An analysis of the utilization of an inoculated C57BL/6 mouse model in studies of Human Papillomavirus and cervical cancer.
Written in 2002; 2,950 words; 9 sources; MLA; $ 87.95
Paper Summary:
This paper takes a close look at cervical cancer including its causes and symptoms. It also examines the role of Human Papillomavirus in inducing cervical cancer. It then proceeds to study the use of inoculated C57BL/6 murine model to study disease in woman. The treatment is analyzed for its accuracy and efficiency.
From the Paper:
"In order to fully understand the genetic link between HPV and high risk for cervical cancer, one must closely examine the mechanism by which HPV induces cervical cancer. HPV is in a class of viruses known as adenoviruses, that is, viruses that invade a host and make some permanent change to the DNA of the infected host cells. In the cases of HPV-16 and HPV-18, the virus produces the oncoproteins E6 and E7, which interact specifically with human cellular components p53 and retinoblastma, respectively. The role of p53 in human cells is to guard DNA repair processes and ensure chromosomal stability, and the degradation of p53 leads directly to mutational changes and ultimately to the immortalization of human cells. The gene controlling transcription of p53 in humans is polymorphic at amino acid 72, containing either a proline or arginine residue at this position (4). The HPV E6 protein degrades p53, thereby inducing cervical cancer. Furthermore, it has been shown that the arginine form of p53 is more easily degraded than the proline form, because E6 can bind more effectively to the arginine form of p53 (6). Consequently, individuals with the arginine variation at amino acid 72 would be much more likely to develop cervical cancer. Because the specific polymorphic combination is conserved between generations, the greater affinity of E6 for p53 would explain the genetic risk factor involved in the progression from HPV infection to full-blown invasive cervical cancer."
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