SMAD4 is localized to chromosome 18q21, a frequent site for loss of heterozygosity in
advanced stage colon cancers. Although Smad4 is regarded as a signaling mediator of the …

The intestinal epithelium–the cell wall that separates the intestinal tract from the rest of the
body–is constantly renewed by intestinal stem cells that divide continuously. This process is …

Aims To determine whether expression of Smad4, a tumour suppressor found to be absent
in 10% of colorectal cancer (CRC), is associated with outcomes in patients with CRC …

Background: Epithelial cells affected by somatic mutations undergo transition from a tumour-
suppressive to a carcinogenic Smad pathway during sporadic colorectal carcinogenesis …

Extensive genomic analysis of patient samples has identified genes whose mutation or loss
map malignant progression from Barrett's metaplasia, through low-(CDKN2A) and high …

Purpose: We previously reported that loss of SMAD4 promotes chemokine CCL15
expression to recruit CCR1+ myeloid cells via the CCL15–CCR1 axis, which facilitates …

Objective Chromosomal loss within the region of 18q and loss of SMAD4 expression have
been reported to be frequent somatic events during colorectal cancer tumour progression; …

Colorectal cancer progression is intrinsically linked to stepwise deregulation of the intestinal
differentiation trajectory. In this process, sequential mutations of APC, KRAS, TP53, and …

PURPOSE Based largely on in vitro inve stigations and animal studies, investigators believe
that disruptions of transforming growth factor-β (TGF-β) signaling contribute to the …

Upregulation of Smad7, an inhibitor of transforming growth factor-β1 (TGF-β1), occurs in
sporadic colorectal cancer (CRC) and knockdown of Smad7 inhibits CRC cell growth, a …