Endometrial cancer: symptoms, causes and treatment

Endometrial cancer is cancer that begins in the endometrium, the lining of the uterus that thickens and sheds each menstrual cycle. It is by far the most common form of uterine cancer – the type most people mean when they say womb cancer – making up around 90 to 95 per cent of cases, and most of it is driven by oestrogen.¹ The classic early warning sign is abnormal bleeding – especially any bleeding after menopause – which is also why so much of it is caught early, when the outlook is very good.¹

This page is the detailed look at endometrial cancer specifically. For the bigger picture, including the rarer uterine sarcomas that start in the muscle wall, see our overview of uterine cancer.

This is general information and not a substitute for personalised medical advice. If any of this sounds like you, please see a doctor or gynaecological specialist.

What is endometrial cancer?

The uterus has two main layers: a thick muscular wall (the myometrium) and an inner lining (the endometrium). Endometrial cancer grows from the gland cells of that lining, not from the muscle itself.¹ Because the endometrium responds so strongly to hormones, this is fundamentally a hormonally influenced cancer in most people who develop it.

It is mostly, though not only, a disease of later life, and it tends to be picked up early because it announces itself with bleeding.¹ That early presentation is the single biggest reason endometrial cancer has a better outlook than most other gynaecological cancers.

A note on language: this page is for women and for anyone with a uterus, including trans men and non-binary people, who can all develop endometrial cancer.

What are the symptoms of endometrial cancer?

The dominant symptom is abnormal bleeding. After menopause, that means any bleeding at all. Before menopause, it means bleeding that is unusual for you – heavier or longer periods, bleeding between periods, or bleeding after sex.¹

Just how central bleeding is becomes clear from the numbers. In a large meta-analysis, postmenopausal bleeding was present in about 90 per cent of people eventually diagnosed with endometrial cancer.² The reassuring flip side is that only around 9 per cent of people with postmenopausal bleeding turn out to have it – so the symptom is common, mostly benign, but always worth checking.²

Other possible signs include unusual or watery vaginal discharge, sometimes before any bleeding, pelvic pain or pressure, pain during sex, and, in more advanced disease, unexplained weight loss.¹ Occasionally endometrial cells show up unexpectedly on a cervical screening (Pap) test, which can be an early prompt to investigate further.¹

How common is endometrial cancer?

In Australia, an estimated 3,493 new cases of uterine cancer were projected for 2025, making it the fifth most commonly diagnosed cancer among Australian women, with a roughly 1 in 46 risk of diagnosis by the age of 85.³ Endometrial cancer accounts for the great majority of these.³

The bigger story is the trend. Case numbers in Australia have roughly doubled over the past two decades, and endometrial cancer is rising worldwide, largely tracking rising rates of obesity.¹ It is one of the few cancers becoming more common rather than less, which makes understanding its risk factors useful.

What causes it, and who is at higher risk?

Most endometrial cancer is driven by oestrogen that is not balanced by progesterone over a long period. Anything that increases lifetime exposure to this unopposed oestrogen tends to push risk up, which is why the risk factors cluster together.¹

Excess body weight is the largest modifiable factor. Fat tissue converts other hormones into oestrogen, so carrying more of it means more oestrogen reaching the lining – it is estimated that around 40 per cent of endometrial cancers are linked to excess weight.¹ Insulin resistance and type 2 diabetes feed into the same hormonal picture.

Other recognised risk factors include:

• starting periods early or reaching menopause late, both of which lengthen oestrogen exposure
• never having been pregnant, or difficulty ovulating
• polycystic ovary syndrome, recently renamed PMOS, which involves irregular ovulation and often insulin resistance
• untreated endometrial hyperplasia, a thickening of the lining that can precede cancer
• oestrogen-only hormone therapy taken without progesterone
• tamoxifen, a breast cancer medicine that acts like oestrogen on the uterus
• increasing age, high blood pressure and diabetes

There is also an important inherited cause. Lynch syndrome (hereditary non-polyposis colorectal cancer) markedly raises the risk of both bowel and endometrial cancer – affected women have an estimated 20 to 60 per cent lifetime risk of endometrial cancer, and often develop it younger.¹ If endometrial or bowel cancer runs in your family, this is worth raising with your doctor.

