Biological and genetic properties of the p53 null preneoplastic mammary epithelium

被引:81
作者
Medina, D
Kittrell, FS
Shepard, A
Stephens, LC
Jiang, C
Lu, JX
Allred, DC
McCarthy, M
Ullrich, RL
机构
[1] Baylor Coll Med, Dept Cellular & Mol Biol, Houston, TX 77030 USA
[2] Univ Texas, MD Anderson Canc Ctr, Dept Vet Med & Surg, Houston, TX 77030 USA
[3] AMC Canc Res Ctr, Denver, CO USA
[4] Baylor Coll Med, Breast Ctr, Houston, TX 77030 USA
[5] Univ Texas, Med Branch, Dept Microbiol, Galveston, TX 77550 USA
[6] Colorado State Univ, Dept Radiol Hlth Sci, Ft Collins, CO 80523 USA
关键词
mammary; premalignant; p53; null; immortal; model;
D O I
10.1096/fj.01-0885fje
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The absence of the tumor suppressor gene p53 confers an increased tumorigenic risk for mammary epithelial cells. In this report, we describe the biological and genetic properties of the p53 null preneoplastic mouse mammary epithelium in a p53 wild-type environment. Mammary epithelium from p53 null mice was transplanted serially into the cleared mammary fat pads of p53 wild-type BALB/c female to develop stable outgrowth lines. The outgrowth lines were transplanted for 10 generations. The outgrowths were ductal in morphology and progressed through ductal hyperplasia and ductal carcinoma in situ before invasive cancer. The preneoplastic outgrowth lines were immortal and exhibited activated telomerase activity. They are estrogen and progesterone receptor-positive, and aneuploid, and had various levels of tumorigenic potential. The biological and genetic properties of these lines are distinct from those found in most hyperplastic alveolar outgrowth lines, the form of mammary preneoplasia occurring in most traditional models of murine mammary tumorigenesis. These results indicate that the preneoplastic cell populations found in this genetically engineered model are similar in biological properties to a subset of precurser lesions found in human breast cancer and provide a unique model to identify secondary events critical for tumorigenicity and invasiveness.
引用
收藏
页码:881 / +
页数:26
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