Research article

Wnt1 is epistatic to Id2 in inducing mammary hyperplasia, ductal side-branching, and tumors in the mouse

Susan Marino¹ , Claire Romelfanger¹ , Yoshifumi Yokota² and Roel Nusse¹

¹  Department of Developmental Biology, Howard Hughes Medical Institute, Beckman Center, Stanford University Medical School Stanford, CA 94305, USA

²  Department of Biochemistry, Fukui Medical University, Shimoaizuki 23-3, Matsuoka, Fukui 910-1193, Japan

author email corresponding author email

BMC Cancer 2004, 4:91doi:10.1186/1471-2407-4-91

Published:	15 December 2004

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.