Tsc1iDeltaEC Tumor model for lymphangiosarcoma mouse

Loss of Tsc1 can cause hyper-activation of mTORC1 signaling in endothelial cells, which results in the development of lymphatic malformation (LM) and progression to vascular tumors that recapitulate salient features of human lymphangiosarcoma (LAS), including local invasion and systemic metastasis.

Contributors

Institute
University Of Cincinnati
Cat. #: 160865
Cancer types: Sarcoma
Research Fields: Cancer;Drug development
Target: Tsc1/Hamartin
disease: Angiosarcoma
Model: Conditional KO
Zygosity: Homozygous
Strain: C57BL/6
Product description: Angiosarcoma/lymphangiosarcoma is a rare cancer that currently has no effective treatment. The mechanism of angiosarcoma development is largely unknown, and there is no animal model for the disease with molecularly defined pathogenesis. Loss of Tsc1 can cause hyper-activation of mTORC1 signaling in endothelial cells, which results in the development of lymphatic malformation (LM) and progression to vascular tumors that recapitulate salient features of human lymphangiosarcoma (LAS), including local invasion and systemic metastasis.
Conditional: Yes
Production details: Cohorts of Tsc1f/f;Scl-Cre and control littermates mice at 8-10 weeks of age were intraperitoneally injected with tamoxifen for three times (2 mg each time, every other day) to induce activation of Cre recombinase to delete floxed Tsc1 gene in endothelial cells.
References:

Yang et al. 2020. Br J Cancer. 122(12):1791-1802. PMID: 32336756.

Sun et al. 2015. Cancer Cell. 28(6):758-772. PMID: 26777415.

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