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dc.contributor.authorChen, Yaoyu
dc.contributor.authorLi, Shaoguang
dc.date2022-08-11T08:08:29.000
dc.date.accessioned2022-08-23T15:56:55Z
dc.date.available2022-08-23T15:56:55Z
dc.date.issued2013-06-06
dc.date.submitted2014-03-11
dc.identifier.citationChen Y, Li S. Molecular signatures of chronic myeloid leukemia stem cells. Biomark Res. 2013 Jun 6;1(1):21. doi: 10.1186/2050-7771-1-21. <a href="http://dx.doi.org/10.1186/2050-7771-1-21">Link to article on publisher's site</a>
dc.identifier.issn2050-7771 (Linking)
dc.identifier.doi10.1186/2050-7771-1-21
dc.identifier.pmid24252550
dc.identifier.urihttp://hdl.handle.net/20.500.14038/30077
dc.description.abstractBCR-ABL tyrosine kinase inhibitors (TKIs) are effective in controlling Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) are unlikely to cure the disease because TKIs are unable to eradicate leukemia stem cells (LSCs) responsible for the disease relapse even after tyrosine kinase inhibition. In addition, the TKI resistance of LSCs is not associated with the BCR-ABL kinase domain mutations. These observations indicate that TKI-insensitive LSCs and TKI-sensitive leukemic progenitor cells are biologically different, which leads us to believe that LSCs and more differentiated leukemic cells have different genetic mechanisms. Further study of LSCs to identify the novel gene signatures and mechanisms that control the function and molecular phenotype of LSCs is critical. In this mini-review, we will discuss our current understanding of the biology of LSCs and novel genes that could serve as a molecular signature of LSCs in CML. These novel genes could also serve as potential targets for eradicating LSCs in CML.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=24252550&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsCopyright 2013 Chen and Li; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<a href="http://creativecommons.org/licenses/by/2.0">http://creativecommons.org/licenses/by/2.0</a>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.subjectBCR-ABL
dc.subjectLeukemic stem cells
dc.subjectCML
dc.subjectBiomarker
dc.subjectHematopoietic stem cells
dc.subjectCancer stem cells
dc.subjectCancer Biology
dc.titleMolecular signatures of chronic myeloid leukemia stem cells
dc.typeJournal Article
dc.source.journaltitleBiomarker research
dc.source.volume1
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1309&amp;context=faculty_pubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/faculty_pubs/310
dc.identifier.contextkey5319122
refterms.dateFOA2022-08-23T15:56:55Z
html.description.abstract<p>BCR-ABL tyrosine kinase inhibitors (TKIs) are effective in controlling Philadelphia-positive (Ph+) chronic myeloid leukemia (CML) are unlikely to cure the disease because TKIs are unable to eradicate leukemia stem cells (LSCs) responsible for the disease relapse even after tyrosine kinase inhibition. In addition, the TKI resistance of LSCs is not associated with the BCR-ABL kinase domain mutations. These observations indicate that TKI-insensitive LSCs and TKI-sensitive leukemic progenitor cells are biologically different, which leads us to believe that LSCs and more differentiated leukemic cells have different genetic mechanisms. Further study of LSCs to identify the novel gene signatures and mechanisms that control the function and molecular phenotype of LSCs is critical. In this mini-review, we will discuss our current understanding of the biology of LSCs and novel genes that could serve as a molecular signature of LSCs in CML. These novel genes could also serve as potential targets for eradicating LSCs in CML.</p>
dc.identifier.submissionpathfaculty_pubs/310
dc.contributor.departmentDepartment of Medicine, Division of Hematology/Oncology
dc.source.pages21


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