Radiological techniques have improved diagnoses many-fold and therefore are used much more frequently and effectively versus exploratory surgeries, which were the gold standard of diagnosing cancer only a few decades ago. Today, we find cancerous lesions without so much as scratching a patient with Magnetic Resonance Imaging (MRI), Computerized Tomography (CT), and UltraSound imaging (US). We will look at the techniques used, how effective they are at finding many types of the cancer and what the treatments to be determined are once a full diagnoses is given. A brief examination of the pathophysiology and the epidemiology will enhance our understanding and give a full picture of the process of Ovarian Cancer.
Pathophysiology and Epidemiology of those affected by Ovarian Cancer
Ovarian cancer is unique only to women, but the strata of women affected by the several types of ovarian cancer is also fairly unique as well. In the UK, Table 1 taken from the UK
Office for National Statistics (Cancer Statistics: Registrations Series MB1), we find that the rate of ovarian cancer incidence by an Age-Standardised rate is 16.2 per 100,000 women in the UK. Comparatively the US has a dramatically higher rate of 33 per 100,000 while Asian and African rates are well below 5 per 100,000. Only if they move to western Europe or the USA does the risk of ovarian cancer increase among this population. The major link to this variant seems to be related to dietary considerations among other things, however it should be noted that genetics of this disease are very strong which will be why the European and US populations remain statistically more likely to develop this cancer. Further, it should be noted, that if a family member has ovarian cancer or has survived it, the risk for it occurring later in the family is 10% compared with 1.6% in the general population.(Bankhead et al, 2008) Ironically, men who have women in the family with ovarian cancer have increased risk of prostate cancer and should be screened properly by their physician. The cancer itself has a predominant affect on women who are post-menopausal. Table 2 shows the ages affected by ovarian cancer and that the increase in incidence occurs at or around the age of 45-49 when the rate jumps 60% from 11.4 for those 40-44 to over 19. This jump occurs at or around the age of menopause, which suggests that a genetic insult may occur due to a decrease in the amount of hormones being produced by a formerly fertile female. Further similar increases are found as the female population ages. Table 1 Table 2 The pathophysiology of the disease was mentioned earlier concerning BRCA-1. This particular gene is responsible for an increased risk causing 50% of hereditary breast cancers and 80% of hereditary ovarian cancers. It is autosomal dominant in nature and is not located on the X chromosome. BRCA1, located on chromosome 17q12-21, and BRCA2, on 13q12-13 are identified as the loci with associations to further processes which affect genomic integrity and cause a single cell to become cancerous given the proper stimuli. (Green 2011) Genetically, BRCA-1 gene product is involved in DNA repair and transcription regulation. It is said to act as a "caretaker gene" preventing DNA damage from leading to cancer. It complexes with RAD51, a protein involved in the repair of dsDNA breaks. When functioning properly, of course, there are many times a DNA strand