Abstract
G2A is a lymphocyte-expressed G protein-coupled receptor whose genetic ablation results in the development of autoimmunity. Using HSV-TK reporter gene directed positron emission tomography (PET), we demonstrate that prior to any indication of the onset of illness, mice transplanted with BCR-ABL transduced G2A-deficient bone marrow harbor expanded populations of leukemic cells compared to recipients of wild-type bone marrow. The target cell type and anatomical locations of leukemia development are indistinguishable in animals transplanted with G2A+/+ or G2A-/- cells. Shorter disease latency in the G2A-deficient background is associated with an increased rate of cellular expansion. PET can be successfully applied to the temporal and spatial analysis of Bcr-Abl driven leukemic progression and should have utility for the study of other leukemias and lymphomas.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Bone Marrow / pathology
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Cell Cycle Proteins / genetics
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Cell Cycle Proteins / metabolism*
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Cell Transformation, Neoplastic
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DNA Primers / chemistry
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Fusion Proteins, bcr-abl / physiology*
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Herpesvirus 1, Human
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Humans
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Leukemia, Experimental / diagnostic imaging*
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Leukemia, Experimental / genetics
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Leukemia, Experimental / metabolism
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Lymphoma / diagnostic imaging*
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Lymphoma / metabolism
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Mice
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Mice, Inbred BALB C
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Mice, Knockout
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Oncogene Proteins / genetics*
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RNA / metabolism
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Receptors, G-Protein-Coupled*
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Retroviridae / genetics
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Reverse Transcriptase Polymerase Chain Reaction
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Sensitivity and Specificity
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Simplexvirus / enzymology
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Simplexvirus / genetics
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Thymidine Kinase / genetics
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Thymidine Kinase / metabolism
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Tomography, Emission-Computed
Substances
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Cell Cycle Proteins
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DNA Primers
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G2A receptor
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Oncogene Proteins
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Receptors, G-Protein-Coupled
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RNA
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Thymidine Kinase
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Fusion Proteins, bcr-abl