"Incessant Ovulation" and Ovarian Cancer

Casagrande, John T.; Pike, Malcolm C.; Ross, Ronald K.; Louie, E.W.; Roy, Subir; Henderson, Brian E.

doi:10.1016/s0140-6736(79)91435-1

Cited by 435 publications

(202 citation statements)

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“…Early menarche is associated with a more rapid onset of ovulatory cycles, and with the tendency to sustain higher levels of luteal phase estradiol and progesterone (Vihko and Apter, 1984). Thus, a protective effect of late menarche, observed here in premenopausal women, is consistent with hypotheses regarding incessant ovulation (Fathalla, 1971;Casagrande et al, 1979) and ovarian inflammation (Ness and Cottreau, 1999), but inconsistent with the hypothesis that higher levels of progesterone are associated with reduced risk (Risch, 1998). Similar to most previous reports (for example, Hartge et al, 1988;Chen et al, 1992), we found no evidence of an association between age at natural menopause and ovarian cancer risk.…”

Section: Discussionsupporting

confidence: 86%

“…Our findings are considered in light of several current hypotheses regarding ovarian cancer pathogenesis. Briefly, the incessant ovulation hypothesis suggests that risk is increased by chronic post-ovulatory trauma to the epithelial surface of the ovary, and the tendency to form inclusion cysts (Fathalla, 1971;Casagrande et al, 1979). The gonadotrophin hypothesis proposes that excessive gonadotropin secretion and consequent increases in oestrogen stimulation lead to proliferation and malignant transformation of ovarian epithelium .…”

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confidence: 99%

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Menstrual and reproductive factors in relation to ovarian cancer risk

et al. 2001

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The reduced risk of epithelial ovarian cancer associated with parity and oral contraceptive use suggests that pituitary and/or ovarian hormones or ovulatory events are important in the aetiology of these tumours (Cramer, 1986). Nevertheless, despite extensive study, the influence of menstrual and reproductive factors, with the exception of parity, remains uncertain. In this report, we evaluate menstrual and reproductive characteristics in relation to ovarian cancer risk overall, and in relation to the major tumour histologic subtypes. Our findings are considered in light of several current hypotheses regarding ovarian cancer pathogenesis. Briefly, the incessant ovulation hypothesis suggests that risk is increased by chronic post-ovulatory trauma to the epithelial surface of the ovary, and the tendency to form inclusion cysts (Fathalla, 1971;Casagrande et al, 1979). The gonadotrophin hypothesis proposes that excessive gonadotropin secretion and consequent increases in oestrogen stimulation lead to proliferation and malignant transformation of ovarian epithelium . More recent hypotheses have suggested a role for chronic ovarian inflammation (Ness, 1999), androgens and progesterone (Risch, 1998), and the possibility that pregnancies reduce risk by clearing transforming cells from the ovaries (ovarian clearance) (Adami et al, 1994). METHODSWe conducted a population-based, case-control study of epithelial ovarian cancer in eastern Massachusetts (MA) and New Hampshire (NH). The methods used have been previously described Harlow et al, 1998). Briefly, 1033 potentially eligible case women (ages 20 to 74) were ascertained between May 1992 and March 1997 through state-wide cancer registries (NH, MA) and hospital tumour boards (MA). After exclusion of patients who had nonepithelial tumours (n = 52), and those who had died (n = 91), moved out of state (n = 27), had no telephone (n = 24), or did not speak English (n = 14), 825 case women were eligible for the study. Physicians denied permission to contact 126 (14%) of these women, and 136 (16%) of women declined to participate. This analysis is based on 563 cases of epithelial ovarian cancer, including lesions of borderline malignancy.Control women were identified primarily by random digit dialing (RDD) (Waksberg, 1978), and matched to case women by age (within 4 years) and telephone sampling unit. Of approximately 5400 residential households contacted, 10% declined to provide a household census, and 80% provided a census, but lacked a potentially eligible control subject. In the remaining 10% of households, a potentially eligible control was identified. 72% of the potential control women agreed to participate in the study. In MA, control women of age 60 or older were randomly chosen from Town Books, and matched to case women by age and precinct. Of 328 control women selected from Town Books, 21% Summary We assessed menstrual and reproductive factors in relation to ovarian cancer risk in a large, population-based, case-control study. 563 cases in Massachusetts and New Hampsh...

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Section: Discussionsupporting

confidence: 86%

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confidence: 99%

Menstrual and reproductive factors in relation to ovarian cancer risk

et al. 2001

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“…(2,(46)(47)(48)(49)(50). Although the mechanism responsible for this protective effect is not fully understood, the findings are supportive of the "incessant ovulation" hypothesis which states that the ovarian epithelium is subject to genetic damage during the wound and repair processes associated with ovulation (5).…”

Section: Discussionsupporting

confidence: 60%

“…OVAC risk correlates with the number of ovulatory cycles in a woman's lifetime, whereas factors associated with decreased ovulation, such as increased parity, breast feeding, and oral contraceptive use, have a protective effect (2-4). These observations have led to the "incessant ovulation" hypothesis which purports that repeated cycles of epithelial disruption and repair may facilitate neoplastic transformation of the ovarian epithelium in susceptible individuals and that the risk of OVAC may be proportional to the number of ovulatory cycles in a woman's lifetime (5). Repeated cycles of rupture and repair of the ovarian epithelium associated with ovulation may predispose the ovarian epithelium to DNA damage, inclusion cyst formation, and dysplastic changes which can lead to neoplastic transformation.…”

