ArticleThe American journal of pathology2002
Acceleration of mouse mammary tumor virus-induced murine mammary tumorigenesis by a p53 172H transgene: influence of FVB background on tumor latency and identification of novel sites of proviral insertion.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Identification and Analysis of Three Hub Prognostic Genes Related to Osteosarcoma Metastasis.Journal of oncology · 2021Article
- Article
- Analysis of tumor heterogeneity and cancer gene networks using deep sequencing of MMTV-induced mouse mammary tumors.PloS one · 2013Article
- Integrin-associated CD151 drives ErbB2-evoked mammary tumor onset and metastasis.Neoplasia (New York, N.Y.) · 2012Article
- Novel common integration sites targeted by mouse mammary tumor virus insertion in mammary tumors have oncogenic activity.PloS one · 2011Article
- Animal models of breast cancer for the study of pathogenesis and therapeutic insights.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2009Review
- Article
- Common integration sites for MMTV in viral induced mouse mammary tumors.Journal of mammary gland biology and neoplasia · 2008Review
- Deciphering the molecular basis of breast cancer metastasis with mouse models.Reviews in endocrine & metabolic disorders · 2007Review
- Rorgamma (Rorc) is a common integration site in type B leukemogenic virus-induced T-cell lymphomas.Journal of virology · 2004Article
- Genes involved in breast cancer progression: analysis of global changes in gene expression or retroviral tagging?The American journal of pathology · 2002Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
We previously showed that a mammary-specific dominant-negative p53 transgene (WAP-p53(172H)) could accelerate ErbB2-induced mammary tumorigenesis in mice, but was not tumorigenic on its own. To identify other genes that cooperate with WAP-p53(172H) in tumorigenesis, we performed mouse mammary tumor virus (MMTV) proviral mutagenesis. We derived F1, N2, and N4/N5 mice from p53(172H) transgenic FVB mice backcrossed onto MMTV+ C3H/He mice. Results show the latency of MMTV tumorigenesis is correlated with FVB contribution. F1 tumors had the shortest latency (217 days), had a higher rate of metastasis, and were less differentiated than the N2 and N4/N5 tumors. The latency was 269 days in N2 mice, and lengthened to 346 days in N4/N5 mice. p53(172H) significantly accelerated MMTV tumorigenesis only in N2 mice, indicating cooperativity between p53(172H) and MMTV in this cohort. To identify genes that may be causally involved in MMTV-induced mammary tumorigenesis, we identified 60 sites of proviral insertion in the N2 tumors. Among the insertions in p53(172H) transgenic tumors were 10 genes not previously found as sites of MMTV insertion including genes involved in signaling (Pdgfra, Pde1b, Cnk1), cell adhesion (Cd44), angiogenesis (Galgt1), and transcriptional regulation (Olig1, Olig2, and Uncx4.1). These may represent cellular functions that are likely not deregulated by mutation in p53.
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