Histological and biochemical analyses of tenascin in various human tumors have indicated that tenascin is expressed in various cancer stroma and increased in the serum, getting strong with advancement of its malignancy. Of interest, the prognostic analysis of breast and colon cancers revealed favorable survival and no lymphogenous metastasis in patients whose cancer expressed tenascin strongly. Injection of tenascin nonproducing A431 human epidermoid cancer cells into nude mice resulted in tenascin production by these cells, suggesting cancer cells can make tenascin if necessary. Thus, both carcinoma and adjacent stroma cells may produce tenascin to coordinate the microenvironment surrounding the cancer tissues. Several tenascin variants have been clearly demonstrated to date. With these findings in mind, we would propose that epithelial tenascin supports the carcinoma cell outgrowth, whereas stromal tenascin may block cancer invasion by covering the cancer nest. No obvious phenotype in tenascin gene knockout mice would indicate that tenascin is functionally redundant in developmental processes, yet it may well be very important in progression of cancer.