Section: Introductionmentioning

confidence: 99%

Reduction of Ovarian and Oviductal Cancers in Calorie-Restricted Laying Chickens

Carver

Barnes

Anderson

et al. 2011

Cancer Prevention Research

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Epithelial ovarian cancer (OVAC) remains a highly lethal malignancy. It is a leading cause of cancer deaths among women in the United States causing more deaths than all other gynecologic malignancies combined. The pathogenesis of OVAC is not completely understood, but the process of repeated ovulation is believed to lead to genetic damage in the ovarian epithelium. As part of a prospective trial designed to evaluate OVAC chemopreventive strategies using the chicken model, caloric restriction (55% less energy) was used to inhibit ovulation in groups of hens receiving chemopreventives, thereby minimizing the impact of ovulation on the incidence of reproductive tract cancer. A separate group of chickens was maintained concurrently in the same environment, and managed similarly, except that caloric intake was not restricted. Among birds not receiving chemopreventive agents, we compared caloric versus noncaloric restricted birds to determine the relations between calorie restriction and risk of developing adenocarcinoma of the reproductive tract. Mortality in the calorie-restricted group was almost half that of those on full feed. Calorie-restricted chickens maintained body weights averaging 1.423 kg compared with the full-fed birds at 1.892 kg. Ovulation rate varied with the full-fed group producing 64% more eggs than the calorierestricted group. Total reproductive cancers occurred in 57 (33.3%) birds for the full-fed group and 26 (10.3%) birds for the calorie-restricted group. On the basis of histopathology, 45 (26.3%) birds in the fullfed group had ovarian adenocarcinoma compared with 16 (6.3%) birds in the calorie-restricted group. Calorie restriction in laying hens resulted in a near five-fold reduction in OVAC. Cancer Prev Res; 4(4); 562-7. Ó2011 AACR.

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“…13,14 The risk of ovarian cancer is reduced by use of oral contraceptive pills, the number of live births, and long-term breastfeeding, promoting the hypothesis that suppression of ovulation protects against ovarian malignancy. 15,16 In support of this belief, several investiga- [17][18][19] Under this hypothesis, repeated cellular damage to the ovarian epithelium leads to aberrant DNA repair, the inactivation of tumor suppressor genes, and other events that increase the potential for malignant transformation. 20 Alternatively, the pituitary gonadotropin hypothesis suggests that persistent stimulation of entrapped surface epithelium (inclusion cysts), formed during ovulation in adult women by estrogen or its precursors in the presence of high levels of luteinizing and follicle-stimulating hormones, leads to ovarian carcinogenesis.…”

Section: Epidemiology Of Ovarian Cancermentioning

confidence: 96%

Descriptive epidemiology of ovarian cancer in the United States, 1992-1997

Goodman

Howe

2003

Cancer

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Ͼ 30 demographic and clinical variables. The unprecedented size of the file, which includes information for Ͼ 653,000 cases submitted from registries meeting national standards of high data quality, provides extensive opportunities for research on cancer incidence patterns that would not otherwise be possible. This supplement represents one area of research produced from this resource. A description of the NAACCR file data elements can be found in the Table 1. No additional data collection or pathology verification were conducted. Purpose of the SupplementOvarian cancer is relatively uncommon, and therefore to our knowledge little has been published concerning racial or ethnic variations in ovarian cancer incidence or mortality. As the U.S. population becomes more diverse, the interest in health problems and disparities in outcomes among minority and economically disadvantaged groups increases. To address this issue, NAACCR received funding from the Centers for Disease Control and Prevention to conduct a descriptive study of ovarian cancer. NAACCR formed a research group from interested representatives of organization members (the Ovarian Cancer Research Group). The group analyzed race-related and ethnicity-related variations in ovarian cancer incidence and outcome. In this supplement, we focus on epidemiology, pathology and classification issues, multiple primary tumors, staging, and incidence and mortality for race/ethnic groups. We also focused on epidemiologic differences between borderline tumors of low malignant potential and carcinomas because borderline tumors will no longer be reportable in 2003. TrendsIn most parts of Europe and North America, the incidence of ovarian cancer was constant during the decades prior to the 1990s.1 A significant increase in ovarian cancer death rates among white women in the U.S. was observed in the 1980s. 2 Both incidence and death rates from ovarian cancer among black women reportedly remained level from 1973-1997. 3 Among white women, ovarian cancer incidence rates were reported to have declined from 1973-1981, increased from 1981-1991, and then reversed again to significantly decline from 1991-1997. 3 Ovarian cancer death rates were stable before 1976, declined from 1976 -1980, leveled off from 1980 -1994, and declined nonsignificantly through 1997. 3 A focus on recent trends between 1992 and 1998 revealed a significant decline in incidence rates of 1.4% per year for all races combined, as well as significant annual declines in white women and Hispanic women. 4 Death rates during the same period (1992)(1993)(1994)(1995)(1996)(1997)(1998)) also demonstrated significant declines of 1.2% per year for all races combined, as well as significant annual declines in white women (-1.1% per year) and Asian/Pacific Islander women (-4.1% per year). Nonsignificant downward trends in death rates also were observed for black, American Indian, and Hispanic women. 4 Epidemiology of Ovarian CancerThe lifetime risk of ovarian cancer is reported to be 1.7%5 and approximately 23,40...

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"Incessant Ovulation" and Ovarian Cancer

Cited by 435 publications

References 16 publications

Menstrual and reproductive factors in relation to ovarian cancer risk

Menstrual and reproductive factors in relation to ovarian cancer risk

Reduction of Ovarian and Oviductal Cancers in Calorie-Restricted Laying Chickens

Descriptive epidemiology of ovarian cancer in the United States, 1992-1997

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