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

نویسندگان

  • Takuma Hayashi
  • Akiko Horiuchi
  • Kenji Sano
  • Nobuyoshi Hiraoka
  • Yae Kanai
  • Tanri Shiozawa
  • Susumu Tonegawa
  • Ikuo Konishi
چکیده

The MIT Faculty has made this article openly available. Please share how this access benefits you. Your story matters. License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Uterine leiomyosarcoma (LMS) develops more often in the muscle tissue layer of the uterine body than in the uterine cervix. The development of gynecologic tumors is often correlated with female hormone secretion; however, the development of uterine LMS is not substantially correlated with hormonal conditions, and the risk factors are not yet known. Importantly, a diagnostic-biomarker which distinguishes malignant LMS from benign tumor leiomyoma (LMA) is yet to be established. Accordingly, it is necessary to analyze risk factors associated with uterine LMS, in order to establish a treatment method. LMP2-deficient mice spontaneously develop uterine LMS, with a disease prevalence of ∼40% by 14 months of age. We found LMP2 expression to be absent in human LMS, but present in human LMA. Therefore, defective LMP2 expression may be one of the risk factors for LMS. LMP2 is a potential diagnostic-biomarker for uterine LMS, and may be targeted-molecule for a new therapeutic approach.

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

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تاریخ انتشار 2011