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For example, a combination of TGF- inhibitors with PI3K/Akt pathway inhibitors could reduce myofibroblast activation and ECM production while also diminishing the survival and proliferation of this fibrotic effector cell

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Crizotinib induced apoptosis and greatly decreased the tumor burden in a patient derived xenograft in vivo model

This is the core reason telomerase upregulation is such a central target in aging research: if you can keep telomerase active, you can theoretically delay the point at which cells stop dividing

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