In our clinic, the lining is rarely the whole story. For most people endometrial risk builds over years from hormones and metabolism slipping out of balance; for others it runs in the family. Either way, we look at the whole person, not just the lining.

Types and grades of endometrial cancer

Endometrial cancers are not all the same, and the differences matter for treatment and outlook. Historically they have been divided into two broad groups: type 1, which is oestrogen-driven, usually lower grade and generally favourable; and type 2, which is less common, not especially oestrogen-driven, and more aggressive.¹

Endometrioid carcinoma

This is the classic type 1 cancer and makes up roughly 80 per cent of endometrial cancers.¹ It is graded 1 to 3 according to how abnormal the cells look and how much they still resemble normal gland tissue – grade 1 is the most favourable, grade 3 the least. Many endometrioid cancers carry mutations in genes such as PTEN.¹

Non-endometrioid and rarer types

The type 2 group includes serous carcinoma, clear cell carcinoma and carcinosarcoma. These are less common but tend to behave more aggressively and are more likely to have spread by the time they are found, so they are usually treated more intensively.¹ Getting the exact subtype right is a key part of planning care.

The molecular classification, and why it changed everything

The biggest shift in how we understand endometrial cancer came from large-scale genetic analysis. In a landmark study, researchers sorted endometrial cancers into four molecular groups based on their underlying genetics, rather than on appearance alone.⁴ Those four groups are now central to modern care:^4–5

• POLE-mutated (ultramutated) – uncommon, and with the best outlook of the four
• mismatch repair deficient (also called MSI-high or hypermutated) – often linked to Lynch syndrome, with an intermediate outlook
• no specific molecular profile – the largest group, also intermediate
• p53-abnormal (copy-number high) – the most aggressive, with the poorest outlook

This matters because two cancers that look almost identical under the microscope can sit in different molecular groups and behave very differently.⁵ The classification now helps doctors avoid over-treating low-risk cancers while making sure high-risk ones get enough, and it is built into the current staging system.⁵

How is endometrial cancer diagnosed?

Diagnosis usually begins the moment abnormal bleeding is investigated. The two main first-line tools are a transvaginal ultrasound, which measures the thickness of the endometrial lining, and an endometrial biopsy, which samples the lining to examine under the microscope.¹

In someone with postmenopausal bleeding, a thin lining on ultrasound is reassuring, while a thickened lining or ongoing bleeding prompts a biopsy.¹ If the picture is unclear, a hysteroscopy – a thin camera passed into the uterus, often with a dilation and curettage to sample the lining more thoroughly – gives a definitive answer.¹

There is no routine screening test for endometrial cancer in people at average risk, the way cervical screening works for the cervix.¹ Early detection relies on people noticing abnormal bleeding and acting on it. People at high risk, such as those with Lynch syndrome, are an exception and may be offered regular surveillance.¹

Stages of endometrial cancer

Staging describes how far a cancer has spread and guides treatment, running broadly from stage I (confined to the uterus) to stage IV (spread to distant organs).⁵ Endometrial cancer uses the FIGO system, which was substantially updated in 2023.⁵

The 2023 update was significant because it folded in tumour grade, the specific cell type and, for the first time, the molecular classification – so that staging now reflects how a cancer is likely to behave, not just how far it has physically spread.⁵ In practice this makes treatment planning far more personalised.⁵

How is endometrial cancer treated?

Treatment depends on the type, grade, stage and molecular profile of the cancer, your general health, and whether preserving fertility matters to you. It is always planned by a specialist gynaecological oncology team, and what follows is a general map, not a personal plan.

