Molecular Mechanisms in Murine Syngeneic Leukemia Stem Cells

Michael Chamo, Omri Koren, Oron Goldstein, Nir Bujanover, Nurit Keinan, Ye’ela Scharff, Roi Gazit

Research output: Contribution to journalArticlepeer-review

Abstract

Acute Myeloid Leukemia (AML) is a severe disease with a very high relapse rate. AML relapse may be attributable to leukemic stem cells (LSC). Notably, the “cancer stem cell” theory, which relates to LSCs, is controversial and criticized due to the technical peculiarities of the xenotransplant of human cells into mice. In this study, we searched for possible LSCs in an immunocompetent synergetic mice model. First, we found phenotypic heterogeneity in the ML23 leukemia line. We prospectively isolated a sub-population using the surface markers cKit+CD9CD48+Mac1−/low, which have the potency to relapse the disease. Importantly, this sub-population can pass in syngeneic hosts and retrieve the heterogeneity of the parental ML23 leukemia line. The LSC sub-population resides in various organs. We present a unique gene expression signature of the LSC in the ML23 model compared to the other sub-populations. Interestingly, the ML23 LSC sub-population expresses therapeutic targeted genes such as CD47 and CD93. Taken together, we present the identification and molecular characterization of LSCs in a syngeneic murine model.

Original languageAmerican English
Article number720
JournalCancers
Volume15
Issue number3
DOIs
StatePublished - 24 Jan 2023

Keywords

  • AML
  • leukemic stem cell
  • syngeneic model

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

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