19

Uterine neoplasia

Introduction

The uterus consists of both the cervix and the body (or ‘corpus’ of the uterus). For many reasons, however, including their causative factors and their treatment, tumours arising from the corpus and the cervix are usually regarded as originating from two separate organs. This chapter will consider cancers arising from the uterine body; cancers arising from the cervix are discussed in Chapter 20.

The majority of malignancies arising from the uterine body arise from the endometrium. The endometrium consists of both glandular and supporting (or ‘stromal’) elements and it is possible for either to undergo malignant change. The majority of uterine malignancies are adenocarcinomas arising from the endometrial glands (Figs 19.1 and 19.2A). Sarcomas of the muscle of the uterus, the myometrium or the stromal tissues of the endometrium are much rarer (Fig. 19.2B).

Incidence

In the UK the incidence of endometrial cancer has been increasing and is now the fourth most common cancer in women, after breast, bowel and lung cancers. There are around 7800 cases diagnosed in the UK annually.

Approximately 5% of endometrial carcinomas will develop in women under the age of 40 and 90% will be diagnosed after the menopause. There is evidence that the incidence is rising in developed countries.

Aetiology

The majority of endometrial cancers are associated with conditions in which there are relatively, rather than absolutely, high levels of oestrogen production and it is therefore postulated that oestrogen has a role in the development of the disease (Box 19.1).

High levels of oestrogen may be physiological, as with obesity (due to the aromatization in body fat of peripheral androgens to oestrogens), or with conditions such as polycystic ovarian syndrome (due to long-term anovulation) and late menopause. It is thought that a third of cases are related to obesity. The relationship between diabetes/hypertension and endometrial cancer is probably a result of the increased incidence of obesity in these groups of women. Non-physiological causes of increased oestrogen include unopposed (without progesterone to protect the endometrium) oestrogen hormone replacement therapy (HRT), which increases the risk four-fold. This risk is reduced to a relative risk of < 1.0 with opposed HRT (i.e. with the addition of progestogen for at least 10 days per cycle). Oestrogen-secreting tumours, which are rare, also increase the risk of endometrial carcinoma.

Endometrial cancer is also seen less frequently in women who have used the combined oral contraceptive pill, probably because it administers progestogens throughout the cycle. Women who smoke, and are therefore likely to reach an earlier menopause, also have a lower than expected incidence of the disease.

The more common and oestrogen-dependent type of endometrial cancer is sometimes called type I disease and is seen in women around the time of the menopause or soon after. It is generally diagnosed at an earlier stage and as a result has a better prognosis. There may be premalignant change (see Endometrial hyperplasia, below) and the tumour cells of type I disease usually have oestrogen and progesterone receptors. This form of the cancer has characteristic growth factor alterations, which distinguish it from normal endometrium.

Type II endometrial cancer is probably not related to oestrogen production. It is seen in older women, progresses more rapidly, and is not associated with a hyperplastic or in situ phase. The chances of surviving 5 years with this type of cancer are considerably lower than for the type I form, even with early-stage disease.

Clinical features and diagnosis

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