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dc.contributor.authorPulikkan, John A.
dc.contributor.authorCastilla, Lucio H.
dc.date2022-08-11T08:09:50.000
dc.date.accessioned2022-08-23T16:45:10Z
dc.date.available2022-08-23T16:45:10Z
dc.date.issued2018-04-26
dc.date.submitted2018-06-15
dc.identifier.citation<p>Front Oncol. 2018 Apr 26;8:129. doi: 10.3389/fonc.2018.00129. eCollection 2018. <a href="https://doi.org/10.3389/fonc.2018.00129">Link to article on publisher's site</a></p>
dc.identifier.issn2234-943X (Linking)
dc.identifier.doi10.3389/fonc.2018.00129
dc.identifier.pmid29755956
dc.identifier.urihttp://hdl.handle.net/20.500.14038/40630
dc.description.abstractAcute myeloid leukemia (AML) is a collection of hematologic malignancies with specific driver mutations that direct the pathology of the disease. The understanding of the origin and function of these mutations at early stages of transformation is critical to understand the etiology of the disease and for the design of effective therapies. The chromosome inversion inv(16) is thought to arise as a founding mutation in a hematopoietic stem cell (HSC) to produce preleukemic HSCs (preL-HSCs) with myeloid bias and differentiation block, and predisposed to AML. Studies in mice and human AML cells have established that inv(16) AML follows a clonal evolution model, in which preL-HSCs expressing the fusion protein CBFbeta-SMMHC persist asymptomatic in the bone marrow. The emerging leukemia-initiating cells (LICs) are composed by the inv(16) and a heterogeneous set of mutations. In this review, we will discuss the current understanding of inv(16) preleukemia development, and the function of CBFbeta-SMMHC related to preleukemia progression and LIC activity. We also discuss important open mechanistic questions in the etiology of inv(16) AML.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29755956&dopt=Abstract">Link to Article in PubMed</a></p>
dc.rightsCopyright © 2018 Pulikkan and Castilla. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectCBFB-MYH11
dc.subjectCBFβ-SMMHC
dc.subjectclonal evolution
dc.subjectleukemia
dc.subjectleukemia-initiating cell
dc.subjectmyeloid
dc.subjectpreleukemia
dc.subjectstem cells
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectHemic and Lymphatic Diseases
dc.subjectNeoplasms
dc.subjectOncology
dc.titlePreleukemia and Leukemia-Initiating Cell Activity in inv(16) Acute Myeloid Leukemia
dc.typeJournal Article
dc.source.journaltitleFrontiers in oncology
dc.source.volume8
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=4445&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/3434
dc.identifier.contextkey12326401
refterms.dateFOA2022-08-23T16:45:10Z
html.description.abstract<p>Acute myeloid leukemia (AML) is a collection of hematologic malignancies with specific driver mutations that direct the pathology of the disease. The understanding of the origin and function of these mutations at early stages of transformation is critical to understand the etiology of the disease and for the design of effective therapies. The chromosome inversion inv(16) is thought to arise as a founding mutation in a hematopoietic stem cell (HSC) to produce preleukemic HSCs (preL-HSCs) with myeloid bias and differentiation block, and predisposed to AML. Studies in mice and human AML cells have established that inv(16) AML follows a clonal evolution model, in which preL-HSCs expressing the fusion protein CBFbeta-SMMHC persist asymptomatic in the bone marrow. The emerging leukemia-initiating cells (LICs) are composed by the inv(16) and a heterogeneous set of mutations. In this review, we will discuss the current understanding of inv(16) preleukemia development, and the function of CBFbeta-SMMHC related to preleukemia progression and LIC activity. We also discuss important open mechanistic questions in the etiology of inv(16) AML.</p>
dc.identifier.submissionpathoapubs/3434
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages129


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Copyright © 2018 Pulikkan and Castilla. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
Except where otherwise noted, this item's license is described as Copyright © 2018 Pulikkan and Castilla. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.