Receptor Identified That May Inhibit Crohns Disease Symptoms

A team of researchers from the U. K. Sweden and Ireland has identified a receptor in the human gut that could offer a novel way to control the development of gastric cancer a common type of stomach cancer in experimental models. In their paper published in the journal Proceedings of the National Academy of Sciences the group describes their study of Gastrointestinal Tumors in Experimental Models and what they learned from them.

Gastrointestinal cancer is a cancer caused by an invasion of cells that are nourished by the stomachs natural chemicals. Often very early in the development of a patient cancer cells either grow into large tumors or escape into the bloodstream causing inflammation within the body. In the latter case surgical treatments such as bypassing aortic aneurysm openings or implantation of a catheter to restore blood flow to organs causing it serves to prevent further cancer from developing. Studies carried out by researchers at Sahlgrenska Academy in Sweden and St. Olavska Academy in Finland have shown that genetic mutations in two subtypes of gastric cancer-PTSD6 and PTSD8-promote certain tumor types to cause an aggressive development and progression. While such mutations may be prevented in experimental models they may most often occur in adults under circumstances of stress in which case they pose a risk to severe obesity. Much has been done in the hope of relieving this risk by modifying the cells which are joined by the Wnt signaling pathway.

To date the scientific community has not been able to identify the neural factors that allow for a reduction in the potential of increased demand on the brain areas affected by the signal. A recent finding led by Alexandra Tobin of the Department of Clinical Sciences Radboud University Nijmegen and colleagues it focused on a specific brain region called the somatosensory cortex which is known to play a role in facial processing. This particular somatosensory cortex has high volume and is necessary for many functions such as tracking the bladder and for guiding different parts of the body.

Tobin and colleagues used a PET scan to study the somatosensory cortex of 3 experimental models all of which had a mutation in a gene in the PTSD6 subtype. This disease mutation causes impaired production of a protein called lac1 that can inactivate more of the signal needed for the development of gastric cancer. From the variants in each model they identified a gene called FOXF1 as a candidate for possible regulatory cells to target for treatment in future experiments. The researchers note that combining the use of PET scan and genetic approach in the case of programmed cell death makes it possible to explore why mutations in this molecular subtype of the cancer can be of limited relevance just as mutations in other cancers do.

The team also notes that the strange outcome observed in experimental models was a result of a severe neurodevelopmental deficit that compensated for the mutant FOXF1 gene in all but one of the experimental mice. In their penultimate paper the team describes how well this work has inhibited the morphological features of mice that exposed a combination of temporarily deficient vs. normal levels of FOXF1. The team concludes by suggesting that this discovery could be used to explore therapeutic options against gastric cancer in humans.

Research Abstracts: The gut is the largest organ of the body containing around 200 trillion pounds in mass. A special function is to offer a healthy nourishment for the organism. Recent research has begun to show that gut microbiota levels of vitamins B and C iron and specific proteins. Proteomic analysis of bacteria from patients with severe alcoholism and so-called acute alcoholic hepatitis has revealed large differences between group. Food-related bacteria were found to be reduced in patients with gastric cancer. FoxF1 patients displayed enhanced protein turnover and survival rate compared to the control groups. The modified genes of FOXF1 patients exhibited more cell proliferation and maintenance improved function decreased tissue damage and reduced pancreatic damage. By combined gene targeting approach FOXF1-deficient mice exhibited low IPD8 expression were well tolerated and survived highly aggressive Western-type (HT-Zola vesicle injection). All dominant mutations of FOXF1 affected neurons and buffered pyroptosis.

Full research abstracts available online.