Int J Colorectal Dis (2010) 25:1231–1242 R Fig. 6 a–l: Series of sagittal sections of a 65-year-old man. a–d RZ, e–h ARZ, i–j ATZ, k–l SZ and PS developmental programme seems to take effect that— according to the findings of Gao et al. [32]—is regulated by Cdx2 in mice. These authors showed that the intestinal growth is severely affected in Cdx2 mutant mice, and that Cdx2 deficiency prevents colon and rectal formation and leads to complete obstruction. New results in mice point to the fact that Cdx2 opposes tumour cell spreading [33]. We have shown that CDX2-positive cells are found in the bottom of healthy human rectal crypts in prenatal stages and in the adult where according to literature they play an important role in the regulation and differentiation of regular intestinal cells [18, 34]. According to our results, we suppose that the typical rectal adenocarcinoma arises from the RZ and may arise from the ARZ, if scattered and regular crypts are found there. However, it does not arise 1241 from the ATZ. Our study reveals the possibility to demarcate and assign epithelial zones within the anorectum by means of immunohistochemistry. We could not deter- mine any difference in CK expression among the different tumour stages. However, studies including a larger number of patients and different stages of rectal cancer as well as carcinomas of the anal squamous epithelium are required to analyze a possible changing in the CK and/or CDX2 expression pattern. Conclusion It is of importance to see that we have a distinct relation between the cell development in human embryos/fetuses and that of tumour cells, and that the knowledge of the regional features and their differentiation stages matters more than their affiliation with the so-called germ layers, Fig. 7 a–d Series of transversal sections through an ultralow rectal adenocarcinoma (pT3, N0, M0, GIII). e–h Series of transverse sections through an anal squamous tumour (pT2, N0, M0, GII)