Endometrial cancers are age dependent. The risk of developing endometrial cancers increases with advancing age. The peak of occurrence is between 55 and 70 years of age and the average age is 61 years. More than 90 % of the patients are over the age of 50. Only 5 % or less develops before the age of 40 [3]. A woman under the age of 40 has 1 in 1423 chances of developing the disease but a woman older than 70 has a risk of 1 in 81 [9].

Race, as stated before, White women are more likely to be afflicted as compared to African, Asian, Hispanic, Chinese or Japanese women. In general, incidence is higher in North America, Australia and Europe than in South Asia, Central America and Africa. But once the women from other regions start living in the United States, the incidence of acquiring the disease increases as compared to those who choose to remain in the country of their origin. However, once the disease occurs, morbidity and mortality rates in Afro-American women are more than in White and Asian women [1].

Obese women have a higher risk of endometrial carcinomas. Nearly 70 % of the patients are obese women. With increase in BMI, the risk of getting the disease and concurrent morbidity and mortality also increase [17]. With a BMI of >30 kg/m2, the risk is 3 times and it becomes 4 times with BMI of >32 kg/m2. A BMI of >35 kg/m2 will increase the risk of developing endometrial carcinomas to 6 times as compared to a woman of BMI 23 kg/m2 [1, 12]. An abrupt increase in weight gain, especially during early adulthood, is also predictive of increased risk. Upper body obesity is also a risk factor independent of body weight. Both obesity and distribution of adipose tissue accumulated during adult life increase the risk of endometrial carcinoma substantially. In addition morbidly obese women have highest risk of cancer-related deaths [1, 17]. As compared to other cancers, the relative risk of obesity-related deaths is highest in endometrial cancers [6].

Obesity increases endogenous oestrogen by peripheral conversion of androstenedione to oestrogen by aromatase in adipose tissues. This increases the endometrial exposure to endogenous oestrogen and decreases serum sex-binding globulins, thereby leading to hyperoestrogenic state [1, 6].

A diet high in carbohydrates and high glycaemic index influences insulin secretion and insulin-like growth factors, which may exert relevant effects on obesity and diabetes mellitus. Both of these are important risk factors for endometrial carcinoma [7]. Food rich in fat and red meat significantly increases the risk [6].

Diabetes mellitus is an independent risk factor, and an increased incidence of type II diabetes mellitus is noted in patients of endometrial cancers since many years [1]. There is also a strong relationship between increased insulin resistance and endometrial cancer. An obese, diabetic menopausal woman has 2–3 times more risk of developing endometrial cancer [3].

Hypertension is often associated with obesity and hence also termed a risk factor [3]. The presence of a triad of obesity, diabetes and hypertension in a woman increases the risk of endometrial cancer and is commonly termed corpus cancer syndrome.

Parity has a positive association with the risk of development of endometrial cancer. Nulliparous women are 2–3 times more at risk than parous women. The observed beneficial effects of pregnancies may be related to a strong exposure to progesterone during pregnancies [8]. Moreover, childbearing at an older age is associated with a lower risk. According to a study, women who give birth at age 40 or even more have 44 % less chances of disease when compared to women who had their last childbirth at age 25. The reduced risk persists for many years [4, 9].

Infertility, which may be a manifestation of nulliparity, has a three- to fivefold increase in the risk for disease as compared to fertile women although treatment for infertility may alter the woman’s cancer risk [1].

Menstrual history also plays a role in risk development. The extremes of spectrum, i.e. early menarche (11–12 years) and late menopause (more than 50 years), have both been associated with increased risk [1]. The longer the menstruation span, the greater is the risk. The increase in menstruation span may be related to an accumulation of PTEN or p53 mutation [5].

Most of the risk factors are associated with exposure to excessive oestrogen (hyperoestrogenic states). The initial cases of endometrial carcinoma were reported relating to oestrogen replacement therapy (ERT) without concomitant progesterone. ERT increased the risk 4.5–8 times [3]. The risk which persisted for many years even after the treatment was stopped. In addition the risk increased with longer duration and higher dosages of oestrogen. A single year of unopposed oestrogen use increased the risk by 40 % of baseline [1].

Oestrogen-producing tumours were first reported by Schroeder in 1992 to be related to endometrial cancers. Since then, a large number of patients (6–12 %) with oestrogen-producing tumours have been found to have developed endometrial carcinoma [1].

Polycystic ovary syndrome is also related with risk of endometrial carcinoma. Elevated endogenous oestrogen levels along with certain comorbidities prevalent in PCOS like obesity, insulin resistance, type II diabetes mellitus and hypertension lead to an increase in the risk. Chronic anovulation leading to proliferative endometrial pathologies, polyps, hyperplasia and unopposed oestrogen exposure all cause an increase in the risk of development of endometrial carcinoma [11].

Hereditary nonpolyposis colorectal cancer (HNPCC) or Lynch syndrome is an inherited autosomal dominant disease in which women are at a risk of more than one primary cancer of colon, rectum, ovaries, small intestine, renal pelvis or endometrial cancer developing in their lifetime. Thirty-nine percent of these women may develop endometrial carcinoma by the age of 70 [1, 3].

A strong association has been found between endometrial cancer and BRCA mutation gene carriers. But it is difficult to differentiate whether there is an increased susceptibility on account of BRCA mutation or a consequence of tamoxifen usage in BRCA carriers with a history of breast carcinoma. Since 1985 multiple authors have confirmed the relation between endometrial carcinoma and the duration and use of tamoxifen. As the benefits of tamoxifen to breast cancer patients outweigh the risk of endometrial cancer, a high index of suspicion and close monitoring is warranted in tamoxifen users complaining of abnormal uterine bleeding [10].