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Molecular mechanisms in Murine Syngeneic Leukemia Stem Cells

ABSTRACT: Molecular mechanisms in Murine Syngeneic Leukemia Stem Cells

PROVIDER: PRJNA911837 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22720343.fastq.gz	Fastqsanger.gz
	SRR22720344.fastq.gz	Fastqsanger.gz
	SRR22720345.fastq.gz	Fastqsanger.gz
	SRR22720346.fastq.gz	Fastqsanger.gz
	SRR22720347.fastq.gz	Fastqsanger.gz

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Molecular mechanisms in Murine Syngeneic Leukemia Stem Cells

Project description:Cancer treatments usually gain good response, but some tumors relapse frequently. Acute My-eloid Leukemia (AML) is notorious for its robust relapse. This is attributed to the Leukemic Stem Cells (LSCs). We use a murine syngeneic leukemia model, ML23, in search for possible identifi-cation and study of LSCs in syngeneic settings. Hereby, we present prospective isolation of a de-fined LSC sub-population, encompassing the potency to passage disease from mouse to mouse. We further provide molecular insights of whole transcriptome analysis. Importantly, the ML23 LSC sub-population is expressing therapeutic targeted genes and provides a model for research in immune-competent animals.

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Project description: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+CD9-CD48+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.

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Project description:This study compared gene expression in murine bcr-abl positive acute lymphoblastic leukemia cells in vivo in allogeneic BMT recipients compared to syngneneic BMT recipients. Experiment Overall Design: The goal of the experiment was to compare gene expression in leukemia cells that were in either an allogeneic transplant (5 samples) or syngeneic transplant (5 samples) immune environment in vivo. The bone marrow transplant model involved preparation of C57BL/6 recipients with total body irradiation and 5-fluoruracil. These recipients were then infused IV with either allogeneic C3.SW marrow and spleen cells or syngeneic C57BL/6 marrow and spleen cells. The leukemia cells were mixed in with the marrow and spleen cells. After a few weeks (2-3) the C57BL/6 leukemia cells were purified by flow cytometry and passed into other freshly transplanted animals. After three serial transplants the leukemia cells were flow purified and RNA prepared. Leukemia was C57BL/6 background (cells contain the human p210 bcr/abl oncogenic fusion gene and also have a deletion in the Ink4a/Arf locus, see: Biology of Blood and Marrow Transplantation. 14:622-630, 2008).

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