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nature portfolio permissions reprints research progress privacy policy advertising g1/s-promoting mechanism parallel social media nature med author information authors yan geng & piotr sicinski core cell-cycle machinery mammary gland development nature 369 nature 398 nature 384 nature 411 nature dana-farber cancer institute mmtv/v-ha-ras author correspondence beta-catenin regulates expression pbabe-puro-ras-v12 fsh-responsive gene involved cyclin d1-deficient mice dfci/harvard medical school mmtv/c-myc genes anti-cyclin d1 therapy beta-casein gene expression e2f-dependent signaling pathway personal data springerlink instant access data protection cell-cycle machinery permissions activated neu–ras pathways human breast cancer breast cancer therapy mammary epithelial cells activated c-neu oncogene breast cancer detected cyclin d1 ablation hc11 cell line harvard medical school privacy development situ breast carcinomas gonadal cell proliferation ras signaling pathway cyclin d1 expression p38/hogmapk pathway

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         description:Breast cancer is the most common malignancy among women. Most of these cancers overexpress cyclin D1, a component of the core cell-cycle machinery. We previously generated mice lacking cyclin D1 using gene targeting. Here we report that these cyclin D1-deficient mice are resistant to breast cancers induced by the neu and ras oncogenes. However, animals lacking cyclin D1 remain fully sensitive to other oncogenic pathways of the mammary epithelium, such as those driven by c-myc or Wnt-1. Our analyses revealed that, in mammary epithelial cells, the Neu–Ras pathway is connected to the cell-cycle machinery by cyclin D1, explaining the absolute dependency on cyclin D1 for malignant transformation in this tissue. Our results suggest that an anti-cyclin D1 therapy might be highly specific in treating human breast cancers with activated Neu–Ras pathways.
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