Ovarian cancer is defined as a condition of abnormal cells growth of ovarian cells as that have become cancerous. It is one of most common cancer in US, according to the statistics adapted from the American Cancer Society's publication, Cancer Facts & Figures 2010, an estimated 21,880 women in the United States will be diagnosed with ovarian cancer and 13,850 deaths.
Ovarian cancer can be divided to the types below
A. Epithelial ovarian Cancer
Epithelial ovarian tumor also known as Surface epithelial-stromal tumor, as the name, it is a result of the cells on the surface of the ovary have become cancerous. Epithelial ovarian tumor is the most common form of ovarian cancer accounted for over 90% of ovarian cancer of all cases, including serous tumor, endometrioid tumor and mucinous cystadenocarcinoma.
B. Germ cell ovarian cancer
C. Sex cord stromal ovarian cancer
Sex cord stromal ovarian tumor is a cancer of the tissue of the ovary accounted for 8% of ovarian cancers. The excess estrogen produced by Sex cord stromal ovarian tumor can lead to certain symptoms, such as adult granulosa cell tumours and thecomas, postmenopausal bleeding, menorrhagia, amenorrhea, endometrial hyperplasia, etc. The cancer tend to develop in older age group.
D. Secondary cancer
Types of food to prevent and treat Ovarian cancer
1. Grapes and berries
Myricetin is a flavonol, belong to the flavonoid in Flavonoids (polyphenols), found in many grapes, berries, etc.. In the research of inverse associations with certain flavonoids or flavonoid subclasses (myricetin, kaempferol, quercetin, luteolin, and apigenin) and ovarian cancer risk, found that In analyses of each individual flavonoid, only intake of apigenin was associated with a borderline significant decrease in risk (RR, highest vs. lowest quintile = 0.79, 95% CI = 0.59-1.06; p-trend = 0.26), and this association was significant after adjustment for intake of the other 4 individual flavonoids (comparable RR = 0.72, 95% CI = 0.53-0.98; p-trend = 0.09), according to "Flavonoid intake and ovarian cancer risk in a population-based case-control study" by Gates MA, Vitonis AF, Tworoger SS, Rosner B, Titus-Ernstoff L, Hankinson SE, Cramer DW.(1)
2. Green tea
a. In prospective cohort study to investigate whether tea consumption can enhance the survival of patients with epithelial ovarian cancer conducted in Hangzhou, China, found that Compared to non-drinkers, the adjusted hazard ratios were 0.55 (95% CI = 0.34-0.90) for tea-drinkers, 0.43 (95% CI = 0.20-0.92) for consuming at least 1 cup of green tea/day, 0.44 (95% CI = 0.22-0.90) for brewing 1 batch or more of green tea/day, 0.40 (95% CI = 0.18-0.90) for consuming more than 500 g of dried tea leaves/year, and 0.38 (95% CI = 0.15-0.97) for consuming at least 2 g of dried tea leaves/batch. The corresponding dose-response relationships were significant (p < 0.05)(2).
b. Other suggested that studies on the health benefits of drinking tea, particularly green tea, are finding exciting results, particularly in cancer research. Modern studies in both Asia and the West have provided encouraging results indicating that drinking green tea contributes to fighting many different kinds of cancers including stomach, oesophageal, ovarian and colon(3).
a. In the study to analyze the impact of sphingosine kinase-1 (SphK-1) inhibition on ceramides production, and evaluated SphK1 inhibitor II (SKI-II) as a potential curcumin chemo-sensitizer in ovarian cancer cells, found that inhibition of SphK1 by SKI-II or by RNA interference (RNAi) knockdown dramatically enhanced curcumin-induced apoptosis and growth inhibition in ovarian cancer cells. SKI-II facilitated curcumin-induced ceramides production, p38 activation and Akt inhibition. Inhibition of p38 by the pharmacological inhibitor (SB 203580), a dominant-negative expression vector, or by RNAi diminished curcumin and SKI-II co-administration-induced ovarian cancer cell apoptosis, and, to restore Akt activation by introducing a constitutively active Akt (CA-Akt), or to inhibit ceramides production by fumonisin B1 also inhibited curcumin plus SKI-II co-administration-induced in vitro anti-ovarian cancer effect(4).
b. Others found that curcumin exhibited time- and dose-dependent cytotoxicity against monolayer cultures of ovarian carcinoma cell lines with differing p53 status (wild-type p53: HEY, OVCA429; mutant p53: OCC1; null p53: SKOV3). In addition, p53 knockdown or p53 inhibition did not diminish curcumin killing of HEY cells, confirming p53-independent cytotoxicity. Curcumin also killed OVCA429, and SKOV3 cells grown as multicellular spheroids(5).
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