PTGS2 & MSR1

PTGS2:
The very existence of the amplification of this gene attests to the fact that in Esophageal cancer the stress imposed by chemical and traumatic irritants will involve inflammatory pathways and over-expression of Cyclins and growth Factors. Over-expression of COX-2 that this gene amplification represents leads to the formation of prostaglandins which decrease membrane protection by PGH2 and PGI2, with ulceration at the tumor level resulting. When you see an ulcerated cancer in the stomach or at the base of the Esophagus, you understand what happened!
It points to the potential importance of Interferon treatment as an adjunct therapy.

MSR1  (Macrophage Scavanger Receptor 1):
This gene amplification may stop Macrophages from removing irritated and altered cancer cells,. Irritated neoplastic cells often contain HSP (Heat shock proteins) altered proteins that should trigger action by the scavenger.  But Mutation at MRS1 leads to a tolerance of the existence of these neoplastic cells.  The HSP are normally generated by HSPA1A, a gene " located in the major histocompatibility complex class III region, in a cluster with two closely related genes which encode similar proteins."<sup>(wikipedia) 

In a normal cell, HSP will interact with ASK1 (Apoptosis  Signal-Regulating Kinase1)  and trigger independently Apoptosis, or use the same molecule as MAP3K5 to stimulate c-JUN (the stress pathway).  And don't tell me we didn't warn you that, in the pathogenesis of Esophageal cancers, irritants will stimulate C-JUN the stress related family member of the MAP Kinases.  ASK1 interacts with TNF alpha Receptor and a bunch of DNA protein Kinases that will lead to the production of inflammatory factors including the Autoimmune Antigen Ku! 
There you have it, do not be surprised that HSP has much to do with other altered proteins called Amyloids...and you start getting the right idea that Alzheimer's disease is around the corner!  Yes, the tolerance induced by Mutated MSR1 and HSP has something to do with the disposition of Amyloid deposits!</sup>

Hypothesis for Cancer Research: Mucinous Cancer

One of the bad types of gastroenterologic cancers such as Gastric and Colon cancers is the one known as Mucinous Cancer.  Basically, this cancer produces a Mucin assumed to be a viscous liquid surrounding the cell.  This tumor spreads early and deeply. At the time it is found, most of the time, the cancer is in advanced stage.  Researchers have explained this phenomenon by stating that this Mucin contains many ingredients suppressive to immunity (including Cytokines), and soluble Molecules (such as Prostaglandin E2) that may down regulate local immunity against the cancer.  It may also have those metalloproteases that we discussed in our earlier post for research suggestions on Oct, 14, 2012
Prostaglandins in general respond to anti inflammatory agents.
CAN WE MEASURE THE LEVEL OF TISSUE PROSTAGLANDINS IN MUCINOUS CANCERS AS A PREDICTOR OF ANTI-INFLAMMATORY (ASPIRIN) MAINTENANCE THERAPY POST PRIMARY TREATMENT TO DECREASE RATE OF METASTASIS IN COLON AND GASTRIC CANCERS?

CAN ANTI-MUCIN (AFTER WE KNOW THE REAL CONTENT FOR SPECIFIC CANCER TISSUE) PROVIDE AN INCREASE OF ANTIBODY BINDING TO CANCER CELLS?

TREG CELLS are cells involved in tolerance of our own cells.  They work to stop us from killing our own cells.  ARE THEY INCREASED IN CANCERS TO DECREASE CELLULAR IMMUNITY AGAINST CANCERS?

CANCER CELLS SEEMS TO HAVE A SELF GROWTH HORMONE WHICH IS SECRETED IN ITS IMMEDIATE SURROUNDING.  THIS HORMONE ACTS THROUGH RECEPTORS ON THE EXTERNAL MEMBRANE OF THE CELL.  THE PROFILE OF RECEPTORS ON CANCER MEMBRANES IS DEFINITELY DIFFERENT FROM THE NORMAL CELL.  WHY CAN'T WE PRACTICE "PROFILING" BY INVENTORYING ALL THE RECEPTORS (OR CRITICAL RECEPTORS)?
RECEPTORS ARE MADE BY GENES MOSTLY, WE CAN CONTROL THESE THROUGH OUR KNOWLEDGE OF GENETICS.  IF WE KNOW RECEPTORS EXCLUSIVE TO CANCER CELLS,
CAN WE DEVELOP ANTIBODY TO THESE RECEPTORS?