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dc.contributor.authorCastilla, Lucio H.
dc.contributor.authorBushweller, John H.
dc.date2022-08-11T08:09:21.000
dc.date.accessioned2022-08-23T16:27:12Z
dc.date.available2022-08-23T16:27:12Z
dc.date.issued2017-03-16
dc.date.submitted2017-05-25
dc.identifier.citationAdv Exp Med Biol. 2017;962:229-244. doi: 10.1007/978-981-10-3233-2_15. <a href="https://doi.org/10.1007/978-981-10-3233-2_15">Link to article on publisher's site</a>
dc.identifier.issn0065-2598 (Linking)
dc.identifier.doi10.1007/978-981-10-3233-2_15
dc.identifier.pmid28299661
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36727
dc.description.abstractAcute myeloid leukemia (AML) is characterized by recurrent chromosomal rearrangements that encode for fusion proteins which drive leukemia initiation and maintenance. The inv(16) (p13q22) rearrangement is a founding mutation and the associated CBFbeta-SMMHC fusion protein is essential for the survival of inv(16) AML cells. This Chapter will discuss our understanding of the function of this fusion protein in disrupting hematopoietic homeostasis and creating pre-leukemic blasts, in its cooperation with other co-occurring mutations during leukemia initiation, and in leukemia maintenance. In addition, this chapter will discuss the current approaches used for the treatment of inv(16) AML and the recent development of AI-10-49, a selective targeted inhibitor of CBFbeta-SMMHC/RUNX1 binding, the first candidate targeted therapy for inv(16) AML.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=28299661&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttps://doi.org/10.1007/978-981-10-3233-2_15
dc.subjectAI-10-49
dc.subjectAML
dc.subjectCBF
dc.subjectCBFb-MYH11
dc.subjectCBFbeta-SMMHC
dc.subjectLeukemia
dc.subjectPPI
dc.subjectProtein-protein interaction inhibitor
dc.subjectRUNX1
dc.subjectTargeted therapies
dc.subjectinv(16)
dc.subjectBiochemistry
dc.subjectCancer Biology
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleMolecular Basis and Targeted Inhibition of CBFbeta-SMMHC Acute Myeloid Leukemia
dc.typeJournal Article
dc.source.journaltitleAdvances in experimental medicine and biology
dc.source.volume962
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/metnet_pubs/94
dc.identifier.contextkey10212159
html.description.abstract<p>Acute myeloid leukemia (AML) is characterized by recurrent chromosomal rearrangements that encode for fusion proteins which drive leukemia initiation and maintenance. The inv(16) (p13q22) rearrangement is a founding mutation and the associated CBFbeta-SMMHC fusion protein is essential for the survival of inv(16) AML cells. This Chapter will discuss our understanding of the function of this fusion protein in disrupting hematopoietic homeostasis and creating pre-leukemic blasts, in its cooperation with other co-occurring mutations during leukemia initiation, and in leukemia maintenance. In addition, this chapter will discuss the current approaches used for the treatment of inv(16) AML and the recent development of AI-10-49, a selective targeted inhibitor of CBFbeta-SMMHC/RUNX1 binding, the first candidate targeted therapy for inv(16) AML.</p>
dc.identifier.submissionpathmetnet_pubs/94
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Molecular, Cell and Cancer Biology
dc.source.pages229-244


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