Please use this identifier to cite or link to this item: https://doi.org/10.3324/haematol.2018.189928
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dc.titleASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion
dc.contributor.authorMadan, V.
dc.contributor.authorHan, L.
dc.contributor.authorHattori, N.
dc.contributor.authorWoon Teoh, W.
dc.contributor.authorMayakonda, A.
dc.contributor.authorSun, Q.-Y.
dc.contributor.authorDing, L.-W.
dc.contributor.authorMohd Nordin, H.B.
dc.contributor.authorLim, S.L.
dc.contributor.authorShyamsunder, P.
dc.contributor.authorDakle, P.
dc.contributor.authorSundaresan, J.
dc.contributor.authorDoan, N.B.
dc.contributor.authorSanada, M.
dc.contributor.authorSato-Otsubo, A.
dc.contributor.authorMeggendorfer, M.
dc.contributor.authorYang, H.
dc.contributor.authorSaid, J.W.
dc.contributor.authorOgawa, S.
dc.contributor.authorHaferlach, T.
dc.contributor.authorLiang, D.-C.
dc.contributor.authorShih, L.-Y.
dc.contributor.authorNakamaki, T.
dc.contributor.authorWang, Q.T.
dc.contributor.authorKoeffler, H.P.
dc.date.accessioned2021-12-16T07:54:31Z
dc.date.available2021-12-16T07:54:31Z
dc.date.issued2018
dc.identifier.citationMadan, V., Han, L., Hattori, N., Woon Teoh, W., Mayakonda, A., Sun, Q.-Y., Ding, L.-W., Mohd Nordin, H.B., Lim, S.L., Shyamsunder, P., Dakle, P., Sundaresan, J., Doan, N.B., Sanada, M., Sato-Otsubo, A., Meggendorfer, M., Yang, H., Said, J.W., Ogawa, S., Haferlach, T., Liang, D.-C., Shih, L.-Y., Nakamaki, T., Wang, Q.T., Koeffler, H.P. (2018). ASXL2 regulates hematopoiesis in mice and its deficiency promotes myeloid expansion. Haematologica 103 (12) : 1980-1990. ScholarBank@NUS Repository. https://doi.org/10.3324/haematol.2018.189928
dc.identifier.issn03906078
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/210856
dc.description.abstractChromosomal translocation t(8;21)(q22;q22) which leads to the generation of oncogenic RUNX1-RUNX1T1 (AML1-ETO) fusion is observed in approximately 10% of acute myelogenous leukemia (AML). To identify somatic mutations that co-operate with t(8;21)-driven leukemia, we performed whole and targeted exome sequencing of an Asian cohort at diagnosis and relapse. We identified high frequency of truncating alterations in ASXL2 along with recurrent mutations of KIT, TET2, MGA, FLT3, and DHX15 in this subtype of AML. To investigate in depth the role of ASXL2 in normal hematopoiesis, we utilized a mouse model of ASXL2 deficiency. Loss of ASXL2 caused progressive hematopoietic defects characterized by myeloid hyperplasia, splenomegaly, extramedullary hematopoiesis, and poor reconstitution ability in transplantation models. Parallel analyses of young and >1-year old Asxl2-deficient mice revealed age-dependent perturbations affecting, not only myeloid and erythroid differentiation, but also maturation of lymphoid cells. Overall, these findings establish a critical role for ASXL2 in maintaining steady state hematopoiesis, and provide insights into how its loss primes the expansion of myeloid cells. © 2018 Ferrata Storti Foundation.
dc.publisherFerrata Storti Foundation
dc.rightsAttribution-NonCommercial 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by-nc/4.0/
dc.sourceScopus OA2018
dc.typeArticle
dc.contributor.departmentCANCER SCIENCE INSTITUTE OF SINGAPORE
dc.contributor.departmentMEDICINE
dc.contributor.departmentDUKE-NUS MEDICAL SCHOOL
dc.description.doi10.3324/haematol.2018.189928
dc.description.sourcetitleHaematologica
dc.description.volume103
dc.description.issue12
dc.description.page1980-1990
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