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子宫平滑肌肉瘤的分子研究方法:LMP2基因缺陷小鼠作为自发性子宫平滑肌肉瘤的动物模型

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

作者信息

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

机构信息

Department of Immunology and Infectious Disease, Shinshu University Graduate School of Medicine, 3-1-1, Asahi Matsumoto, Nagano 390-8621, Japan.

出版信息

Sarcoma. 2011;2011:476498. doi: 10.1155/2011/476498. Epub 2011 Mar 8.

Abstract

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.

摘要

子宫平滑肌肉瘤(LMS)在子宫体的肌肉组织层中比在子宫颈中更常发生。妇科肿瘤的发生通常与女性激素分泌相关;然而,子宫LMS的发生与激素状况没有实质性关联,且风险因素尚不清楚。重要的是,区分恶性LMS与良性肿瘤平滑肌瘤(LMA)的诊断生物标志物尚未确立。因此,有必要分析与子宫LMS相关的风险因素,以便建立一种治疗方法。LMP2基因缺陷的小鼠会自发发生子宫LMS,到14月龄时疾病患病率约为40%。我们发现LMP2在人类LMS中不表达,但在人类LMA中表达。因此,LMP2表达缺陷可能是LMS的风险因素之一。LMP2是子宫LMS的一种潜在诊断生物标志物,可能是一种新治疗方法的靶向分子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4cfa/3061316/d58c156f54f4/SRCM2011-476498.001.jpg

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