Provided are transgenic Caenorhabditis elegans (C. elegans) overexpressing DNA methyltransferase 3a (Dnmt3a) and a method of producing the same. According to the method, a specific mechanism and related factors for DNA methylation mediated by Dnmt3a may be found, and a critical gene for regulating the life span of C. elegans may be identified, and therefore C. elegans may be used as an animal model for screening a drug for a DNA methylation-related disease.

Compositions including recurrent hepatocellular carcinoma (HCC) model generating systems are disclosed. The HCC model generating system contains a CRISPR-Cas expression vector, a transposase expression vector, and a transposon expression vector. Also provided is a non-human animal model of recurrent HCC containing genetic modifications introduced by integration of the model generating system into target liver cells of target animals. Upon stable integration, the model generating system modifies expression of Tp53 and expresses the oncogene in the target liver cells of the target animal, resulting in the development of a HCC tumors in the liver. Methods of using the non-human animal model of recurrent HCC are also provided. The non-human animal model of recurrent HCC can be used for research purposes such as investigating the molecular and genetic mechanisms underlying recurrent HCC tumor development, identifying potential therapeutic targets, and evaluating/screening potential compounds for the treatment of recurrent HCC.

This disclosure provides a rodent model of prostate cancer. The rodents disclosed herein comprise a transgene that provides prostate-specific expression of an oncogenic protein (e.g, an SV40 tumor antigen) under the control of 5 and 3 regulatory regions of a mouse probasin gene. The rodents develop progressive forms of prostate tumor that resemble the development of human prostate cancer.

Non-human animal cancer models are provided herein for identifying and characterizing agents useful for therapy and prophylaxis of cancers, including agents useful for diminishing side effects related to cancer therapies and reducing metastatic disease.

Provided are transgenic Caenorhabditis elegans (C. elegans) overexpressing DNA methyltransferase 3a (Dnmt3a) and a method of producing the same. According to the method, a specific mechanism and related factors for DNA methylation mediated by Dnmt3a may be found, and a critical gene for regulating the life span of C. elegans may be identified, and therefore C. elegans may be used as an animal model for screening a drug for a DNA methylation-related disease.

The present disclosure is directed, in some embodiments, to compositions and methods for inducible modification of a cell genome.

Chimeric transmembrane immunoreceptors (CAR) targeted to PSCA are described.