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As an organ-specific, chronic inflammation-carcinoma sequence, it is well known that colorectal neoplasia is prone to appear in long-standing ulcerative colitis (UC) (LennardJones et al., 1983). It has been shown that the tumor suppressor gene, p53 mutation, which results from chromosomal instability due to inflammation-driven DNA damage plays an important role in the early stage of tumorigenesis (Hussain et al., 2000; Yoshida et al., 2003; 2006). However, the incidence of p53 mutation is approximately up to 50% in dysplasia and carcinoma lesions in UC, according to our examination with our novel combined method of microdissection and polymerase chain reaction (PCR)-direct sequencing of the full-length p53 gene from single crypts in long-standing UC (Yoshida et al., 2004). Instead, we have shown that mucosal remodeling and stromal genomic instability can be raised as another factor for carcinoma development. In this chapter, we describe the mucosal remodeling and genomic instability of stromal cells as well as epithelial cells, suggesting insufficient cross-talk between epithelium and stroma in longstanding UC.

Mucosal Remodeling and Alteration of Stromal Microenvironment in Ulcerative Colitis as Related to Colorectal Tumorigenesis