MassIVE MSV000098728

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Overexpression of the signaling-coordinator GAB2 can play an important role in Acute Myeloid Leukemia progression

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Description

Label free quantification (LFQ) proteomics experimental data from a study of murine acute myeloid leukemia (AML) that spontaneously develops in mice with Dnmt3aR878H/+ x Npm1cA/+ bone marrow. These mice spontaneously develop myelomonocytic AML in 6-15 months. We characterized pre-leukemic bone marrow samples, and 11 independent spontaneous AMLs that developed in these doubly-mutant mice ("mAML1-11").10 of 11 AMLs contained an amplification of murine chromosome 7 (chr7), usually as the only structural variant. Furthermore, we identified two non-leukemic mice where whole genome sequencing revealed amplification of chromosome 7 (+7) and no other cooperating mutations in identifiable driver genes (pre-tumor, +7 only). One of these clonal expansions was tested twice in secondary transplant assays, and did not commonly yield fatal disease when transplanted into recipients, suggesting that +7 is an intermediate step in AML progression. Further experiments identified Gab2 as an important gene on chromosome 7 for AML pathogenesis in this model. Retroviral overexpression of Gab2 in Dnmt3aR878H/+ x Npm1cA/+ bone marrow led to expansion of bone marrow cells both in vitro and in vivo in transplanted, recipient mice, as well as to accelerated development of AML; the resulting AML samples are called GAB2 mAML in this dataset. Measurements were performed from bulk bone marrow of mice. Data can be explored further at mAML.leylab.org. Note that data uploaded here were analyzed using the publicly available FragPipe software, with full workflow details available for download. In the JCI publication in press and on the mAML.leylab.org website, data were analyzed as described in the methods section, with expected slight variation in the protein quantification results. The conclusions presented in the publication are supported by both analyses. [doi:10.25345/C52V2CP5F] [dataset license: CC0 1.0 Universal (CC0 1.0)]

Keywords: acute myeloid leukemia ; AML ; DatasetType:Proteomics

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Principal Investigators:
(in alphabetical order) 		Timothy J. Ley, Washington University in St. Louis, United States of America
Submitting User: saimukund
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