Selected work.

Selected Publications

• 2026

  Human haematopoietic stem cells remember inflammatory stress.

  Zeng AGX, Nagree MS, Jakobsen NA, Shah S, Varesi A, Kang JRW, et al. Dick JE, Xie SZ.

  Nature, 655(8122), 458–467 · DOI

• 2026

  ATP2B1 expression identifies human hematopoietic stem cells with superior repopulation and self-renewal.

  Varesi A, Nagree MS, Di Biasio I, Zeng AGX, Shah S, Zhang M, et al. Dick JE, Xie SZ.

  Proc Natl Acad Sci USA, 123(19), e2604380123 · DOI

• 2025

  Metformin reduces the competitive advantage of Dnmt3a^R878H HSPCs.

  Hosseini M, Voisin V, Chegini A, Varesi A, Cathelin S, Ayyathan DM, et al. Xie SZ, Trowbridge JJ, Chan SM.

  Nature, 642(8067), 421–430 · DOI

• 2024

  Selective advantage of mutant stem cells in human clonal hematopoiesis is associated with attenuated response to inflammation and aging.

  Jakobsen NA, Turkalj S, Zeng AGX, Stoilova B, Metzner M, Rahmig S, et al. Dick JE, Xie SZ, Vyas P.

  Cell Stem Cell, 31(8), 1127–1144.e17 · DOI

• 2021

  TFEB-mediated endolysosomal activity controls human hematopoietic stem cell fate.

  García-Prat L, Kaufmann KB, Schneiter F, Voisin V, Murison A, Chen J, et al. Xie SZ*, Dick JE*. (*co-senior authors)

  Cell Stem Cell, 28(10), 1838–1850.e10 · DOI

• 2021

  Sphingosine-1-phosphate receptor 3 potentiates inflammatory programs in normal and leukemia stem cells to promote differentiation.

  Xie SZ, Kaufmann KB, Wang W, Chan-Seng-Yue M, Gan OI, Laurenti E, et al. Dick JE.

  Blood Cancer Discovery, 2(1), 32–53 · DOI

• 2019

  Sphingolipid modulation activates proteostasis programs to govern human hematopoietic stem cell self-renewal.

  Xie SZ, García-Prat L, Voisin V, Ferrari R, Gan OI, Wagenblast E, et al. Dick JE.

  Cell Stem Cell, 25(5), 639–653.e7 · DOI

• 2015

  CDK6 levels regulate quiescence exit in human hematopoietic stem cells.

  Laurenti E, Frelin C, Xie S, Ferrari R, Dunant CF, Zandi S, et al. Dick JE.

  Cell Stem Cell, 16(3), 302–313 · DOI

For a complete list of publications, please visit our Google Scholar profile.