Attempts to stimulate proliferation of the germinal epithelium of the ovary

Stein, Kathryn F.; Allen, E. J.

doi:10.1002/ar.1090820102

Cited by 39 publications

(7 citation statements)

References 16 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ovulation exposes ovarian epithelium to recurrent minor traumas and contact with follicular fluid, may thus, induce inclusions in the surface epithelium, relevant to cancer development. Animal data have shown that ovarian epithelium proliferates rapidly after ovulation and mitotic figures are concentrated near the site of ovulation (80) . The subsequent model based on`ovulatory age' (ie period from starting to cessation of menses minus`protected time' constituted by pregnancies OC use and lactation) is not, however, at least at its present state, satisfactory, perhaps on account of different proportions of ovulatory years at different ages.…”

Section: Discussionmentioning

confidence: 99%

The epidemiology of female genital tract cancers

Parazzini

Franceschi

Vecchia

et al. 1997

Int J Gynecol Cancer

View full text Add to dashboard Cite

Endometrial, ovarian and cervical cancer are among the leading causes of death in women. The role of unopposed estrogens in endometrial carcinogenesis is well established. Any factor that increases the exposure of the endometrium to unopposed estrogen, such as menopausal replacement treatment, obesity, or irregular menstrual cycles tends to raise the risk of the disease, while factors that lower exposure to estrogens or increase progesterone levels, such as oral contraceptives (OC) or smoking, decrease the risk. These well‐established risk factors can have different effects at different ages, particularly in pre‐ and postmenopausal women: more generally, the interaction between various factors is still not totally defined. With reference to ovarian cancer, OC and parity, late menopause and lifelong regular menstrual periods increase the risk of the disease. In terms of biologic mechanisms, these factors are thought to act on ovarian cancer risk by affecting lifetime number of ovulations. Along this line, ‘incessant ovulation’ could be the relevant exposure that defines the incidence of the neoplasm. Among the factors other than reproductive or hormonal, diet is likely to be the most relevant, but it is still. however, poorly quantified. There is now consistent evidence that Human Papillomavirus (HPV) has a causal role in the ethiology of cervical cancer and that sexual habits and reproductive/hormonal factors are associated with the risk of invasive cervical cancer. Less clear is the role of smoking and dietary habits, but recent studies have shown a direct relationship between smoking and the risk of invasive cervical cancer and an inverse one between selected vitamin intake and risk of the disease. In this paper we review and discuss these evidences.

show abstract

Section: Discussionmentioning

confidence: 99%

The epidemiology of female genital tract cancers

Parazzini

Franceschi

Vecchia

et al. 1997

Int J Gynecol Cancer

View full text Add to dashboard Cite

show abstract

“…In biological terms, the association between OCs and risk of ovarian cancer has been interpreted in the context of the "incessant ovulation" theory, according to which ovulatory cycles are the relevant exposure which determines a woman's risk of developing epithelial ovarian cancer (Casagrande et al, 1979). Animal data have shown that ovarian epithelium proliferates rapidly after ovulation and mitotic figures are concentrated near the site of ovulation (Stein and Allen, 1942). Alternatively, the OC-related decrease in the secretion of pituitary gonadotropins [which stimulates the growth of cell lines derived from human ovarian carcinomas (Simon et al, 1983)] per se might explain the negative association between OCs and ovarian cancer risk.…”

Section: Discussionmentioning

confidence: 99%

Pooled analysis of 3 european case‐control studies of epithelial ovarian cancer: III. Oral contraceptive use

Franceschi

Parazzini

Negri

et al. 1991

Intl Journal of Cancer

143

View full text Add to dashboard Cite

The relationship between use of oral contraceptives (OCs) and other contraceptive methods and the risk of ovarian cancer was examined in a combined analysis of 3 hospital-based case-control studies conducted in Italy, the United Kingdom, and Greece, for a total of 971 ovarian cancer cases and 2,258 controls under age 65. Compared with never-users, the combined multivariate relative risk (RR) for ever-users was 0.6 (95% confidence interval, CI = 0.4-0.8) and the estimates were consistent in the 3 datasets. The protection was also similar across strata of age and parity. Considering various measures of OC use, available in the Italian and British datasets only, the protection conveyed on ovarian cancer risk increased with the duration of use and persisted in the medium-long period: the RR in women reporting their last OC use greater than or equal to 15 years prior to diagnosis was 0.5 (95% CI = 0.2-1.0). The risks in ever-users were appreciably lower in those women who reported their first OC use before 25 years of age (RR = 0.3 for first use before age 25, 0.8 for first use at age 25-34 and 0.7 at 35 years or after). Such findings emerged similarly from Italian and British data. This combined analysis, besides offering further quantitative estimates of the protective effects of OCs on ovarian cancer risk in European populations, provides useful insights into the time pattern of the relationship between OC use and ovarian carcinogenesis, suggesting that the protection persists for 15 years or more after cessation of use and may be larger for use at younger age.

show abstract

“…Increased OSE proliferation was also observed in the hilum region of mice and rats after estrogen administration. 70 It was also reported that the extent of OSE proliferation around the ovary was insufficient for post-ovulatory regeneration of OSE in adult mice. 71 Consistent with this observation, it has been proposed that the OSE/mesothelium cells of the hilum might be responsible for providing additional cells for closure of ovulatory wounds.…”

Section: Cancer-prone Stem Cell Nichesmentioning

confidence: 99%

Role of the stem cell niche in the pathogenesis of epithelial ovarian cancers

Flesken‐Nikitin¹,

Odai-Afotey

Nikitin

2014

Molecular & Cellular Oncology

View full text Add to dashboard Cite

Ovarian cancer is the fifth leading cause of cancer-related deaths among women in the United States. Recent extensive genomic analyses of epithelial ovarian cancer (EOC), particularly the most common and deadly form of high-grade serous ovarian carcinoma, have provided important insights into the repertoire of molecular aberrations that are characteristic for this malignancy. However, interpretation of the discovered aberrations is complicated because the origin and mechanisms of progression of EOC remain uncertain. Here, we summarize current views on the cell of origin of EOC and discuss recent findings of a cancer-prone stem cell niche for ovarian surface epithelium, one of the major likely sources of EOC. We also outline future directions and challenges in studying the role of stem cell niches in EOC pathogenesis.

show abstract

Attempts to stimulate proliferation of the germinal epithelium of the ovary

Cited by 39 publications

References 16 publications

The epidemiology of female genital tract cancers

The epidemiology of female genital tract cancers

Pooled analysis of 3 european case‐control studies of epithelial ovarian cancer: III. Oral contraceptive use

Role of the stem cell niche in the pathogenesis of epithelial ovarian cancers

Contact Info

Product

Resources

About