Dataset Information


Gene expression profiling in pre-leukemic hematopoietic stem cells carrying both NrasG12D/+ and Tet2+/- mutations

ABSTRACT: By using a genetically accurate mouse model, we demonstrate that endogenous expression of oncogenic N-RasG12D and Tet2 haploinsufficiency collaborate to accelerate CMML development in mice. Gene expression was compared across all genotypes (WT, Tet2+/-, NrasG12D/+ and double mutants) in bone marrow-derived hematopoietic stem cells (CD150+CD48-Lin-Sca1+cKit+) using RNA-seq. N-RasG12D and Tet2 haploinsufficiency cooperate to induce both unique and overlapping effects on HSC gene expression programs. Overall design: Gene expression profiling in FACS-sorted SLAM HSCs from 10-12 week old wild type control (n=3), NrasG12D/+ single mutant (n=3), Tet2+/- single mutant (n=3) and NrasG12D/+;Tet2+/- double mutant (n=3) mice.

INSTRUMENT(S): Illumina HiSeq 2500 (Mus musculus)

ORGANISM(S): Mus musculus  


PROVIDER: GSE97640 | GEO | 2018-06-22


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Oncogenic N-Ras and Tet2 haploinsufficiency collaborate to dysregulate hematopoietic stem and progenitor cells.

Jin Xi X   Qin Tingting T   Zhao Meiling M   Bailey Nathanael N   Liu Lu L   Yang Kevin K   Ng Victor V   Higashimoto Tomoyasu T   Coolon Rosemary R   Ney Gina G   Figueroa Maria E ME   Li Qing Q  

Blood advances 20180601 11

Concurrent genetic lesions exist in a majority of patients with hematologic malignancies. Among these, somatic mutations that activate RAS oncogenes and inactivate the epigenetic modifier ten-eleven translocation 2 (TET2) frequently co-occur in human chronic myelomonocytic leukemias (CMMLs) and acute myeloid leukemias, suggesting a cooperativity in malignant transformation. To test this, we applied a conditional murine model that endogenously expressed oncogenic NrasG12D and monoallelic loss of  ...[more]

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