Intestinal GUCY2C prevents TGF-β secretion coordinating desmoplasia and hyperproliferation in colorectal cancer.

Tumorigenesis is a multistep process that reflects intimate reciprocal interactions between epithelia and underlying stroma. However, tumor-initiating mechanisms coordinating transformation of both epithelial and stromal components are not defined. In humans and mice, initiation of colorectal cancer is universally associated with loss of guanylin and uroguanylin, the endogenous ligands for the tumor suppressor guanylyl cyclase C (GUCY2C), disrupting a network of homeostatic mechanisms along the crypt-surface axis.

Perioperative management of a patient with a nonresectable pheochromocytoma.

Objective: To describe the clinical course of a patient with a nonresectable pheochromocytoma during urgent hip surgery.

Methods: To describe the clinical management and postoperative outcome of the patient and review the relevant literature.

Results: An 85-year-old male with a nonresectable pheochromocytoma required urgent hip surgery following a traumatic hip fracture.

Phenyl groups versus tert-butyl groups as solubilizing substituents for some [5]phenacenes and [7]phenacenes.

In recent years, we have used the photocyclizations of diarylethylenes to synthesize a number of [n]phenacenes in the hope that they might be useful as the bridging groups for electron transfer processes in donor-bridge-acceptor molecules. Because [n]phenacenes with n > 5 are very insoluble, their synthesis and characterization has required the attachment of solubilizing substituents such as tert-butyl. The studies of Pascal and co-workers of some large polynuclear aromatic compounds having multiple phenyl substituents prompted us to explore the use of phenyls as alternative solubilizing groups for [n]phenacenes.

The hormone receptor GUCY2C suppresses intestinal tumor formation by inhibiting AKT signaling.

Background & Aims: GUCY2C is the intestinal receptor for the paracrine hormones guanylin and uroguanylin that converts guanosine-5'-triphosphate to cyclic guanosine monophosphate (cGMP). It functions as a tumor suppressor; its loss disrupts intestinal homeostasis and promotes tumorigenesis. We investigated the effects of GUCY2C loss on intestinal cell proliferation, metabolism, signaling, and tumorigenesis in mice.

Overexpression of matrix metalloproteinase 9 in tumor epithelial cells correlates with colorectal cancer metastasis.

Colorectal cancer mortality largely reflects metastasis, the spread of the disease to distant organs. Matrix metalloproteinase 9 (MMP-9) is a key regulator of metastasis and a target for anticancer strategies in colon cancer. Here, the overexpression of MMP-9 in pure tumor epithelial, but nor stromal, cell populations was associated with metastatic progression of colorectal cancer, as defined by reverse transcriptase-polymerase chain reaction (qRT-PCR) and confirmed by immunostaining.