Quiz questions on prevention of endometrial cancer
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I now have sufficient material from the textbooks to generate a comprehensive, clinically rigorous quiz. Here are 20 mixed-format questions on the prevention of endometrial cancer, pitched at postgraduate/resident level.
🩺 Quiz: Prevention of Endometrial Cancer (Postgraduate Level)
Section A — Multiple Choice Questions (MCQs)
Q1. A 52-year-old postmenopausal woman is prescribed hormone replacement therapy for vasomotor symptoms. She has an intact uterus. Which of the following is the most important modification to her regimen to prevent endometrial cancer?
- A) Use the lowest effective estrogen dose
- B) Add cyclic or continuous progestogen to the estrogen
- C) Use a transdermal rather than oral estrogen formulation
- D) Limit duration of use to 6 months
Answer: B
Rationale: Progestogens oppose unopposed estrogen stimulation of the endometrium. Women with an intact uterus must receive progestin alongside estrogen to prevent endometrial hyperplasia and carcinoma. The lowest dose of estrogen should also be used, but progestin addition is the primary protective measure. — Lippincott Illustrated Reviews: Pharmacology
Q2. Which molecular pathway is most frequently dysregulated in endometrioid endometrial carcinoma, making it a hallmark of this tumour type?
- A) MAPK/ERK pathway
- B) PI3K/AKT pathway
- C) WNT/β-catenin pathway
- D) JAK/STAT pathway
Answer: B
Rationale: Endometrial carcinomas harbour higher-frequency mutations in the PI3K/AKT pathway than any other tumour type studied. Key alterations include PTEN loss (30–80%), PIK3CA mutations (~40%), and KRAS mutations (~25%). — Robbins, Cotran & Kumar: Pathologic Basis of Disease
Q3. A 38-year-old woman with PCOS does not wish to conceive and does not respond to clomiphene. She has persistent anovulation. Which of the following interventions is MOST effective in preventing endometrial cancer in this patient?
- A) Progesterone supplementation during the luteal phase only
- B) Combined oral contraceptive pill (OCP)
- C) Metformin alone
- D) Annual endometrial biopsy without further intervention
Answer: B
Rationale: In PCOS with persistent anovulation, prevention of endometrial cancer requires continuous progestogenic influence. Combined OCPs provide this most reliably. If ovulation induction or OCPs are not used, periodic progestational agents should be given to induce secretory transformation. Annual biopsy monitors but does not prevent malignancy. — Berek & Novak's Gynecology
Q4. Tamoxifen is used as adjuvant therapy for oestrogen receptor–positive breast cancer. Its effect on the endometrium is best described as:
- A) Purely anti-oestrogenic, fully protective
- B) Weak agonist, increasing endometrial cancer risk 2–3 fold
- C) Strong agonist, equivalent to postmenopausal oestrogen therapy
- D) Neutral — no effect on endometrial risk
Answer: B
Rationale: Tamoxifen exhibits antioestrogen activity in breast tissue but weak oestrogen agonist activity in uterine epithelium, increasing endometrial cancer incidence 2–3 fold, particularly in postmenopausal women treated for >2 years. — Goodman & Gilman's; Harrison's Principles of Internal Medicine 22E
Q5. A 45-year-old woman is found to carry a germline MLH1 mutation (Lynch syndrome). Her lifetime risk of endometrial cancer is approximately:
- A) 5–10%
- B) 15–20%
- C) 40%
- D) 75%
Answer: C
Rationale: Women with Lynch syndrome (HNPCC) have approximately a 40% lifetime risk of endometrial cancer and a 10% lifetime risk of ovarian cancer. Middle-aged women with HNPCC carry a 4% annual risk of endometrial cancer. — Schwartz's Principles of Surgery; Harrison's Principles 22E
Q6. Which of the following selective oestrogen receptor modulators (SERMs) has a more favourable uterine safety profile compared to tamoxifen when used for breast cancer chemoprevention?
- A) Raloxifene
- B) Bazedoxifene
- C) Clomiphene
- D) Ospemifene
Answer: A
Rationale: Raloxifene is 24% less effective than tamoxifen in reducing breast cancer risk, but carries a 45% reduction in endometrial cancer risk compared to tamoxifen, owing to its purely antioestrogen effect on the uterus. — Sabiston Textbook of Surgery; Harrison's Principles 22E
Q7. Which FIGO endometrial carcinoma stage classification correctly identifies the stage associated with invasion confined to the uterine corpus without deep myometrial invasion?
