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Indeed, the mechanisms involved in E2-mediated proliferation are associated with the inhibition of the tumor suppressor protein, p53, which, in turn, generates the downstream activation of cyclin-dependent kinases (CDKs) and, consequently, the release of the retinoblastoma protein (Rb) that promote the progression of the cell cycle by activating diverse transcription factors (Gompel et al., 2004)

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It is administered through small subcutaneous injections