There may be a new, more definitive reason for why people develop oral or esophageal cancer.
New research developed by the University of Pennsylvania School of Medicine shows that a protein that enables cells to stick together is often not present or out of place when a person has oral or esophageal cancer. It’s not certain at this point, however, that the loss of the protein correlates to the presence of tumors.
Cancer in the oral cavity and esophagus affects more than 650,000 people every year.
The investigators made this finding by creating mice that did not have the protein, p120-catenin, in their oral-upper digestive tract. The results were that these mice developed squamous cell cancers.
This study, which was published in the journal Cancer Cell, gives credence to the idea that p120-ctn is involved with suppressing tumors. The tumors the mouse developed mirrored the tumors that generally develop in humans.
When the tissue is healthy, the p120-ctn is part of a larger group of proteins that enable the cells to maintain their position in tightly packed sheets. If the proteins are not present, the following cancers may develop: prostate, breast, colon, pancreas, bladder, skin and endometrial.
When the previous animals that were created did not have the protein, problems arose because they cannot survive during the embryonic process or directly after birth unless they have the protein. The problem was solved by a process known as Cre-Lox, which enables the animals to be created without a certain gene in only a subset of tissues.
The mice were created without p120-ctn in their oral cavity, esophagus and forestomach. After surviving, the mice showed signs of precancerous lesions after about four to six months. By the time they reached nine to 12 months, 70 percent of the animals developed full-blown tumors. To compare, none of the mice born with the protein showed signs of cancer.
This information could be vital in developing new approaches to tumor treatment in humans.