Endometrial cancers

Question 1

what is simple endometrial hyperplasia?

Answer 1

general distribution
glands and stoma
dilated (not crowded glands)
normal cytology

Question 2

what is complex endometrial hyerplasia?

Answer 2

focal distribution
glands (crowded)
normal cytology

Question 3

what is atypical (precursor of carcinoma) endometrial hyperplasia?

Answer 3

focal distribution
glands crowded
atypical cytology

Question 4

what causes endometrial hyperplasia?

Answer 4

not known but potentially persistent oestrogen simulation

Question 5

how does endometrial hyperplasia present?

Answer 5

abnormal bleeding (dysfunctional uterine bleeding or postmenopausal bleeding)

Question 6

what is endometrial carcinoma?

Answer 6

There are 2 main groups with different precursor lesions
o Endometrioid carcinoma – precursor atypical hyperplasia
o Serous carcinoma – precursor serous intraepithelial carcinoma

Question 7

who gets it?

Answer 7

peak incidence is 50-60
uncommon under 40
young women RF are PCOS, lynch syndrome
obesity

Question 8

how does obesity increase the risk of endometrial carcinoma?

Answer 8

o Endocrine and inflammatory effects of adipose tissue
o Endometrial proliferation induced by adipocytes expressing aromatase that converts ovarian androgens into oestrogens
o Sex hormone-binding globulin levels lower in obese women (higher levels of biologically active hormones)

Question 9

what is lynch syndrome?

Answer 9

o High risk of endometrial cancer and ovarian cancer
o Inheritance of a defective DNA mismatch repair gene (autosomal dominant inheritance)
o Immunohistochemistry staining of the tumour for mismatch repair proteins can help identify tumours due to Lynch syndrome

Question 10

how does it present?

Answer 10

Generally presents with abnormal bleeding

Macroscopic
• Large uterus
• Polypoid

Microscopic
• Most are adenocarcinomas
• Most are well-differentiated

Spread
• Directly into myometrium and cervix
• Lymphatic
• Haematogenous

Question 11

type 1 tumours

Answer 11

Endometriod and mucinoid (80%)

• Related to unopposed oestrogen
• Associated with atypical hyperplasia
• Typically infiltrates myometrium
• Serous carcinoma may spread early to the peritoneal cavity
• Good prognosis

Question 12

type 2 tumours

Answer 12

serous and clear cell

• Not associated with unopposed oestrogen
• Affect elderly post-menopausal women
• TP53 often mutated
• Spreads along fallopian tube mucosa and peritoneal surfaces so can present with extrauterine disease
• More aggressive than type 1 cancers
• Surgery usually more extensive and adjuvant chemo/radiotherapy used more frequently

Question 13

how is it managed?

Answer 13

Surgical treatment is the mainstay - Total abdominal hysterectomy and bilateral salpingo-oophorectomy (TAH-BSO)
Controversy over the role of lymphadenectomy
Adjuvant radiotherapy
- Vault brachytherapy
- External beam
Chemotherapy - Adjuvant chemotherapy – depending on grade

Question 14

where does a endometrial stromal sarcoma arise from?

Answer 14

the endometrial stroma

Question 15

what is an endometrial stromal sarcoma?

Answer 15

High grade endometrial stromal sarcoma (increased atypical proliferative activity) – more likely to disease
Rare – cells resemble endometrial stroma, infiltrate myometrium and often lymphovascular spaces

Question 16

how does endometrial stromal sarcoma present?

Answer 16

typically with abnormal uterine bleeding

initial presentation may be as metastasis (most commonly ovarian or lung)

Question 17

what is a carcinosarcoma?

Answer 17

• Under 5% of uterine malignancies
• High grade carcinomatous and sarcomatous elements
• Heterogenous elements commonly seen in about 50% of cases (rhabdomyosarcoma – worst prognosis, chondrosarcoma, osteosarcoma)
• Usually associated with a poor outcome