It is believed that the decreased levels of a protein named p120 catenin, can help in order to prevent the formation of tumor, may elaborate why a few patients basically occur the resistance to the epidermal growth factor receptor targeted cancer therapy.
According to an early-stage study, held at the Penn State University College of Medicine demonstrated that cells with high epidermal growth factor receptor levels single handedly were responsive to the therapy, but patients with the increased epidermal growth factor receptor levels and decreased level of p120 catenin quickly developed the resistance. The EGFR gene encodes a transmembrane protein, which has an absolutely crucial role in order to the division of cells as well as survival. Mutations in the EGFR are responsible for the overexpression of protein and out of controlled cell division. This process is directly associated with numerous cancers including lung cancer, anal cancers and glioblastoma, among several others. The gefitinib was developed in order to target the abnormal epidermal growth factor receptor expression, it was approved in the year of 2003. From then to now minimum 4 more medications in this family have been developed such as erlotinib and afatinib. Although epidermal growth factor receptor targeting therapies are useful in about 75% of patients, many developed resistance as well as relapse within the initial year of treatment. Approximately 70% of reasons for relapses are known, and can be because of the epidermal growth factor receptor mutations, or blocking of the cell pathways required for the protein in order to act precisely. However, 30 percent of cases are not accounted for. According to Stairs, a Penn State Cancer Institute researcher, "Alluding scientists are the still some reasons for resistance". "A few factors have indicated that the excess EGFR and less p120 catenin is mainly responsible for causing the cancer". "Apart from this, less p120 catenin protein is also responsible in order to cause resistance to the therapies of EGFR,” He added. On behalf of Journal PLoS ONE, Stairs and team cultured genetically-engineered esophageal cancer cells prior to treating them with the EGFR targeted medication named gefitinib. Single cell lines carried normal levels of epidermal growth factor receptor as well as p120 catenin, one had increased epidermal growth factor receptor, one increased p120 catenin, and one increased epidermal growth factor receptor and decreased p120 catenin. Of the couple of groups of cells with increased epidermal growth factor receptor, those with the normal levels of p120 catenin died as if the therapy was effective. But, the cells in the group with increased epidermal growth factor receptor and decreased p120 catenin resisted treatment with the drug named gefitinib 250 mg. All these outcomes are promising, but still at an initial stage. Scientists are going to look at cells from the patients with epidermal growth factor receptor positive cancers, resistant to the therapies to research the working of protein named p120 catenin. They also need to determine whether this resistance develops across all medications targeting epidermal growth factor receptor cancers. According to the words of Stairs, "It is crucial to find out how the p120 catenin loss is responsible in order to cause this resistance. “It is also necessary to find out if in case any patient with excess epidermal growth factor receptor (EGFR) in their samples also should be tested for the p120 catenin levels. In order to do so, it may be helpful to know who is at the risk for resistance to EGFR-targeting therapies or relapse, "He added.
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