Endometrial Endometrioid Carcinoma: Understanding Your Pathology Report

Section Editor: Kianoosh Keyhanian MD FRCPC
September 3, 2026

Endometrial endometrioid carcinoma is a cancer that begins in the endometrium, the inner lining of the uterus. It is by far the most common type of endometrial cancer, and it most often affects women after menopause.

Most of these cancers are found early, while still confined to the uterus, because they cause bleeding that prompts investigation. Most are also low-grade and slow-growing. The outlook for this diagnosis is generally good, and considerably better than for the uncommon high-grade types of endometrial cancer.

This cancer frequently develops from a precancerous condition called atypical endometrial hyperplasia, also called endometrioid intraepithelial neoplasia. In that condition, the lining cells are already abnormal but have not yet invaded.

What causes endometrial endometrioid carcinoma?

This cancer is strongly linked to long-term exposure to estrogen without enough progesterone to balance it. Estrogen makes the lining grow, and progesterone matures it and prepares it to shed. When that balance is lost over years, the lining can progress through hyperplasia to cancer.

Excess body weight — The most important risk factor. Fat tissue converts other hormones into estrogen, increasing the amount that reaches the lining.
Irregular or absent ovulation — Progesterone is produced only after an egg is released. Polycystic ovary syndrome and the years approaching menopause both reduce how often this happens.
Estrogen-only hormone therapy — Taken by someone who still has a uterus.
Tamoxifen — A medication used in breast cancer treatment that acts like estrogen in the uterus.
Diabetes — Associated with a higher risk, partly through its link with body weight.
Lynch syndrome — An inherited condition. Cancer of the uterus is the most common Lynch-related cancer in women, and it often appears at a younger age than usual.

What are the symptoms?

Abnormal uterine bleeding — The most common symptom, including bleeding between periods and any bleeding after menopause. Always assess bleeding after menopause promptly.
Unusual vaginal discharge — Sometimes the first change noticed.
Pelvic discomfort or pain during intercourse — Less common.

How is the diagnosis made?

The process usually begins with an endometrial biopsy, in which a small sample of the lining is removed and examined under the microscope by a pathologist.

If cancer is found, surgery generally follows to remove the uterus, and usually the ovaries and fallopian tubes. Doctors often assess lymph nodes at the same time. The removed tissue determines the grade, the depth of invasion, whether the cancer has spread, and which biomarkers are present.

What does endometrial endometrioid carcinoma look like under the microscope?

Endometrioid carcinoma forms abnormal glands that resemble the normal lining glands but are irregular in size and shape and crowded together.

Gland formation — The defining feature. The tumor cells arrange themselves into gland shapes, unlike the higher-grade endometrial cancers.
Solid growth — Some tumors contain areas where cells form sheets rather than glands. The proportion of solid growth determines the grade.
Squamous differentiation — Areas resembling squamous cells are common. This is common and does not, by itself, indicate a worse outlook.
Invasion of the muscle wall — The pathologist assesses whether the tumor has grown out of the lining and into the muscle beneath.

Immunohistochemistry

Immunohistochemistry is a laboratory test that uses antibodies to detect specific proteins inside cells. Here it confirms the tumor type and separates it from cancers that start in the cervix.

Estrogen receptor and progesterone receptor. Usually strongly positive in most tumor cells in low-grade tumors. This fits with a cancer driven by hormones and has treatment consequences.
p16. Usually patchy, meaning only some cells stain.
p53. Usually normal, described as wild-type. An abnormal result is more common in high-grade tumors and changes how the tumor is managed.
ARID1A, PTEN, and mismatch repair proteins. Loss of one of these supports an endometrial origin rather than a cervical one.

The p16 result is more useful than it sounds. A cancer starting in the cervix and caused by HPV typically shows strong p16 staining throughout with negative hormone receptors, which is close to the opposite of the pattern here. When the tumor sits near the junction of the uterus and cervix, this combination is often what determines where it started.

FIGO grade

Grade describes how much of the tumor forms solid sheets rather than glands, and how abnormal the cells look. It is one of the two most important pieces of information in your report, alongside the stage.

Grade 1 — Less than 5 percent solid growth.
Grade 2 — Between 6 and 50 percent solid growth.
Grade 3 — More than 50 percent solid growth.

Grades 1 and 2 are considered low grade. Grade 3 is high, and it is staged and treated differently, as described in the staging section below. If your report gives a grade, note which one, because much of what follows depends on it.

Biomarkers

Biomarkers are tests performed on tumor tissue to understand how a cancer is likely to behave and which treatments may work.

Mismatch repair proteins

Mismatch repair proteins fix small errors that occur when DNA is copied. The four tested are MLH1, PMS2, MSH2, and MSH6. Results are reported as retained, meaning normal, or lost, meaning abnormal.

Loss means the tumor is mismatch repair deficient. This identifies tumors likely to respond to immunotherapy, and it is also how patients with Lynch syndrome are identified. Testing is now recommended for all endometrial cancers regardless of grade or stage.

