Ovarian follicular steroidogenesis

The major genetic risk factor for ovarian cancer is a mutation in BRCA1 or BRCA2 DNA mismatch repair genes, which is present in 10% of ovarian cancer cases. Only one allele need be mutated to place a person at high risk. The gene can be inherited through either the maternal or paternal line, but has variable penetrance . [16] [19] Though mutations in these genes are usually associated with increased risk of breast cancer, they also carry a substantial lifetime risk of ovarian cancer, a risk that peaks in a person's 40s and 50s. The lowest risk cited is 30% and the highest 60%. [18] [16] [19] Mutations in BRCA1 have a lifetime risk of developing ovarian cancer of 15–45%. [21] Mutations in BRCA2 are less risky than those with BRCA1 , with a lifetime risk of 10% (lowest risk cited) to 40% (highest risk cited). [16] [21] On average, BRCA-associated cancers develop 15 years before their sporadic counterparts, because people who inherit the mutations on one copy of their gene only need one mutation to start the process of carcinogenesis, whereas people with two normal genes would need to acquire two mutations. [19]

Women, who have a high number of dysfunctional follicles to begin with, due to xenobiotic exposure in the womb, will have worse problems if their diets are high in sugary foods and low in nutrition. Since this is exactly the type of diet favored by teens and young women, it's easy to understand why there is so much PCOS in that age group. Fifty years ago, the average person age one pound of sugar a year. Today the average teenager today eats one pound a week! Potato chips, corn chips, pasta and white rice are all highly refined carbohydrates that also act on the body much the same as sugars do.

Ovarian follicular steroidogenesis

ovarian follicular steroidogenesis


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