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Evaluating The Mechanism Of Chemotherapy Essay

896 words - 4 pages

Powerful genotoxic reagents such as Mitoxantrone, Docetaxel, Hydrogen Peroxide, Bleomycin and radiation have been recently investigated in PSC27(Normal Human Prostate Stromal Cell Lines) cell lines and prostate cancer cell lines such as PC-3, LNCaP, DU145, BPH1 and M12 cells. These chemotherapy reagents are ultimately DNA-damaging mechanisms that break hydrogen bonds and DNA strands in DNA. There are great implications associated with the employment of chemotherapy agents. Patients who have prostate cancer are often subjected to one or five of those core treatments. But recent studies have shown that 90% of patients with metastatic carcinomas experience some type of resistance, because these chemotherapy agents essentially induce the overexpression of the WNT16B protein in PSC27 cells that are located in surrounding tumor areas. Once this expression has occurred significantly, it reduces the overall competency of chemotherapy agents and results in its ineffectiveness. This is a huge problem for the patient and those who make these chemotherapy agents. To test for the expression of the WNT16B protein, an RT-PCR (Reverse-Transcription Polymerase Chain Reaction) analysis will be conducted for LNCaP and PC-3 cells treated with Mitozantrone, Docetaxel and Hydrogen peroxide before and after treatment process.

Current research has profoundly indicated that there are negative implications associated with the employment of chemotherapy agents among prostate cancer patients. The recently publish article from 2012, titled “Treatment Induced damage to the tumor microenvironment promotes prostate cancer resistance through WNT16B,” showed a clear analysis of how genotoxic reagents such as Mitoxantrone, Bleomycin, Docetaxel, hydrogen peroxide, and radiation are all core mechanisms in promoting high production of WNT16B protein, when PSC27 (Normal Human Prostate Stromal Cell Lines) cells in surrounding tumor areas are subjected to chemotherapy agents. The rendered chemotherapy agents ultimately damage the DNA of normal prostate cells, eventually causing breaks in hydrogen bonds and DNA strands. The WNT16B protein is artificially induced by chemotherapy agents. The results were statistically important. The study was also conducted in other prostate cancer lines such as PC-3, LNCaP, DU145, BPH1 and M12 cells. When chemotherapy agents were subjected to these cancer lines the production of the WNT16B protein was relatively low. In the article, Yu Sun and his colleagues greatly suggests that the production of this protein is a presented problem because it causes chemotherapy agents to be ineffective in which prostate cancer patients use. The expression of this particular protein leads to later resistance in cancer patients. They also suggested that there was a core discrepancy in the production of WNT16B protein before and after the chemotherapy agents were administered. LNCaP and PC-3...

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