<span>Field of the invention: The present invention pertains to the identification and characterization of a nucleic acid sequence of the human involucrin gene which targets expression of any desired nucleic acid sequence to specific tissues and specific cells. In particular, this invention relates to nucleic acid sequences which target expression of nucleic acid sequences to suprabasal cells in stratifying squamous epithelial tissue and to uroepithelial cells. In another aspect, this invention pertains to transgenic animals which exhibit certain cancers and hyperplasias. In yet another aspect, this invention pertains to methods of screening for therapeutics for epithelial neoplasia. Background of the invention: Diseases of epithelial cells are the single most common cause of morbidity and mortality of humans. Foremost among these diseases is cancer. Other diseases which are epithelial in origin include, for example, blistering disease (e.g., epidermolytic hyperkeratosis, and Dowling-Meara disease) proliferative disease (e.g., psoriasis, epidermal lysis, and Bulosa simplex) and Ichthyosis disease (e.g. Ichthyosis bullosa Simens, and recessive X-linked ichthyosis). The location of the epithelium as the lining of tissue surfaces in the body places it at a particularly high risk for repeated damage from a variety of agents in the environment. For example, most of the prevalent epithelial cancers (e.g., cancer of the lung, breast, colon, liver, cervix, etc.) are associated with exposure to </span><span>carcinogens such as cigarette smoke, hydrocarbons in grilled foods, toxic molds, and infection with genital DNA tumor viruses. The evaluation of candidate therapeutics directed at the treatment of epithelial disease has traditionally focused on animal models in which the animal is repeatedly exposed to one or a combination of chemicals. For example, models for cancer development and treatment rely on administration of carcinogenic and co-carcinogenic compounds. However, one drawback to such a model is that animals treated with chemicals exhibit a multitude of genetic and metabolic alterations. The multiplicity of genetic and metabolic changes makes it difficult to determine which of this multitude of changes is causally related to the resulting disease state, and hence makes it also difficult, if not impossible, to identify candidate therapeutics which target only relevant genetic and/or metabolic lesions. The further problems of unpredictability and variability of genetic and metabolic changes in response to chemical treatment make such animals poor models for the evaluation of therapeutics. More recently, trangenic animals which harbor known genetic alterations and which express epithelial disease have been used. In particular, transgenic animal models which develop cancer and in which selected genes are expressed in epithelial cells in general (e.g., U.S. Pat. No. 5,550,316; Griep et al. (1994) Proc. Soc. Exp. Biol. Med. 206:24-34; Kondoh et al. (1995)http://www.google.com/patents?vid=USPAT6313373</span>

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