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A major clinical aim remains the identification and elimination of low-level disease persistence, termed \u201cminimal residual disease\u201d. The phenomenon of disease persistence suggests that despite targeted therapeutic approaches, BCR-ABL-independent mechanisms exist which sustain the survival of leukemic stem cells (LSCs). Although other markers of a primitive CML LSC population have been identified in the preclinical setting, only CD26 appears to offer clinical utility. Here we demonstrate consistent and selective expression of CD93 on a lin\n                    <jats:sup>\u2212<\/jats:sup>\n                    CD34\n                    <jats:sup>+<\/jats:sup>\n                    CD38\n                    <jats:sup>\u2212<\/jats:sup>\n                    CD90\n                    <jats:sup>+<\/jats:sup>\n                    CML LSC population and show in vitro and in vivo data to suggest increased stem cell characteristics, as well as robust engraftment in patient-derived xenograft models in comparison with a CD93\n                    <jats:sup>\u2212<\/jats:sup>\n                    CML stem\/progenitor cell population, which fails to engraft. Through bulk and single-cell analyses of selected stem cell and cell survival-specific genes, we confirmed the quiescent character and demonstrate their persistence in a population of CML patient samples who demonstrate molecular relapse on TKI withdrawal. Taken together, our results identify that CD93 is consistently and selectively expressed on a lin\n                    <jats:sup>\u2212<\/jats:sup>\n                    CD34\n                    <jats:sup>+<\/jats:sup>\n                    CD38\n                    <jats:sup>\u2212<\/jats:sup>\n                    CD90\n                    <jats:sup>+<\/jats:sup>\n                    CML LSC population with stem cell characteristics and may be an important indicator in determining poor TKI responders.\n                  <\/jats:p>","DOI":"10.1038\/s41375-019-0684-5","type":"journal-article","created":{"date-parts":[[2020,1,2]],"date-time":"2020-01-02T09:03:00Z","timestamp":1577955780000},"page":"1613-1625","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":59,"title":["CD93 is expressed on chronic myeloid leukemia stem cells and identifies a quiescent population which persists after tyrosine kinase inhibitor therapy"],"prefix":"10.1038","volume":"34","author":[{"given":"Ross","family":"Kinstrie","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9741-7352","authenticated-orcid":false,"given":"Gillian A.","family":"Horne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heather","family":"Morrison","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Irvine","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chinmay","family":"Munje","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7355-2960","authenticated-orcid":false,"given":"Eduardo G\u00f3mez","family":"Casta\u00f1eda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hothri A.","family":"Moka","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6532-970X","authenticated-orcid":false,"given":"Karen","family":"Dunn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jennifer E.","family":"Cassels","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Narissa","family":"Parry","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cassie J.","family":"Clarke","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary T.","family":"Scott","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard E.","family":"Clark","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tessa L.","family":"Holyoake","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helen","family":"Wheadon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7655-016X","authenticated-orcid":false,"given":"Mhairi","family":"Copland","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,1,2]]},"reference":[{"key":"684_CR1","doi-asserted-by":"publisher","first-page":"2056","DOI":"10.1182\/blood.V94.6.2056","volume":"94","author":"T Holyoake","year":"1999","unstructured":"Holyoake T, Jiang X, Eaves C, Eaves A. 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MC has received research funding from Novartis, Bristol-Myers Squibb, Cyclacel and Ariad\/Incyte is an advisory board member for Bristol-Myers Squibb, Novartis, Incyte and Pfizer and has received honoraria from Astellas, Bristol-Myers Squibb, Novartis, Ariad\/Incyte, Pfizer, Takeda and Celgene. REC, received research funding from Novartis, Bristol-Myers Squibb and Pfizer, was an advisory board member for Novartis, Bristol-Myers Squibb, Jazz pharmaceuticals, Abbvie and Pfizer, and received honoraria from Novartis, Bristol-Myers Squibb, and Pfizer. The other authors declare that they have no conflict of interests.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflict of interest"}}]}}