Abstract
The Mutant Mouse Regional Resource Center (MMRRC) Program serves as the National Institutes of Health (NIH) premier repository of spontaneous and induced mutant mouse lines. The MMRRC Program was established in 1997 through a U01 funding mechanism from the NIH National Center for Research Resources. The purpose of the MMRRC Program is to ensure the continued availability of scientifically valuable, genetically engineered mice and to distribute these mice to qualified researchers studying human and animal biology and disease. The MMRRC Program is made up of a national network of regional breeding and distribution centers, in which UC Davis participates as the West Coast regional Center. The facilities and personnel of the MMRRC regional Centers cryopreserve and distribute mouse strains with potential value in the research of human disease and biology. These strains are then made available for distribution to qualified researchers. Mice are supplied either from a production colony or from a colony recovered from cryopreservation. MMRRC Centers also offer cryopreserved material from some strains for resuscitation at the recipient scientist's institution. The MMRRC at UC Davis is made up from contributions of a number of UC Davis campus resources and units, including the UC Davis Mouse Biology Program, the Center for Comparative Medicine, and the Center for Laboratory Animal Sciences. We provide a host of services in support of the MMRRC Program, including importation of mouse strains by rederivation, cryopreservation and reanimation of frozen embryos and germplasm, assisted reproduction techniques (in vitro fertilization, intracytoplasmic sperm injection, intracytoplasmic nuclear injection), and comprehensive genotyping (including speed congenics) and phenotyping (pathology, behavior, clinical pathology, etc.) capabilities. As part of its participation in the MMRRC Program, the MMRRC at UC Davis provides a comprehensive list of services and procedures to insure safe and expedient importation, maintenance, archiving, genotyping, phenotyping, and distribution of mutant mouse lines. A number of these services and procedures are provided at no charge to the Donating Investigator, while others are offered for a fee to Requesting Investigators. In addition, using the type 3 submission mechanism, a Donating Investigator can negotiate with the MMRRC at UC Davis to perform selected services and procedures on their mouse strain. For more information on the MMRRC National Program, or to donate mice to, or request mice from, the MMRRC please visit the website (www.mmrrc.org) or go to the MMRRC at UC Davis website http://mbp.compmed.ucdavis.edu/modules.php?name=mmrrc.
Highlights
The remarkable generation of scores of increasingly sophisticated mouse models of mammary cancer over the past two decades has provided tremendous insights into molecular derangements that can lead to cancer
We report that somatic mutations of p53 in mouse mammary epithelial cells lead to ERα-positive and ERαnegative tumors. p53 inactivation in pre-pubertal/pubertal mice, but not in adult mice, leads to the development of ERα-positive tumors, suggesting that developmental stages influence the availability of ERα-positive tumor origin cells
Genetic alterations commonly observed in human breast cancer including c-myc amplification and Her2/Neu/erbB2 activation were seen in these mouse tumors
Summary
Transgenic Oncogenesis Group, Laboratory of Cell Regulation and Carcinogenesis, National Cancer Institute, Bethesda, Maryland, USA. The remarkable generation of scores of increasingly sophisticated mouse models of mammary cancer over the past two decades has provided tremendous insights into molecular derangements that can lead to cancer. The relationships of these models to human breast cancer, remain problematic. P53 inactivation in pre-pubertal/pubertal mice, but not in adult mice, leads to the development of ERα-positive tumors, suggesting that developmental stages influence the availability of ERα-positive tumor origin cells. These tumors have a high rate of metastasis that is independent of tumor latency. Since it is feasible to isolate ERα-positive epithelial cells from normal mammary glands and tumors, molecular mechanisms underlying ERα-positive and ERα-negative mammary carcinogenesis can be systematically addressed using this model
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