Estrogen receptor and progesterone receptor

These proteins allow tumor cells to respond to estrogen and progesterone. Results are reported as positive or negative, often with a percentage.

These tumors are frequently positive, particularly when low grade. Positive results are associated with a better outlook, and they mean hormone-blocking treatment may be an option for advanced or recurrent disease, or for someone hoping to preserve fertility.

p53

p53 is a protein that helps control cell growth and repair damaged DNA. In most low-grade endometrioid carcinomas, it is normal, reported as wild-type.

An abnormal result, reported as aberrant or mutant-type, is uncommon in low-grade tumors and more frequent in grade 3. It matters a great deal when found. Such tumors behave more like serous carcinoma and are often treated the same way, even when they look endometrioid under the microscope. For tumors confined to the uterus, an abnormal result also raises the stage.

POLE

POLE is a gene involved in copying DNA accurately. Tumors with a POLE mutation carry very large numbers of DNA changes yet behave better than any other group.

These tumors have an excellent outlook and a very low risk of recurrence, even when other features look concerning. A POLE mutation lowers the stage under the current staging system, and it can mean less treatment rather than more.

Other genetic changes

PTEN loss is very common and is usually an early event, but it is not used on its own to guide treatment. PIK3CA changes are also common. KRAS changes occur in a subset.

CTNNB1 deserves a separate mention. Changes in this gene are found in some low-grade tumors. They have been linked to a higher risk of recurrence even in early-stage disease. This is one of the few findings that can raise concern in an otherwise favorable tumor.

Molecular subtypes

Large genomic studies group endometrial cancers into four molecular subtypes. Endometrioid carcinomas appear in all four, which is why the testing is worth doing.

POLE ultramutated — Excellent outlook, even when other features look high risk.
Mismatch repair deficient — Intermediate outlook, and often eligible for immunotherapy in advanced disease.
p53 abnormal — The least favorable group, and often managed like serous carcinoma.
No specific molecular profile — The largest group for this diagnosis. Many are hormone receptor positive with typical endometrioid behavior, although a CTNNB1 change can raise the risk within this group.

What other findings will be described in the report?

Myometrial invasion

The myometrium is the thick muscular wall of the uterus. Myometrial invasion means the tumor has grown from the lining into that wall. The pathologist measures the depth and reports it as a percentage of the full thickness.

For low-grade endometrioid carcinoma, the 50 percent threshold still matters, and it separates stage IA from stage IB. Invasion of half or more of the wall is associated with a higher risk of spread to lymph nodes.

Cervical stromal invasion

Cervical stromal invasion means the tumor has grown from the body of the uterus into thecervix’ supporting tissue. Involvement of only the surface lining of the cervix does not count. This finding raises the stage and may influence whether radiation therapy is recommended.

Spread to surrounding organs.

In more advanced cases,s the tumor spreads beyond the uterus to the ovaries, fallopian tubes, vagina, bladder, bowel, or the lining of the abdomen. The pathologist examines the removed tissue and reports whether tumor cells are present. Spread beyond the uterus raises the stage.

Lymphovascular invasion

Lymphovascular invasion means tumor cells have been seen inside small lymphatic channels or blood vessels. These are pathways by which cells can reach lymph nodes or distant organs.

Your report should describe it as absent, focal, or substantial, and that distinction now carries real weight. Under the current staging system, substantial lymphovascular invasion in a low-grade tumor raises the stage to IIB even when the tumor has not left the uterus. If your report says only “present,” ask whether it was focal or substantial.

Margins

A margin is the edge of the tissue removed during surgery. The pathologist examines the margins for tumor cells. Depending on the operation, these may include the cervical margin, the vaginal cuff margin, the tissue on either side of the uterus, and the peritoneal surface.

A positive margin means tumor cells reach the cut edge and some cancer may remain. A negative margin means no tumor cells were found at the edges. Positive margins may lead to a recommendation for radiation therapy.

Lymph nodes

Lymph nodes are small immune organs that filter fluid draining from tissues. Cancer cells can travel to them and form a metastasis. They are a common first site of spread for endometrial cancer.

Surgeons may remove nodes during surgery and examine them individually. Many centers now use sentinel node mapping, which identifies the few nodes that drain the uterus directly so that only those need to be removed. When cancer is found, the size of the largest deposit determines the nodal stage.

Isolated tumor cells — A group measuring 0.2 mm or less. These are recorded as N0(i+) and are not counted as node-positive disease.
Micrometastasis — A deposit measuring more than 0.2 mm and up to 2 mm. This gives a nodal stage of N1mi or N2mi, depending on which nodes are involved.
Macrometastasis — A deposit measuring more than 2 mm. This gives a nodal stage of N1a or N2a and is associated with a less favorable outlook.

Pathologic stage

The pathologic stage uses the TNM system from the American Joint Committee on Cancer, which describes the tumor (T), the lymph nodes (N), and distant spread (M).

Tumor stage (pT):

T1 — The tumor involves only the body of the uterus.
T2 — The tumor has grown into the supporting tissue of the cervix.
T3 — The tumor has reached the outer surface of the uterus, or has spread to the fallopian tubes, ovaries, or vagina.
T4 — The tumor has grown into the lining of the bladder or the bowel.

