Register for Somatic mutations in murine mammary cancer mirror human breast features
Breast CancerJuly 20, 2004
2004 JUL 20 - (NewsRx.com & NewsRx.net) -- Somatic mutations in murine mammary cancer mirror human breast features.
According to a study from the United States, "approximately 70% of human breast cancers are estrogen receptor alpha (ERalpha)-positive, but the origins of ERalpha-positive and -negative tumors remain unclear. Hormonal regulation of mammary gland development in mice is similar to that in humans; however, most mouse models produce only ERalpha-negative tumors. In addition, these mouse tumors metastasize at a low rate relative to human breast tumors."
"We report here that somatic mutations of p53 in mouse mammary epithelial cells using the Cre/loxP system leads to ERa-positive and -negative tumors. p53 inactivation under a constitutive active WAPCre(c) in prepubertal/pubertal mice, but not under MMTVCre in adult mice, leads to the development of ERalpha-positive tumors, suggesting that target cells or developmental stages can determine ERalpha status in mammary tumors," according to S.C.J. Lin and colleagues, University of California Irvine, Department of Developmental and Cell Biology.
"Importantly, these tumors have a high rate of metastasis. An inverse relationship between the number of targeted cells and median tumor latency was also observed. Median tumor latency reaches a plateau when targeted cell numbers exceed 20%, implying the existence of saturation kinetics for breast carcinogenesis. Genetic alterations commonly observed in human breast cancer including c-myc amplification and Her2/Neu/erbB2 activation were seen in these mouse tumors."
"Thus, this tumor system reproduces many important features of human breast cancer and provides tools for the study of the origins of ERalpha-positive and -negative breast tumors in mice," researchers suggested.
Lin and colleagues published the results of their research in Cancer Research (Somatic mutation of p53 leads to estrogen receptor alpha-positive and -negative mouse mammary tumors with high frequency of metastasis. Cancer Res, 2004;64(10):3525-3532).
For additional information, contact E.Y.H.P. Lee, University California Irvine, Department Development & Cell Biology, Sprague Hall, Room 140, 839 Hlth Science Court, Irvine, CA 92697 USA.
The publisher of the journal Cancer Research can be contacted at: American Association for Cancer Research, 615 Chestnut St., 17TH Floor, Philadelphia, PA 19106-4404 USA.
The information in this article comes under the major subject areas of Endocrinology, Mutagenesis, and Oncology. This article was prepared by Cancer Weekly editors from staff and other reports. Copyright 2004, Cancer Weekly via NewsRx.com & NewsRx.net.
©Copyright 2004, Cancer Weekly via NewsRx.com & NewsRx.net
