@article {cite-key,
	title = {Amplification and proviral activation of several Wnt genes during progression and clonal variation of mouse mammary tumors.},
	journal = {Oncogene},
	volume = {7},
	number = {3},
	year = {1992},
	month = {Mar},
	pages = {487{\textendash}492},
	address = {Howard Hughes Medical Institute, Beckman Center, Stanford University, California 94305.},
	abstract = {Mammary tumors in the GR strain are caused by a dominant locus containing an endogenous mouse mammary tumor provirus. Expression of this locus results in high virus titers, inducing tumors that progress from a hormone-dependent to a hormone-independent tumor state. We previously studied the activation of the Wnt-1 and int-2 oncogenes in several series of transplanted GR tumors and found that hormone-dependent early passages are generally oligoclonal for proviral integration at these genes. We have now re-examined several such tumor series for activation of other Wnt genes. In one series, the transition to hormone-independent growth was marked by the loss of the oligoclonal genotype and outgrowth of a hormone-independent cell population, clonal for the activation of Wnt-3. We show two examples of series of transplanted tumors that in later hormone-independent passages contain an amplified and overexpressed Wnt-2 gene, a novel mode of activation of these genes.},
	issn = {0950-9232 (Print); 0950-9232 (Linking)},
	author = {Roelink, H and Wagenaar, E and Nusse, R}
}