Surgery is the mainstay for most endometrial cancers, typically a hysterectomy to remove the uterus and cervix, usually with the fallopian tubes and ovaries, and sometimes nearby lymph nodes.¹ Depending on the findings, this may be followed by radiotherapy or chemotherapy to lower the chance of recurrence.¹

For early, low-grade, oestrogen-driven cancer in carefully selected younger people who wish to preserve fertility, hormonal (progestin) treatment can sometimes be used instead of immediate surgery.¹ And in a major recent shift, immunotherapy has changed the outlook for advanced and recurrent disease: drugs that release the brakes on the immune system, given alongside chemotherapy, have produced practice-changing results, especially in mismatch-repair-deficient tumours.⁶

Endometrial cancer survival rates and outlook

The outlook for endometrial cancer is generally good, largely because so much of it is found early. Across all cases, around 81 per cent of people are alive five years after diagnosis, and outlook falls as the stage rises – which is exactly why early bleeding should never be ignored.⁷

Survival is closely tied to how far the cancer has spread when it is found. Using the SEER groupings, the five-year relative survival rate is about 95 per cent when it is still confined to the uterus, around 70 per cent once it has spread to nearby tissues or lymph nodes, and about 18 per cent if it has reached distant organs.⁷ These are broad averages from large datasets, not a prediction for any one person.

Increasingly, the molecular group also shapes the outlook – POLE-mutated cancers do very well, while p53-abnormal cancers are more serious – which is why accurate classification matters as much as stage.⁵

Can endometrial cancer be prevented?

You cannot change your age or your genes, but several of the biggest levers are modifiable. Maintaining a steady, healthy weight is the most powerful, because it directly affects how much oestrogen reaches the lining.¹ Managing insulin resistance, diabetes and conditions like PCOS all feed into the same protective picture, and there is good evidence that physical activity lowers risk.¹

Some hormonal approaches are protective too. Combined oral contraceptives and progestin-containing treatments reduce endometrial cancer risk, and where oestrogen hormone therapy is used after menopause in someone with a uterus, it should always be paired with progesterone to protect the lining.¹ Treating endometrial hyperplasia and addressing relative oestrogen excess early are part of the same upstream approach. If you carry a known genetic risk such as Lynch syndrome, your specialist can discuss surveillance and risk-reducing options with you.¹

Frequently asked questions

What is the difference between endometrial cancer and uterine cancer?

Uterine cancer is the umbrella term for any cancer of the uterus. Endometrial cancer is the most common type, starting in the lining; the rarer type, uterine sarcoma, starts in the muscle wall. Most of the time, the two terms are used to mean the same thing.

What is the most common first sign of endometrial cancer?

Abnormal bleeding, especially any bleeding after menopause. It is present in about 90 per cent of people who are eventually diagnosed, which is why it should always be checked.²

Does a Pap smear detect endometrial cancer?

Not reliably. Cervical screening is designed to find cervical cell changes, not endometrial cancer, though it occasionally picks up endometrial cells by chance. Abnormal bleeding still needs separate investigation.

Can you get endometrial cancer after menopause?

Yes – in fact most cases occur after menopause. That is precisely why bleeding after menopause is treated as a red flag worth assessing.¹

Is endometrial cancer curable?

Often, yes, particularly when it is found early and confined to the uterus.¹ Outcomes are strongly tied to stage and to the specific type and molecular group of the cancer.

Can younger people get endometrial cancer?

It is much less common before menopause, but risk rises with obesity, PCOS, insulin resistance and Lynch syndrome.¹ Persistent abnormal bleeding at any age deserves assessment.

What to do next

If you have had any bleeding after menopause, or new and persistent abnormal bleeding before it, book in to have it assessed. It is usually nothing serious, but it is the single most useful step you can take, and acting early is what gives the best outcomes.

If you would like to understand your own risk, it helps to look at the conditions that sit upstream of endometrial cancer – oestrogen balance, insulin resistance, weight and ovulation – and to address them as part of your wider health rather than in isolation. For the broader context on all uterine cancers, see our uterine cancer overview above.

If you would like to talk something through, you can use Aunt Vadge’s Assistant, the chat in the bottom-left of your screen, or book in with one of our practitioners. For anything involving suspected cancer, our role is to support you alongside, not instead of, your gynaecological and oncology team.

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