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The combination of SS1P with chemotherapy is based on results from in vivo mouse models showing marked synergy between SS1P and chemotherapy [23] [26].
These are the first mouse models showing that IGF-IR or IRS overexpression leads to tumorigenesis in vivo.
Several mouse models showing diminished dendritic arborization do not have reduced brain size (Krey et al., 2013; Hoogenraad et al., 2005; Henkemeyer et al., 2003).
Genetic models of SIRT1 overexpression have provided more clarity with multiple mouse models showing that SIRT1 is protective against mutant huntingtin neurotoxicity.
This is confirmed in mouse models, showing that stimulation of NK cell function protected against NSCLC metastasis [ 11, 12], while depletion enhanced lung cancer metastasis [ 13].
However, most mouse models showing prevention or cure of colitis with Foxp3+ Treg have been conducted in lymphopenic animals, in which homeostatic expansion of Foxp3+ Treg may facilitate their impact on disease.
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Both mouse models show that TLX1 can induce T-ALL.
Since all circadian gene-mutant mouse models show increased sensitivity to γ-radiation, we conclude that the molecular clock functions in tumor suppression in vivo.
However, current humanized mouse models show sub-optimal human T cell reconstitution and limited ability to support immunoglobulin class switching by human B cells.
In vivo primary glioblastoma mouse models show efficacy.
OA cartilage in both humans and mouse models shows increased expression of HIF-2α.
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