Epidemiology of endometrial cancer

Voigt, Lynda F.; Weiss, Noel S.

doi:10.1007/978-1-4613-0867-6_1

Cited by 13 publications

(10 citation statements)

References 97 publications

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“…[1][2][3], the mechanisms by which estrogens might act to influence the development of this disease remain unclear. One widely accepted hypothesis emphasizes the role of unopposed estrogen in stimulating cellular proliferation (4,5).…”

Section: Introductionmentioning

confidence: 99%

Interindividual Variation in Nucleotide Excision Repair Genes and Risk of Endometrial Cancer

Weiss

Ulrich

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Exposure to estrogens is a likely cause of endometrial cancer, but the means by which estrogens exert this effect are not entirely clear. One hypothesis is that certain estrogen metabolites bind to the DNA, forming bulky adducts that damage the DNA and initiate carcinogenesis. A woman's reduced capacity to repair such damage may increase her risk of endometrial cancer. We conducted a population-based case-control study in western Washington State to address the role of variation in nucleotide excision repair genes on the risk of endometrial cancer. Case women (n = 371), ages 50 to 69 years, were diagnosed with invasive endometrial cancer between 1994 and 1999. Control women (n = 420) were selected using random-digit dialing (ages 50-65 years) and by random selection from Health Care Financing Administration data files (ages 66-69 years). Genotyping assays were done for ERCC1, ERCC2 (XPD), ERCC4 (XPF), ERCC5 (XPG), XPA, and XPC. No appreciable differences between cases and controls were observed in the genotype distributions of ERCC1 (c8092a and c19007t), ERCC2 (D312N, K751Q, and c22541a), ERCC4 (R415Q and t30028c), or ERCC5 (D1104H). Carriage of at least one variant allele for XPA G23A was associated with decreased risk of endometrial cancer [odds ratio (OR), 0.70; 95% confidence interval (95% CI), 0.53-0.93]. Carriage of at least one XPC A499V variant allele was associated with a modest decrease in risk (OR, 0.79; 95% CI, 0.59-1.05). Women with variant alleles at both XPC A499V and K939Q had 58% of the risk of women with no XPC variant alleles (OR, 0.58; 95% CI, 0.35-0.96). Our data suggest that interindividual variation in XPA and XPC influences a woman's risk of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14(11):2524 -30)

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Section: Introductionmentioning

confidence: 99%

Interindividual Variation in Nucleotide Excision Repair Genes and Risk of Endometrial Cancer

Weiss

Ulrich

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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132

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“…However, aspects of the descriptive epidemiology of these neoplasms suggest that uterine leiomyosarcoma, and perhaps other histologic types, might share risk factors with the epithelial malignancies of the endometrium, ovary, or breast (Harlow et al, 1986). Since the incidence of these more common tumors is influenced, to varying degrees, by a woman's menstrual and/or reproductive history (Adami et al, 1990;Greene et al, 1984;Voigt and Weiss, 1989), such characteristics may also play a role in the development of some uterine sarcomas. Two small studies which examined this hypothesis have reported conflicting results (Kvale et al, 1988;Schwartz et al, 1989), and neither was able to examine risks associated with specific histologic types of these malignancies.…”

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Incidence of histologic types of uterine sarcoma in relation to menstrual and reproductive history

Weiss¹,

Daling²,

Newcomb³

et al. 1991

Intl Journal of Cancer

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To determine whether the occurrence of one or more histologic types of uterine sarcoma is related to events in a woman's reproductive life, a population-based case-control study was conducted. One-hundred sixty-seven women newly diagnosed with uterine sarcoma among residents of 6 geographic regions were compared to 208 women selected at random from the same populations with regard to histories of menstruation, pregnancy and childbearing, and breast feeding, as reported during a telephone interview. Compared to women whose menstrual periods began at age 13, women whose menses began earlier were at increased risk of leiomyosarcoma (OR = 2.0, 95% CI 0.9, 4.3); other histologic types were less strongly associated with early age at menarche. Women with leiomyosarcoma and endometrial stromal sarcoma, but not malignant mixed Müllerian tumors, tended to have ceased menstruating 2-3 years later than controls. None of the histologic types was clearly related to parity or to age at first live birth, but each was inversely related to age at last live birth. Associations were observed between leiomyosarcoma and histories of an induced abortion (OR = 4.2, 95% CI 1.2, 14.2) and of breast feeding after a live birth (OR = 0.5, 95% CI 0.3, 1.0); these relationships were not observed for other morphologic variants. These results suggest possible similarities and differences in menstrual and reproductive risk factors among histologic types of uterine sarcoma, and between these malignancies and the more common breast, endometrial and ovarian carcinomas.

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“…Endometrioid and clear cell ovarian tumors, like those of the endometrium (Voigt and Weiss, 1989), may be subject to the influence of estrogens (Weiss et al, 1982;La Vecchia et al, 1982).We were, therefore, encouraged to investigate the association between tubal ligation and endometrial cancer to confirm or refute the findings of Castellsagué et al (1996). The methods used in this study have been described previously (Rosenblatt et al, 1995 (Table II).…”

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Association between tubal ligation and endometrial cancer

Rosenblatt

Thomas

1997

Int. J. Cancer

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Association between tubal ligation and endometrial cancerIn a previous issue of this periodical, Castellsagué et al. (1996) (Rosenblatt et al., 1996). Endometrioid and clear cell ovarian tumors, like those of the endometrium (Voigt and Weiss, 1989), may be subject to the influence of estrogens (Weiss et al., 1982;La Vecchia et al., 1982).We were, therefore, encouraged to investigate the association between tubal ligation and endometrial cancer to confirm or refute the findings of Castellsagué et al. (1996). The methods used in this study have been described previously (Rosenblatt et al., 1995 (Table II).Although tubal ligation appears to affect endogenous hormone levels, the direction of a potential alteration in the estrogen/progesterone ratio has been debated (Corson et al., 1981;Radwanska et al., 1982;Cattanach, 1985). Therefore, it is not clear how tubal ligation would be expected to affect the risk of endometrial cancer.The non-significant and opposite results of these 2 studies are strongly suggestive of the occurrence of random variation due to chance.Yours sincerely,

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Epidemiology of endometrial cancer

Cited by 13 publications

References 97 publications

Interindividual Variation in Nucleotide Excision Repair Genes and Risk of Endometrial Cancer

Interindividual Variation in Nucleotide Excision Repair Genes and Risk of Endometrial Cancer

Incidence of histologic types of uterine sarcoma in relation to menstrual and reproductive history

Association between tubal ligation and endometrial cancer

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