- A) Stage IA — no or less than half myometrial invasion
- B) Stage IB — more than half myometrial invasion
- C) Stage II — cervical stromal involvement
- D) Stage III — extrauterine extension
Answer: A
Rationale: FIGO Stage IA = tumour confined to endometrium or invading less than half the myometrium. Stage IB = ≥50% myometrial invasion. Well-differentiated stage I tumours detected early (including in PCOS patients) carry a cure rate >90%. — Berek & Novak's Gynecology
Q8. Oral contraceptives provide protection against endometrial cancer through which primary mechanism?
- A) Suppression of LH and FSH reducing gonadotrophin stimulation
- B) Progestin component opposing endometrial oestrogen stimulation
- C) Direct anti-proliferative effect via oestrogen receptor downregulation
- D) Reduction of peripheral aromatisation of androgens
Answer: B
Rationale: OCPs contain progestins that counterbalance the proliferative effect of oestrogen on the endometrium, preventing hyperplasia. They provide consistent progestogenic influence similar to the secretory phase of a normal cycle. — Harrison's Principles of Internal Medicine 22E
Section B — True / False
Q9. Endometrial hyperplasia without cytologic atypia carries the same malignant potential as atypical hyperplasia.
Answer: FALSE
Rationale: The classification of hyperplasia is based on the presence or absence of cytologic atypia, which determines risk of progression to endometrioid carcinoma. Atypical hyperplasia has significantly higher malignant potential. — Robbins & Kumar: Basic Pathology
Q10. Obesity is a major risk factor for endometrial cancer primarily because adipose tissue is a significant source of extra-gonadal oestrogen via peripheral aromatisation of androgens.
Answer: TRUE
Rationale: Obesity leads to elevated circulating oestrogens through peripheral aromatisation, as well as hyperinsulinaemia and increased IGF-1 signalling, all of which stimulate endometrial proliferation. Maintaining a healthy body weight is an important cancer prevention recommendation. — Goldman-Cecil Medicine
Q11. Progestin-releasing intrauterine devices (e.g. levonorgestrel IUD) have a protective role in managing endometrial hyperplasia.
Answer: TRUE
Rationale: The levonorgestrel-releasing IUD delivers progestin locally to the endometrium, opposing oestrogen stimulation and providing effective treatment and prevention of hyperplasia. It is a well-established nonsurgical management option. — Berek & Novak's Gynecology
Q12. Lynch syndrome is inherited in an autosomal recessive pattern.
Answer: FALSE
Rationale: Lynch syndrome is autosomal dominant. It involves germline mutations in mismatch repair genes (MLH1, MSH2, MSH6, PMS2) and confers a colorectal cancer risk of up to 75% by age 75, and ~40% lifetime risk of endometrial cancer. — Schwartz's Principles of Surgery
Q13. TP53 mutations are an early molecular event in endometrioid (Type I) endometrial carcinoma.
Answer: FALSE
Rationale: TP53 mutations are early events in Type II (serous) endometrial carcinomas, present even in the precursor serous endometrial intraepithelial carcinoma. In endometrioid carcinoma, TP53 mutations occur in ~50% of poorly differentiated tumours and are considered late events in progression. — Robbins, Cotran & Kumar: Pathologic Basis of Disease
Q14. Risk-reducing hysterectomy with bilateral salpingo-oophorectomy is recommended for women with Lynch syndrome who have completed childbearing.
Answer: TRUE
Rationale: Given the ~40% lifetime risk of endometrial cancer and 10% of ovarian cancer, risk-reducing salpingo-oophorectomy with hysterectomy is recommended for Lynch syndrome carriers who have completed childbearing, ideally 5–10 years before the earliest familial cancer case. — Schwartz's Principles of Surgery
Section C — Short Answer Questions
Q15. List four modifiable risk factors for endometrial cancer that can be targeted in a preventive strategy.
Model Answer:
- Obesity — reduce via diet, exercise, bariatric surgery; decreases circulating oestrogens
- Unopposed exogenous oestrogen — add progestin in women with intact uterus on HRT
- Anovulation / PCOS — induce ovulation or provide progestogenic protection (OCPs or cyclical progestins)
- Type 2 diabetes / insulin resistance — glycaemic control reduces insulin-mediated endometrial proliferation (Additional: tamoxifen use in at-risk women — switch to raloxifene when appropriate)
Q16. A patient on long-term tamoxifen for breast cancer develops postmenopausal vaginal bleeding. What is the most appropriate next step, and why?
