Endometrial cancer.Survey of 610 cases treated at Woman's hospital (1919–1960)

Javert, Carl T.; Renning, Elise L.

doi:10.1002/1097-0142(196308)16:8<1057::aid-cncr2820160813>3.0.co;2-m

Cited by 26 publications

(1 citation statement)

References 7 publications

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“…Substantial epidemiologic data implicate an imbalance of estrogens and progestogens in the etiology of endometrial cancer (Table 1): early menarche (1, 2), late menopause (3,4), anovulation (5,6), prolonged menstruation, obesity (7)(8)(9), polycystic ovary syndrome (10), and diabetes mellitus (11)(12)(13), characteristics or conditions involving a relative increase in exposure to endogenous estrogens, have been associated with an increased risk of the disease. All three prospective studies that have examined hormone levels observed an increase in endometrial cancer risk with increasing circulating levels of estrogen (14)(15)(16).…”

Section: Introductionmentioning

confidence: 99%

Inflammation and Endometrial Cancer: A Hypothesis

Modugno

Ness

Chen

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

229

201

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Endometrial cancer is the most common gynecologic malignancy in the United States. Substantial epidemiologic data implicate an imbalance of estrogens and progestogens in the etiology of this disease. We propose that inflammation also plays a role in endometrial cancer development. Emerging laboratory data suggest that elevated levels of prostaglandin E 2 may underlie the transformation of normal endometrium to neoplastic tissue and that in vitro nonsteroidal anti-inflammatory drugs may inhibit endometrial cancer cell growth. In this review, we suggest that the risk factors for endometrial cancer-unopposed estrogens, anovulation, polycystic ovary syndrome, excessive menstruation, early menarche, and late menopause-may be viewed as factors increasing the exposure of the endometrium to inflammation, whereas pregnancy and smoking, two likely protective factors, have the opposite effect. Chronic inflammation can induce rapid cell division, increasing the possibility for replication error, ineffective DNA repair, and subsequent mutations. A proinflammatory milieu can also directly increase estrogen production. Hence, inflammation may work in conjunction with or in addition to estrogen exposure in the development of endometrial cancer. (Cancer Epidemiol Biomarkers Prev 2005;14 (12):2840 -7)

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Section: Introductionmentioning

confidence: 99%

Inflammation and Endometrial Cancer: A Hypothesis

Modugno

Ness

Chen

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

229

201

View full text Add to dashboard Cite

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Glucose Tolerance and Endometrial Carcinoma

Dunn¹,

Merchant²,

Bradbury³

et al. 1968

Arch Intern Med

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The concept that the triad of diabetes mellitus, obesity, and hypertension is of etiologic and diagnostic significance in endometrial carcinoma was tested in 55 patients with endometrial carcinoma and 114 control patients. Factors which might influence glucose tolerance such as age, parity, obesity, hypertension, family history of diabetes, and anterior pituitary function were evaluated. Both groups consisted of patients who had postmenopausal bleeding and were divided into those with endometrial carcinoma and those with neither endometrial carcinoma nor hyperplasia. Abnormal glucose metabolism and sustained arterial hypertension were no more frequent in patients with endometrial carcinoma than in the controls. There appeared to be no association between increased parity and decreased glucose tolerance nor between the degree of obesity and decreased glucose tolerance. The carcinoma group was significantly more obese and less parous than the control group.The literature dealing with the epidemiology of endometrial carcinoma contains many refer¬ ences to the triad of diabetes mellitus, obesity, and hypertension. It has been postulated that the associ¬ ated triad characteristic of this ma¬ lignancy is of both etiologic and diagnostic significance and that an underlying endocrinopathy is re¬ sponsible not only for the triad but also for the carcinoma itself. A sur¬ vey of the literature, however, es¬ pecially in regard to the frequency of diabetes in patients with endo¬ metrial carcinoma, leads to no clear conclusions (Table 1 and 2). No study has taken into account many of the factors that influence glucose tolerance, such as age, parity, obes¬ ity, hypertension, family history of diabetes, and anterior pituitary func¬ tion. The purpose of this paper is to report observations on these factors and to assess their relationship to glucose tolerance in patients with endometrial carcinoma and in an ap¬ propriately matched control group. Materials and MethodsFifty-five patients with endometrial carcinoma and 114 control patients par¬ ticipated in the study. All were referred to the University of Iowa Hospitals in the years 1963 to 1966. The presence of the malignancy was documented by bi¬ opsy or curettage. No patient received therapy before the endocrine evalua¬ tion. All were patients of the Gynecology Service and participated in a comprehensive investigation of the en¬ docrine factors in endometrial carci¬ noma. This paper represents one phase of the larger study.1 Control Group.-In view of the re¬ ported effects of age, socioeconomic status, obesity, hypertension, and family history of diabetes on glucose tolerance, it is of the utmost importance to have an unbiased control group which is similar to the study group in these fac¬ tors, and yet which is not selected on

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Endometrial adenoacanthoma.A clinicopathological study of 55 cases

Charles

1965

Cancer

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Endometrial cancer.Survey of 610 cases treated at Woman's hospital (1919–1960)

Cited by 26 publications

References 7 publications

Inflammation and Endometrial Cancer: A Hypothesis

Inflammation and Endometrial Cancer: A Hypothesis

Glucose Tolerance and Endometrial Carcinoma

Endometrial adenoacanthoma.A clinicopathological study of 55 cases

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