@article {cite-key,
	title = {Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse.},
	journal = {BMC Cancer},
	volume = {4},
	year = {2004},
	month = {Dec},
	pages = {91},
	address = {Department of Developmental Biology, Howard Hughes Medical Institute, Beckman Center, Stanford University Medical School Stanford, CA 94305, USA. smarino@cmgm.stanford.edu},
	abstract = {BACKGROUND: During pregnancy, the mammary glands from Id2 mutant animals are deficient in lobulo-alveolar development. This failure of development is believed to be due to a proliferation defect. METHODS: We have asked whether functional Id2 expression is necessary for Wnt induced mammary hyperplasia, side branching, and cancer, by generating mice expressing a Wnt1 transgene in an Id2 mutant background. RESULTS: We show in this work that forced expression of Wnt1 in the mammary gland is capable of overcoming the block to proliferation caused by the absence of Id2. We also show that Wnt1 expression is able to cause mammary tumors in an Id2 mutant background. CONCLUSIONS: We conclude that functional Id2 expression is not required for Wnt1 to induce mammary hyperplasia and mammary tumors.},
	issn = {1471-2407 (Electronic); 1471-2407 (Linking)},
	doi = {10.1186/1471-2407-4-91},
	author = {Marino, Susan and Romelfanger, Claire and Yokota, Yoshifumi and Nusse, Roel}
}
