Review Article

Molecular Approach to Uterine Leiomyosarcoma: LMP2-Deficient Mice as an Animal Model of Spontaneous Uterine Leiomyosarcoma

Figure 3

Model of the mechanism for development of uterine leiomyosarcoma. In LMP2-deficient cells, levels of the antioncogenic factor IRF-1, p21WAF are significantly reduced. Reduced expression of the calponin h1 transcript, which contributes to cell proliferation and tumorigenesis in uterine smooth muscle cells, is detected in uterine LMS tissues. Cell cycle regulatory factors, CDK2/Cyclin E, are markedly activated. The inactivation of such antioncogenic factors is considered to transform LMP2-deficient cells into malignant tumor cells.
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