Real-Time Monitoring of Tumorigenesis, Dissemination, & Drug Response in a Preclinical Model of Lymphangioleiomyomatosis/Tuberous Sclerosis Complex
Identifieur interne : 003F42 ( Main/Exploration ); précédent : 003F41; suivant : 003F43Real-Time Monitoring of Tumorigenesis, Dissemination, & Drug Response in a Preclinical Model of Lymphangioleiomyomatosis/Tuberous Sclerosis Complex
Auteurs : Fangbing Liu [États-Unis] ; Elaine P. Lunsford [États-Unis] ; Jingli Tong [États-Unis] ; Yoshitomo Ashitate [États-Unis] ; Summer L. Gibbs [États-Unis] ; Jane Yu [États-Unis] ; Hak Soo Choi [États-Unis] ; Elizabeth P. Henske [États-Unis] ; John V. Frangioni [États-Unis]Source :
- PLoS ONE [ 1932-6203 ] ; 2012.
Abstract
TSC2-deficient cells can proliferate in the lungs, kidneys, and other organs causing devastating progressive multisystem disorders such as lymphangioleiomyomatosis (LAM) and tuberous sclerosis complex (TSC). Preclinical models utilizing LAM patient-derived cells have been difficult to establish. We developed a novel animal model system to study the molecular mechanisms of TSC/LAM pathogenesis and tumorigenesis and provide a platform for drug testing.
TSC2-deficient human cells, derived from the angiomyolipoma of a LAM patient, were engineered to co-express both sodium-iodide symporter (NIS) and green fluorescent protein (GFP). Cells were inoculated intraparenchymally, intravenously, or intratracheally into athymic NCr
We generated homogeneous NIS/GFP co-expressing TSC2-deficient, patient-derived cells that can proliferate and migrate
Url:
DOI: 10.1371/journal.pone.0038589
PubMed: 22719903
PubMed Central: 3376142
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>TSC2-deficient cells can proliferate in the lungs, kidneys, and other organs causing devastating progressive multisystem disorders such as lymphangioleiomyomatosis (LAM) and tuberous sclerosis complex (TSC). Preclinical models utilizing LAM patient-derived cells have been difficult to establish. We developed a novel animal model system to study the molecular mechanisms of TSC/LAM pathogenesis and tumorigenesis and provide a platform for drug testing.</p>
</sec>
<sec><title>Methods and Findings</title>
<p>TSC2-deficient human cells, derived from the angiomyolipoma of a LAM patient, were engineered to co-express both sodium-iodide symporter (NIS) and green fluorescent protein (GFP). Cells were inoculated intraparenchymally, intravenously, or intratracheally into athymic NCr <italic>nu/nu</italic>
mice and cells were tracked and quantified using single photon emission computed tomography (SPECT) and computed tomography (CT). Surprisingly, TSC2-deficient cells administered intratracheally resulted in rapid dissemination to lymph node basins throughout the body, and histopathological changes in the lung consistent with LAM. Estrogen was found to be permissive for tumor growth and dissemination. Rapamycin inhibited tumor growth, but tumors regrew after the drug treatment was withdrawn.</p>
</sec>
<sec><title>Conclusions</title>
<p>We generated homogeneous NIS/GFP co-expressing TSC2-deficient, patient-derived cells that can proliferate and migrate <italic>in vivo</italic>
after intratracheal instillation. Although the animal model we describe has some limitations, we demonstrate that systemic tumors formed from TSC2-deficient cells can be monitored and quantified noninvasively over time using SPECT/CT, thus providing a much needed model system for <italic>in vivo</italic>
drug testing and mechanistic studies of TSC2-deficient cells and their related clinical syndromes.</p>
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</TEI>
<affiliations><list><country><li>États-Unis</li>
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</record>
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