Endometrial and ovarian cancers coexist in approximately 5 % of patients with endometrial cancer and 10 % of cases of ovarian cancer [2]. Synchronous cancers are usually seen in younger premenopausal women usually associated with obesity and nulliparity. They usually have early-stage disease and hence have better prognosis than those with metastatic disease. In endometrial cancer patients less than 45 years, the incidence of synchronous ovarian cancer is higher [3–5]. The median age reported in various series ranges from 41 to 52 years, about a decade younger than median ages for development of endometrial or ovarian cancer alone. Walsh et al. reported a high rate of coexisting malignancy of 25 % in a study of 102 patients of less than 45 years with endometrial carcinoma. Women who are 9–22 kg above their ideal body weight have a threefold increased risk for developing endometrial cancer, and women more than 22 kg above their ideal body weight have a ninefold increased risk [6]. Obese women have excess peripheral conversion of androstenedione to estrone in adipose tissue. This hyperestrogenic state results in endometrial proliferation which may lead to development of endometrial cancer. Other conditions which produce hyperestrogenic state like polycystic ovarian disease, chronic anovulation, unopposed estrogen replacement therapy, and estrogen-producing ovarian tumors also increase their risk of endometrial cancer and synchronous ovarian cancers. Eifel et al. similarly found that 50 % of the women in their study with synchronous endometrioid tumors were nulliparous [7]. Herrinton et al. found that women with synchronous endometrial and ovarian cancers had a lower than expected mean parity compared with women with only one of these cancers [8].

Family history of Lynch II syndrome (hereditary nonpolyposis colorectal cancer) is also associated with synchronous endometrial and ovarian cancers. HNPCC is an autosomal dominant familial cancer risk syndrome that occurs due to a germ line mutation in one of several mismatch repair genes and is associated with an increased risk of colorectal, endometrial, and ovarian cancer. The diagnosis of HNPCC is made when the following three Amsterdam criteria are met: [1] at least three relatives with histologically verified HNPCC-related cancers (colorectal, endometrial, ovarian, gastric, hepatobiliary, small bowel, or transitional cell cancer of the renal pelvis or ureter), one of them a first-degree relative of the other two (familial adenomatous polyposis excluded), [2] at least two successive generations affected, and [3] in one of the individuals, the diagnosis of cancer is made before the age of 50 [9].

There are many postulations on the simultaneous occurrence of two cancers at two anatomical locations. One of the theories suggests that when tissues of same embryonic origin are subjected to hormonal exposure or to carcinogens, they develop synchronous malignancies [10]. The presence of estrogen receptors in these tissues indicate a hormonal field effect which could lead to the development of simultaneous cancers in the endometrium and ovary. Eifel et al. also suggested that the response of the uterine corpus, fallopian tubes, and ovarian epithelium as a morphologic unit could explain the development of synchronous endometrioid tumors in different components of the Müllerian system [5]. The theory of a secondary Müllerian system says that the epithelium of cervix, uterus, fallopian tubes, ovaries, and peritoneal surface have shared molecular receptors responding to carcinogenic stimulus leading to the development of multiple primary malignancies synchronously [8]. They further describe that the hypothesis provides an explanation for synchronous malignancies of similar histology. The epithelial linings of the endometrium, ovaries, and peritoneum have molecular receptors (the so-called secondary Müllerian system) responding to the same carcinogenic stimulus and therefore development of synchronous primary tumors [11–13]. However, this can only explain synchronous tumors of similar histology and not dissimilar types. Future studies are needed to further evaluate the role of estrogen in these synchronous endometrioid cancers of the endometrium and ovary.

It is very important to differentiate synchronous tumors from metastatic tumors. Synchronous tumors involving the ovary and endometrium are both early-stage cancers, have favorable outcome, and do not mandate aggressive adjuvant treatment. On the other hand, metastatic tumors are of advanced stage and need aggressive postoperative treatment in the form of radiotherapy or chemotherapy.

About 5 % of women with endometrial adenocarcinoma of endometrioid type have synchronous ovarian carcinoma. It is usually possible for the pathologists to distinguish between synchronous and metastatic cancers. If the pathological examination of the uterus shows low-grade endometrial cancers confined to the endometrium or with superficial myometrial infiltration and no lymphovascular infiltration, the coexisting adnexal tumor is most probably synchronous cancer. In the presence of high-grade endometrial tumor and lymphovascular invasion, the ovarian mass is usually metastatic disease. If pathological examination of ovaries shows features of borderline or low-grade cancer with associated endometriosis, this indicates synchronous cancer. Metastatic ovarian cancers are usually bilateral with multinodular pattern, vascular invasion, and tubal lumen involvement.

The first attempt to distinguish synchronous cancers from metastatic cancers was by Ulbright and Roth in 1985 [14]. They used pathological features like similar histology, grade, myometrial infiltration, vascular involvement, and tubal lumen involvement. This was later on modified by Scully et al. including clinical and pathological features which are now accepted by pathologists to differentiate synchronous from metastatic cancers.