCORING: Journal article

C2 - 25092303

VL - 111

SP - 12133

EP - 12138

JO - P NATL ACAD SCI USA

JF - P NATL ACAD SCI USA

SN - 0027-8424

IS - 33

ER -