Data from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1 Article Swipe
Evangelia Loizou
,
Ana Banito
,
Geulah Livshits
,
Yu-Jui Ho
,
Richard P. Koche
,
Francisco J. Sánchez‐Rivera
,
Allison Mayle
,
Chi-Chao Chen
,
Savvas Kinalis
,
Frederik Otzen Bagger
,
Edward R. Kastenhuber
,
Benjamin H. Durham
,
Scott W. Lowe
·
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.c.6548093.v1
YOU?
·
· 2023
· Open Access
·
· DOI: https://doi.org/10.1158/2159-8290.c.6548093.v1
Mutations in the TP53 tumor suppressor gene are common in many cancer types, including the acute myeloid leukemia (AML) subtype known as complex karyotype AML (CK-AML). Here, we identify a gain-of-function (GOF) Trp53 mutation that accelerates CK-AML initiation beyond p53 loss and, surprisingly, is required for disease maintenance. The Trp53R172H mutation (TP53R175H in humans) exhibits a neomorphic function by promoting aberrant self-renewal in leukemic cells, a phenotype that is present in hematopoietic stem and progenitor cells (HSPC) even prior to their transformation. We identify FOXH1 as a critical mediator of mutant p53 function that binds to and regulates stem cell–associated genes and transcriptional programs. Our results identify a context where mutant p53 acts as a bona fide oncogene that contributes to the pathogenesis of CK-AML and suggests a common biological theme for TP53 GOF in cancer.Significance:Our study demonstrates how a GOF p53 mutant can hijack an embryonic transcription factor to promote aberrant self-renewal. In this context, mutant Trp53 functions as an oncogene to both initiate and sustain myeloid leukemia and suggests a potential convergent activity of mutant Trp53 across cancer types.This article is highlighted in the In This Issue feature, p. 813
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Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1158/2159-8290.c.6548093.v1
- OA Status
- gold
- Related Works
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- OpenAlex ID
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All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4362545613Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1158/2159-8290.c.6548093.v1Digital Object Identifier
- Title
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Data from A Gain-of-Function p53-Mutant Oncogene Promotes Cell Fate Plasticity and Myeloid Leukemia through the Pluripotency Factor FOXH1Work title
- Type
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preprintOpenAlex work type
- Language
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enPrimary language
- Publication year
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2023Year of publication
- Publication date
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2023-04-03Full publication date if available
- Authors
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Evangelia Loizou, Ana Banito, Geulah Livshits, Yu-Jui Ho, Richard P. Koche, Francisco J. Sánchez‐Rivera, Allison Mayle, Chi-Chao Chen, Savvas Kinalis, Frederik Otzen Bagger, Edward R. Kastenhuber, Benjamin H. Durham, Scott W. LoweList of authors in order
- Landing page
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https://doi.org/10.1158/2159-8290.c.6548093.v1Publisher landing page
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YesWhether a free full text is available
- OA status
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goldOpen access status per OpenAlex
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https://doi.org/10.1158/2159-8290.c.6548093.v1Direct OA link when available
- Concepts
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Biology, Myeloid leukemia, Cancer research, Context (archaeology), Oncogene, Myeloid, Haematopoiesis, Transcription factor, Mutation, Stem cell, Genetics, Cell cycle, Molecular biology, Cancer, Gene, PaleontologyTop concepts (fields/topics) attached by OpenAlex
- Cited by
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0Total citation count in OpenAlex
- Related works (count)
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.article | 181 |
| abstract_inverted_index.complex | 22 |
| abstract_inverted_index.context | 108 |
| abstract_inverted_index.disease | 46 |
| abstract_inverted_index.humans) | 53 |
| abstract_inverted_index.myeloid | 16, 167 |
| abstract_inverted_index.present | 69 |
| abstract_inverted_index.promote | 150 |
| abstract_inverted_index.results | 105 |
| abstract_inverted_index.subtype | 19 |
| abstract_inverted_index.sustain | 166 |
| abstract_inverted_index.aberrant | 60, 151 |
| abstract_inverted_index.activity | 174 |
| abstract_inverted_index.context, | 155 |
| abstract_inverted_index.critical | 87 |
| abstract_inverted_index.exhibits | 54 |
| abstract_inverted_index.feature, | 189 |
| abstract_inverted_index.function | 57, 92 |
| abstract_inverted_index.identify | 28, 83, 106 |
| abstract_inverted_index.initiate | 164 |
| abstract_inverted_index.leukemia | 17, 168 |
| abstract_inverted_index.leukemic | 63 |
| abstract_inverted_index.mediator | 88 |
| abstract_inverted_index.mutation | 33, 50 |
| abstract_inverted_index.oncogene | 117, 161 |
| abstract_inverted_index.required | 44 |
| abstract_inverted_index.suggests | 126, 170 |
| abstract_inverted_index.(CK-AML). | 25 |
| abstract_inverted_index.embryonic | 146 |
| abstract_inverted_index.functions | 158 |
| abstract_inverted_index.including | 13 |
| abstract_inverted_index.karyotype | 23 |
| abstract_inverted_index.phenotype | 66 |
| abstract_inverted_index.potential | 172 |
| abstract_inverted_index.programs. | 103 |
| abstract_inverted_index.promoting | 59 |
| abstract_inverted_index.regulates | 97 |
| abstract_inverted_index.biological | 129 |
| abstract_inverted_index.convergent | 173 |
| abstract_inverted_index.initiation | 37 |
| abstract_inverted_index.neomorphic | 56 |
| abstract_inverted_index.progenitor | 74 |
| abstract_inverted_index.suppressor | 5 |
| abstract_inverted_index.accelerates | 35 |
| abstract_inverted_index.contributes | 119 |
| abstract_inverted_index.highlighted | 183 |
| abstract_inverted_index.demonstrates | 137 |
| abstract_inverted_index.maintenance. | 47 |
| abstract_inverted_index.pathogenesis | 122 |
| abstract_inverted_index.self-renewal | 61 |
| abstract_inverted_index.hematopoietic | 71 |
| abstract_inverted_index.self-renewal. | 152 |
| abstract_inverted_index.surprisingly, | 42 |
| abstract_inverted_index.transcription | 147 |
| abstract_inverted_index.transcriptional | 102 |
| abstract_inverted_index.transformation. | 81 |
| abstract_inverted_index.gain-of-function | 30 |
| abstract_inverted_index.cell–associated | 99 |
| abstract_inverted_index.<i>TP53</i> | 3, 132 |
| abstract_inverted_index.<i>Trp53</i> | 32, 157, 177 |
| abstract_inverted_index.813</i></p></div> | 191 |
| abstract_inverted_index.<div>Abstract<p>Mutations | 0 |
| abstract_inverted_index.types.</p><p><i>This | 180 |
| abstract_inverted_index.cancer.</p>Significance:<p>Our | 135 |
| abstract_inverted_index.<i>Trp53<sup>R172H</sup></i> | 49 |
| abstract_inverted_index.(<i>TP53<sup>R175H</sup></i> | 51 |
| cited_by_percentile_year | |
| countries_distinct_count | 0 |
| institutions_distinct_count | 13 |
| citation_normalized_percentile.value | 0.19300318 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |