Pathophysiology of Ovarian Cancer
Medical health writers at Paper Masters can custom write a research paper on the pathophysiology of ovarian cancer. Various cancers can be overviewed by our writers and more in-depth research is available on any of the following cancers:
- Colon Cancer
- Lung Cancer
- Breast Cancer
- Prostate Cancer
- Leukemia
- Lymphoma
Ovarian Cancer Pathophysiology
When it comes to the pathophysiology of ovarian cancer, despite over 20 years of research on the subject, medical science has been unable to completely solve the riddle of ovarian cancer pathophysiology. "The etiologic factors involved in the pathogenesis of ovarian cancer, the reason for a lack of a durable response to therapy (both chemotherapy and radiotherapy), and the development of resistance to chemotherapeutic agents are poorly understood". However, what is known about the disease's response to chemotherapy has provided a significant amount of insight into the pathophysiology of ovarian cancer.
The process of ovarian cancer starts when cell aptosis in ovary becomes unregulated. Scientists believe that this is due in part to a gene, bcl-2, located on chromosome 18. Bcl-2 encodes for the protein bcl-2, which is necessary for normal cell growth. "Bcl-2 is unique among the proto-oncogens, as it is localized on the mitochondrial membranes and interferes with programmed cell death independently of its ability to promote cell division". Therefore, the same protein that regulates cell growth is also responsible for impeding cell aptosis.
Although this research represents the most recent findings on the pathophysiology of ovarian cancer, researchers have also found that the incidence of many ovarian cancer cases are directly related to deletions or mutations in the p53 gene. An author in a pathophysiology of ovarian cancer research project notes the following:
Mutations or deletions of the p53 gene currently are the most common known molecular alterations in ovarian cancer. Human cells depend on the p53 gene for repair when injury occurs; the gene activates or represses gene transcription, leading to the expression of specific elements that are necessary for the inhibition of cell growth and the induction of cell repair. The absence of functional p53 thus can lead to abnormal cell growth . Despite over 20 years of research, this is the extent of what medical science knows about the pathophysiology of this disease.