Ovarian cancer affects over 6500 patients a year, with an overall lifetime risk of 1 in 50 (NICE, April 2011). Risk associated with ovarian cancer development is multifactorial and includes reproductive factors, exogenous hormones, genetics, and lifestyle.

A consistent finding in epidemiological studies is the link between the number of lifetime ovulations and ovarian cancer risk. Pregnancy, breast feeding, and the combined oral contraceptive pill all reduce ovulation and also decrease ovarian cancer risk. For instance, a 40% reduction in cancer risk has been observed following a woman's first full-term pregnancy in a pooled analysis of 12 US-based case–control and cohort studies, with a further 14% risk reduction with each additional pregnancy (Whittemore et al., 1992). Furthermore, early age at first birth confers a protect effect with a 10% risk reduction with each 5 year increment (Watson and Lynch, 2001).

Conversely, repeated ovulation is thought to increase cancer risk. Ovarian biopsies obtained from women undergoing ovarian stimulation infertility treatment displayed a higher rate of ovarian dysplasia when compared to controls (Chene et al., 2012). It has been theorized that through repeated ovulation, a proinflammatory state is created, predisposing malignant change. However, the effect of infertility and infertility treatments on ovarian cancer risk has been widely debated and the long-term effect of ovarian stimulation fertility treatment on cancer risk is still not clear.

The use of the combined oral contraceptive pill has consistently reduced ovarian cancer risk, with a relative risk of 0.64 (95% CI 0.57–0.73) when compared to those never having used the pill (Hankinson et al., 1992). Hormone replacement therapy (HRT) appears to confer a small risk of developing ovarian cancer, although many trials to date have shown only marginal results.

Lifestyle and environmental factors are assumed to play a role in ovarian cancer risk but evidence is currently inconclusive. Diet, smoking, and alcohol have all been implicated in ovarian cancer risk, but epidemiological studies have produced conflicting results to date.

10% of ovarian cancer cases are familial with 90% of these cases due to the mutated high-penetrance breast-ovarian cancer genes, BRCA1/2 (Gayther and Pharoah, 2010). Mismatch DNA repair mutations, MLH1 and MSH2, as seen in HNPCC (Hereditary nonpolyposis colon cancer), are also associated with ovarian cancer (Adami et al., 1994). More recently genome-wide association analyses have identified susceptibility loci including a locus on chromosome 9 (Song et al., 2011).

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Last Updated on: Jul 03, 2024