Model Answer:
Endometrial biopsy (or transvaginal ultrasound as initial triage, followed by biopsy if endometrial thickness ≥4–5 mm or symptoms persist). Tamoxifen's weak uterine oestrogenic agonism increases endometrial cancer risk 2–3 fold. Any abnormal uterine bleeding in a postmenopausal woman on tamoxifen must be evaluated to exclude endometrial malignancy. — Goodman & Gilman's; Sabiston Textbook of Surgery
Q17. Describe the molecular basis by which PCOS leads to increased endometrial cancer risk, and outline a preventive strategy.
Model Answer:
In PCOS, chronic anovulation results in persistent, unopposed oestrogen stimulation of the endometrium without the counterbalancing secretory phase provided by progesterone. This drives endometrial hyperplasia, which — particularly in the presence of cytologic atypia — is a precursor to endometrioid carcinoma. Underlying molecular events include PTEN inactivation and PI3K/AKT pathway activation.
Prevention: If ovulation induction is not feasible or desired, continuous progestogenic influence should be provided via combined OCPs. If OCPs are not used, regular cyclic progestin or levonorgestrel IUD should be prescribed to induce regular secretory transformation and menstruation. Endometrial surveillance (biopsy) is indicated if the threshold is lowered by abnormal bleeding, increasing weight, or age. — Berek & Novak's Gynecology
Q18. What are the four molecular subtypes of endometrial carcinoma identified by TCGA analysis, and which has the best prognosis?
Model Answer:
- POLE ultramutated — mutations in DNA polymerase epsilon; remarkably high mutation burden; best prognosis
- MSI hypermutated — mismatch repair deficiency (frequently MLH1 promoter hypermethylation in sporadic cases); intermediate prognosis
- Copy-number low — frequent PTEN, CTNNB1, KRAS mutations; endometrioid histology; intermediate prognosis
- Copy-number high — extensive somatic copy number alterations, frequent TP53 mutations; serous/serous-like histology; worst prognosis
— Berek & Novak's Gynecology
Q19. Which DNA mismatch repair genes are most commonly mutated in Lynch syndrome–associated endometrial cancer? Name three.
Model Answer:
MLH1, MSH2, MSH6 (and, less commonly, PMS2 and PMS1).
Loss of these genes leads to microsatellite instability (MSI), now also associated with response to immune checkpoint inhibitors (e.g. pembrolizumab). — Harrison's Principles 22E; Schwartz's Principles of Surgery
Q20. A 36-year-old nulliparous woman with a BMI of 38 kg/m² presents with a 2-year history of irregular periods and infertility. Endometrial biopsy shows atypical endometrial hyperplasia. She wishes to preserve fertility. What is the most appropriate management to prevent progression to carcinoma, and what is the long-term preventive plan?
Model Answer:
Immediate management: Continuous progestin therapy — either high-dose oral progestins (e.g. medroxyprogesterone acetate or megestrol acetate) or levonorgestrel-releasing IUD. Response should be confirmed by repeat biopsy at 3–6 months.
Fertility strategy: Ovulation induction once hyperplasia has regressed, with close endometrial surveillance during any pregnancy attempt.
Long-term prevention:
- Sustained weight loss (targets peripheral aromatisation, insulin resistance, and IGF-1 signalling)
- After childbearing is complete: risk-reducing hysterectomy is the definitive option given the high risk of recurrence
- If fertility preservation continues, ongoing progestogen therapy with regular surveillance biopsies
— Berek & Novak's Gynecology; Robbins, Cotran & Kumar: Pathologic Basis of Disease
Answer Key Summary
| Q | Type | Answer |
|---|---|---|
| 1 | MCQ | B |
| 2 | MCQ | B |
| 3 | MCQ | B |
| 4 | MCQ | B |
| 5 | MCQ | C |
| 6 | MCQ | A |
| 7 | MCQ | A |
| 8 | MCQ | B |
| 9 | T/F | False |
| 10 | T/F | True |
| 11 | T/F | True |
| 12 | T/F | False |
| 13 | T/F | False |
| 14 | T/F | True |
| 15–20 | Short answer | See above |
Sources consulted:
- Berek & Novak's Gynecology
- Robbins, Cotran & Kumar: Pathologic Basis of Disease
- Robbins & Kumar: Basic Pathology
- Harrison's Principles of Internal Medicine, 22nd Ed. (2025)
- Goodman & Gilman's Pharmacological Basis of Therapeutics
- Schwartz's Principles of Surgery, 11th Ed.
- Sabiston Textbook of Surgery
- Goldman-Cecil Medicine
- Lippincott Illustrated Reviews: Pharmacology
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