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将p53突变型卵巢移植到野生型雌性宿主中时的肿瘤形成。

Tumor formation in p53 mutant ovaries transplanted into wild-type female hosts.

作者信息

Chen Chun-Ming, Chang Junn-Liang, Behringer Richard R

机构信息

Department of Molecular Genetics, University of Texas, MD Anderson Cancer Center, Houston, TX 77030, USA.

出版信息

Oncogene. 2004 Oct 7;23(46):7722-5. doi: 10.1038/sj.onc.1208037.

Abstract

P53: gene alterations correlate highly with advanced ovarian carcinoma in women. In mice, p53 deficiency predominantly results in the formation of lymphomas and sarcomas. However, ovarian epithelial tumors have not been documented in p53 homozygous mutant (p53-/-) mice, probably because they die before other tumors can form. To determine whether p53-/- ovaries can develop epithelial tumors, they were transplanted into the ovarian bursae of histocompatible wild-type recipient females. The p53-/- ovarian grafts formed tumors approximately 1 year post-transplantation. The tumor type was angiosarcoma, suggesting that vascular tissues are predisposed to tumor formation in p53-/-ovaries. These findings suggest that p53 deficiency alone is not sufficient for ovarian epithelial tumorigenesis in mice. Thus, other genetic lesions are likely required to develop mouse models of human ovarian cancer.

摘要

P53基因改变与女性晚期卵巢癌高度相关。在小鼠中,p53基因缺失主要导致淋巴瘤和肉瘤的形成。然而,在p53纯合突变(p53-/-)小鼠中尚未记录到卵巢上皮肿瘤,这可能是因为它们在其他肿瘤形成之前就死亡了。为了确定p53-/-卵巢是否能发展为上皮肿瘤,将其移植到组织相容性野生型受体雌性小鼠的卵巢囊中。p53-/-卵巢移植物在移植后约1年形成肿瘤。肿瘤类型为血管肉瘤,表明血管组织在p53-/-卵巢中易发生肿瘤形成。这些发现表明,仅p53基因缺失不足以在小鼠中引发卵巢上皮肿瘤发生。因此,可能需要其他基因损伤来建立人类卵巢癌的小鼠模型。

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