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Most common gynaecological carcinoma in
developed countries
Japan and Asia have 5 times lower incidence

Most cases are post-menopausal
< 5% under age of 40 ( hyperestrogenic )
At diagnosis 75% have Stage 1 disease
OBESITY strong link as peripheral conversion to Estrone
SHBG(sex hormone binding globulin) decrease with an increase in FREE estrogen for uptake in target tissues

Lifetime risk: 1.1%
Lifetime risk of dying: 0.4%
5-year survival rates are considered to be
good at around 75%

The prognosis is generally good because the majority
of patients are diagnosed in an early stage

Role of hormones (estrogen)

Estrogen dependent disease
Prolonged exposure without the balancing effects of progesterone

Conditions of Estrogen excess

Early Menarche and Late Menopause

Associated with more estrogen exposure

Estrogen Replacement Therapy

Place women at high risk
Risk reduced when + progesterone


Anti-estrogenic drug for breast cancer
Side effect
Induces non-cancerous uterine tumors
Some may develop into endometrial cancer
Long term use => endometrial cancer
Only 1 in 500 develop endometrial cancer

Reduced Risk

Oral Contraceptives

Combined OC => 50% reduced rate
Actual reduction number small because uncommon in women of child bearing age
Long term offers protection
Reduced risk presumably => progesterone

Physical exercise and fruit vegetables diet

Endometrial Carcinoma: aetiology

Hyperoestrogenic states

Age - mainly 60-70 years (late menopause)
Parity - nulliparity, relative infertility
Metabolic disorders [Cancer Triad]
Obesity, Diabetes, Hypertension
Ovarian tumours
granulosa cell tumour, PCOD
unopposed Exogenous oestrogens [HRT]

other conditions
leiomyomas; adenomyosis, endometriosis, breast Ca

Risk factors
  • Usually in postmenopausal women
  • Unapposed estrogen stimulation
  • Preceded by endometrial hyperplasia
  • Simple hyperplasia

Adenomatous hyperplasia

Cellular Atypia

Clinical Features

Abnormal bleeding
mainly postmenopausal
intermenstrual or pre-menstrual

Lower abdominal pain
abnormal vaginal discharge / pyometra

Endometrial Carcinoma


Endometrial sampling
Dilation and curettage / Endometrial aspiration

TVS / CT scan / MRI

Hysteroscopy + targeted biopsy

Tumor marker
Ca 125 / 199

Cystoscope / Proctoscope


Early detection is best prevention
Treating precancerous hyperplasia
Hormones (progestin)
10 ~ 30% untreated develop into cancer

Histology/ grade

90% endometrial adenocarcinoma
Arise from the epithelium

Tumor grading
Grade 1
Well differentiated
Grade 2
Moderately differentiated with solid component
Grade 3
Poorly differentiated with solid sheets of tumor

Rare cell types

10% rare cell types
Papillary serous carcinoma
Clear cell carcinoma
Papillary endometrial carcinoma
Mucinous carcinoma
Rarer cancers
Onset at later age
Greater risk for metastases
Poorer prognosis
50% of treatment failure


Direct spread
Through endometrial cavity to the cervix
Through fallopian tubes to ovary / peritoneum
Invade myometrium reaching serosa
Rare: invasion to pubic bone
Lymphatic spread
Pelvic and para-aortic LN
Inguinal LN ( rare )
Hematogenous spread
Rare but may spread to lungs

Adenocarcinoma uterus

Intraoperatively obtained gross specimen of the uterus, bivalved in a sagittal plane, shows deep invasion (50% of the myometrial thickness) of endometrial carcinoma

Stage 1 Tumour confined to corpus
Stage 1a <50% myometrial invasion
Stage 1b >50% myometrial invasion

Stage 2 Tumour invades Cx stroma

Stage 3 Local/regional tumour spread

3a Invades serosa/+- adnexa
3b Vaginal or parametrial spread
3c1 Positive pelvic nodes
3c2 Positive para-aortic nodes
Stage 4 Invades bladder/bowel/distant

Treatment of endometrial hyperplasia/ carcinoma

Endometrial hyperplasia

Excessive stimulation of the uterine endometrium results in endometrial hyperplasia

Imbalance of hormones or hormonal changes can happen around the time of menopause, and contribute to the development of hyperplasia in some women.

Endometrial hyperplasia of the uterus, by itself, is not cancerous, but requires treatment and monitoring to prevent the risk of cancer.

Managing endometrial hyperplasia

Uterine hyperplasia can get worse, leading to atypical and precancerous cellular changes.

This is why any woman with hyperplasia is considered to be at a higher risk for cancer than one without hyperplasias.

investigate thickened endometrium,
hyperplasia can lead to uterine cancer —
early identification and intervention for uterine abnormalities is highly successful.

The evaluation process begins with a
speculum and bimanual exam
(internal exam and external palpation of the pelvic organs)

An ultrasound and tissue sampling
with endometrial biopsy, hysteroscopy and/or D&C

Hormonal treatment of endometrial hyperplasia

hyperplasia without atypia
progesterone/progestin therapy for three months,
then to retest the endometrium.
micronized natural progesterone at high doses

Atypia present
option for women who want to wait or avoid surgery altogether is Megace (megestrol acetate), a very potent, orally administered hormonal agent.

Ca Endometrium Treatment Algorithms

Clinical Stage I

( Grade? Depth? Cell type ?)

Low Risk ~ 75%

High Risk ~ 25%
EBRT to pelvis
(but~13% have PA nodes)

Treatment of endometrial cancer

Stage II
Consider radical hysterectomy
With macroscopic tumor on cervix:

Consider a cervical cancer

Intra-abdominal spread:
Remove all tumor if possible

Advanced stage

Debulking surgery


+/- hormone / chemotherapy


Likely in women with advanced disease
Within 3 years of original diagnosis
Hormone therapy can be considered
External beam pelvic radiation or brachytherapy.

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