Nodal stage (pN): N0 means no tumor cells in the nodes examined. N0(i+) means only isolated tumor cells. N1mi and N1a describe involvement of pelvic nodes. N2mi and N2a describe involvement of nodes higher in the abdomen. The “mi” categories are used for deposits of 2 mm or less. NX means no nodes were examined.

Metastatic stage (pM): M1 means the cancer has spread to a distant site. This can only be assigned when tissue from that site has been examined, so most reports list it as MX and use imaging instead.

FIGO stage

The International Federation of Gynecology and Obstetrics substantially revised the staging system in 2023. The new system separates endometrial cancers into two groups based on how they tend to behave, and for this diagnosis, the grade determines which group applies.

Grade 1 and grade 2 endometrioid carcinoma — The lower-risk group, where the depth of invasion still determines the stage.
Grade 3 endometrioid carcinoma — The higher-risk group, alongside serous and clear cell carcinoma, where any invasion of the muscle wall means stage IIC.

For grade 1 and grade 2 tumors confined to the uterus:

Stage IA1 — Confined to the lining, or contained within a polyp.
Stage IA2 — Invasion of less than half the muscle wall, with no or only focal lymphovascular invasion.
Stage IA3 — A low-grade tumor involving both the uterus and an ovary, in a specific pattern that carries a favorable outlook.
Stage IB — Invasion of half or more of the muscle wall, with no or only focal lymphovascular invasion.
Stage IIA — Invasion of the supporting tissue of the cervix.
Stage IIB — Substantial lymphovascular invasion, whatever the depth of invasion.

For grade 3 tumors: stage IC means the tumor is confined to the lining, and stage IIC means it has grown into the muscle wall to any depth.

For all grades, once the tumor has left the uterus:

Stage IIIA — The outer surface of the uterus, or the ovaries or fallopian tubes.
Stage IIIB — The vagina or the tissue on either side of the uterus.
Stage IIIC — Lymph nodes. IIIC1 is pelvic nodes, and IIIC2 is nodes higher in the abdomen.
Stage IVA — The lining of the bladder or bowel.
Stage IVB — Within the abdomen beyond the pelvis.
Stage IVC — Distant organs such as the lungs or liver.

Molecular results can change the stage for tumors confined to the uterus. A POLE mutation lowers the stage to IAmPOLEmut, whatever the grade or depth. An abnormal p53 result raises it to IICmp53abn. Molecular results do not change stage III or stage IV disease.

Your report or your oncologist may use a stage that does not match what you have read elsewhere. The difference between the 2009 and 2023 systems likely explains this, and it is worth asking which one was used.

What is the prognosis?

The outlook for this diagnosis is generally good. Most tumors are found while confined to the uterus and are low grade, and five-year survival for stage I low-grade disease is around 90 out of 100 or better.

Grade, stage, depth of invasion, and lymphovascular invasion are the traditional factors. The molecular subtype now adds to them in ways that can move the assessment in either direction. A POLE mutation predicts an excellent outcome even when other features look concerning, while an abnormal p53 result predicts a worse one even in an otherwise low-risk tumor.

Published figures come from groups of patients and cannot tell you what will happen in your case. Your own team is far better placed to discuss what the outlook means for you.

How is endometrial endometrioid carcinoma treated?

Surgery — Removal of the uterus, cervix, fallopian tubes, and ovaries, often with sentinel lymph node mapping. For many people with low-grade, early-stage disease, this is the only treatment.
Vaginal brachytherapy — A short course of internal radiation to the top of the vagina, used for tumors with intermediate risk features to reduce local recurrence.
Chemotherapy — Recommended for higher-risk and advanced disease, usually carboplatin and paclitaxel.
Immunotherapy — Now used alongside chemotherapy for advanced or recurrent disease, with the greatest benefit in mismatch repair deficient tumors.
Hormone treatment — An option for advanced or recurrent hormone receptor positive disease.
Fertility-sparing treatment — For a small number of younger patients with grade 1 tumors confined to the lining, progestin treatment with close monitoring is an option. It may allow the uterus to be kept until childbearing is complete. This requires careful selection and a thorough initial assessment.

Molecular results are increasingly used to decide how much treatment is needed, and clinical trials are actively testing whether some people can safely receive less.

Questions to ask your doctor

What is my FIGO grade, and what is my stage?
Was the 2023 FIGO system used?
How deeply did the tumor invade the muscle wall?
Was lymphovascular invasion present, and was it focal or substantial?
Were lymph nodes examined, and did any contain cancer?
Were the margins negative?
What molecular subtype is my tumor?
Was p53 normal or abnormal, and does that change my treatment?
Was a POLE mutation found, and could that mean less treatment?
What did the mismatch repair testing show, and should I be tested for Lynch syndrome?
Do I need radiation or chemotherapy, or is surgery alone enough?
If I hope to become pregnant, is fertility-sparing treatment an option for me?
What will follow-up involve, and how often?