Human 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...Human 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 uterine LMS from benign tumor leiomyoma (LMA), is yet to be established. Accordingly, it is necessary to analyze risk factors associated with uterine LMS, to establish a clinical treatment method. Protea some β-ring subunit LMP2/β1i-deficient mice spontaneously develop uterine LMS, with a disease prevalence of ~40% by 14 months of age. We found LMP2/β1i expression to be absent in human uterine LMS, but present in human LMA. Therefore, defective-LMP2/β1i expression may be one of the risk factors for human uterine LMS. LMP2/β1i is a potential diagnostic-biomarker under the combination of candidate molecules, for instance cyclin B1, cyclin E and calponin h1 and ki-67/MIB1 counts for uterine mesenchymal tumors, especially human uterine LMS, and may be a targeted-molecule for a new therapeutic approach.展开更多
文摘Human 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 uterine LMS from benign tumor leiomyoma (LMA), is yet to be established. Accordingly, it is necessary to analyze risk factors associated with uterine LMS, to establish a clinical treatment method. Protea some β-ring subunit LMP2/β1i-deficient mice spontaneously develop uterine LMS, with a disease prevalence of ~40% by 14 months of age. We found LMP2/β1i expression to be absent in human uterine LMS, but present in human LMA. Therefore, defective-LMP2/β1i expression may be one of the risk factors for human uterine LMS. LMP2/β1i is a potential diagnostic-biomarker under the combination of candidate molecules, for instance cyclin B1, cyclin E and calponin h1 and ki-67/MIB1 counts for uterine mesenchymal tumors, especially human uterine LMS, and may be a targeted-molecule for a new therapeutic approach.
