Abstract

of this work is that the number of ‘‘passenger mutations’’ greatly Recent advances in cancer therapeutics stress the need for a exceeds the number of ‘‘driver mutations.’’ Consequently, more better understanding of the molecular mechanisms driving sequencing will be required to gain a comprehensive view of the tumor formation. This can be accomplished by obtaining a human cancer genome. This is especially true given the relatively more complete description of the genes that contribute to low mutation rate of most cancer genes within a patient cancer. We previously described an approach using the population (1). Sleeping Beauty (SB) transposon system to model hematopoi- We recently described a novel transposon-based insertional etic malignancies in mice. Here, we describe modifications of mutagenesis system, called Sleeping Beauty (SB), which can be used the SB system that provide additional flexibility in generating as a cancer gene discovery tool in mice (5, 6). Our initial version of mouse models of cancer. First, we describe a Cre-inducible LsL the SB system consisted of the RosaSBase knock-in allele (trans- SBase allele, RosaSBase , that allows the restriction of posase source) and the T2/Onc2 allele (transposon source). A transposon mutagenesis to a specific tissue of interest. This