Retained cell–cell adhesion in serrated neoplastic pathway as opposed to conventional colorectal adenomas.

The molecular features of serrated polyps of colorectum remain to be elucidated. The expression pattern of adhesive molecules (E-cadherin, α-catenin, and β-catenin) has not been examined in serrated neoplastic pathway. The expression of E-cadherin, α-catenin, and β-catenin were analyzed by immunohistochemistry in 32 hyperplastic polyps (HPs), 28 sessile serrated adenomas (SSAs), 37 traditional serrated adenomas (TSAs), 51 traditional adenomas (TAs), and 10 normal colonic tissues (NCs).

Opposite expression patterns of Sonic hedgehog and Indian hedgehog are associated with aberrant methylation status of their promoters in colorectal cancers.

Aims: Activation of the Hedgehog (Hh) signalling pathway in colorectal cancers (CRCs) is controversial, and its regulation mechanism remains to be elucidated. In the present study we attempted to clarify the regulatory mechanism of the expression of Hh ligands during colorectal carcinogenesis.

Methods: Reverse transcriptase polymerase chain reaction and immunohistochemistry were used to characterise expressions of the SHH, IHH and GLI1 genes in 36 CRCs, and the findings compared to 21 hyperplastic polyps and 32 colorectal adenomas.

Regulatory properties of polysaccharopeptide derived from Coriolus versicolor and its combined effect with ciclosporin on the homeostasis of human lymphocytes.

Objectives: Lymphocyte homoeostasis is essential in inflammatory and autoimmune diseases. In search of natural fungal metabolites with effects on lymphocyte homoeostasis, we recently reported that polysaccharopeptide (PSP) from Coriolus versicolor exhibited ciclosporin-like activity in controlling aberrant lymphocyte activation. This object of this study was to investigate its effect on lymphocyte homoeostasis.

Indian hedgehog, a neglected member of hedgehog pathway, may offer a novel avenue for colorectal cancer therapy.

Published data on hedgehog (Hh) pathway activation in colorectal cancer (CRC) are conflicting, and the effect of the Hh pathway inhibitor on the viability of colon cancer cells is controversial. This article focuses attention on the often-neglected, yet likely, critical role of Indian Hh in the course of colonic tumor progression and hypothesizes that upregulation of Indian Hh expression may offer a novel therapeutic approach against CRC through inducing differentiation of tumor cells and through abrogating the Sonic Hh signaling that drives CRC growth.