Step 2 CK · Obstetrics & Gynecology

Gynecologic Oncology & Screening

Name: Gynecologic Oncology & Screening
Creator: Veli Bakalov, MD

Master the screening algorithms and treat postmenopausal bleeding as cancer until biopsy

Obstetrics & Gynecology·Gynecologic Oncology·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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HPV 16 and 18 cause ~70% of cervical cancers (E6 degrades p53, E7 inactivates Rb); most are squamous cell carcinomas of the transformation zone.
Cervical screening starts at 21 regardless of sexual history: cytology every 3 years at 21–29; primary HPV every 5 years preferred (co-testing every 5 or cytology every 3 acceptable) at 30–65; stop at 65 after adequate negative screening.
ASC-US reflexes to HPV testing at 25 or older with colposcopy if positive (ages 21 to 24: repeat cytology in 1 year); LSIL and HSIL go straight to colposcopy with biopsy; CIN2–3 is excised by LEEP or cone, while CIN1 is observed.
The 9-valent HPV vaccine is routine at 11–12 (2 doses before 15, 3 if older or immunocompromised), with catch-up through 26; it does not replace screening.
Endometrial cancer, the most common US gynecologic malignancy, is driven by unopposed estrogen (obesity, PCOS, tamoxifen, nulliparity) and Lynch syndrome.
Postmenopausal bleeding is cancer until proven otherwise: an endometrial stripe >4 mm (or persistent bleeding) mandates endometrial biopsy.
Atypical endometrial hyperplasia is precancerous: hysterectomy, or high-dose progestin to preserve fertility.
Ovarian cancer presents late with bloating and early satiety; CA-125 is nonspecific, no general screening works, and staging is surgical; germ cell markers are LDH (dysgerminoma), AFP (yolk sac), β-hCG (choriocarcinoma).
In-utero DES exposure causes vaginal clear-cell adenocarcinoma; biopsy persistent vulvar lesions and any dominant breast mass even with a negative mammogram.

Cervical cancer: HPV and screening

HPV biology. High-risk HPV types 16 and 18 cause about 70% of cervical cancers. Viral E6 degrades p53 and E7 inactivates Rb, removing two key brakes on the cell cycle. Most cervical cancer is squamous cell carcinoma arising in the transformation zone. Risk factors are early intercourse, multiple partners, smoking, and immunosuppression/HIV. Cervical cancer classically presents with postcoital bleeding; advanced disease can obstruct the ureters and cause renal failure.

Cervical cancer screening (average risk)

Age	Strategy
<21	No screening, regardless of sexual history
21–29	Pap cytology every 3 years
30–65	Primary HPV every 5 years is preferred (USPSTF 2024 draft; self-collection allowed); co-testing (Pap + HPV) every 5 years or cytology alone every 3 years remain acceptable
>65	Stop after adequate negative prior screening

Women with HIV or other immunosuppression are screened more often; no screening is needed after hysterectomy with cervix removal for benign disease.

Abnormal cytology, CIN, and HPV vaccination

ASC-USage 25 or older: reflex HPV testing; colposcopy if HPV-positive, repeat HPV-based testing in 3 years if negative. Age 21 to 24: repeat cytology in 1 year preferred
LSIL or HSILcolposcopy with directed biopsy (acetic acid turns abnormal epithelium white)
High-grade lesion (HSIL, CIN2–3)excision by LEEP or cone

CIN grading guides treatment. CIN1 (low grade) usually regresses and is observed. CIN2/3 (high grade) is treated with excision (LEEP, cold-knife cone) or ablation; excision can later cause cervical insufficiency and preterm birth. Invasive cervical cancer is treated by stage: surgery for early disease and cisplatin-based chemoradiation for advanced disease.

Colposcopy and biopsy are safe in pregnancy, but endocervical curettage is avoided and treatment of preinvasive disease is deferred until after delivery.

HPV vaccine is primary prevention. The 9-valent vaccine (covering 16 and 18 plus other oncogenic and wart-causing types) is routine at 11–12 (may start at 9), with catch-up through 26. Give two doses if started before 15, and three doses if started at 15 or older or if immunocompromised. Vaccination does not replace screening.

Endometrial hyperplasia and cancer

Epidemiology and risk. Endometrial carcinoma is the most common gynecologic malignancy in the US. Anything that raises unopposed estrogen raises risk: obesity, nulliparity, early menarche or late menopause, estrogen-only therapy, tamoxifen, PCOS, and chronic anovulation. Lynch syndrome (mismatch-repair mutations) confers a high lifetime risk. Combined OCPs and progestins are protective.

Endometrial carcinoma types

Feature	Type I (endometrioid)	Type II (serous, clear cell)
Driver	Estrogen-driven; arises from atypical hyperplasia	Estrogen-independent; arises in atrophic endometrium
Patient	Obese, perimenopausal or early postmenopausal	Older, often thin
Molecular	PTEN loss, mismatch-repair defects	p53 mutation
Behavior	Low grade, good prognosis	High grade, aggressive

Postmenopausal bleeding is endometrial cancer until proven otherwise, even though atrophy is its most common cause.

Transvaginal ultrasoundendometrial thickness ≤4 mm makes cancer very unlikely
Endometrial biopsyif thickness >4 mm, bleeding persists, or the patient is high risk; biopsy is the definitive test
Hysteroscopy with D&Cif biopsy is nondiagnostic or bleeding continues despite a benign result

Hyperplasia. Endometrial hyperplasia with atypia (endometrial intraepithelial neoplasia) is precancerous, driven by unopposed estrogen: manage with hysterectomy or, to preserve fertility, high-dose progestin (oral or levonorgestrel IUD) with surveillance biopsies. Hyperplasia without atypia is treated with progestins.

Ovarian cancer and tumor markers

The silent presentation. Ovarian cancer presents late with vague symptoms—bloating, early satiety, pelvic or abdominal pain, and urinary frequency—so most cases are found after peritoneal spread. Epithelial (serous) tumors are most common. Risk rises with BRCA1/2 mutations, family history, Lynch syndrome, nulliparity, and age; oral contraceptives, pregnancy, breastfeeding, and tubal ligation or salpingectomy are protective.

A postmenopausal woman with new persistent bloating and a pelvic mass has ovarian cancer until proven otherwise—refer to a gynecologic oncologist for surgical staging.

CA-125 aids evaluation and monitoring of epithelial ovarian cancer but is nonspecific, rising with endometriosis, fibroids, and PID, especially before menopause. Evaluate a pelvic mass with transvaginal ultrasound and CA-125. There is no effective general-population screening; diagnosis and staging are surgical, followed by platinum-taxane chemotherapy. BRCA carriers are offered risk-reducing salpingo-oophorectomy after childbearing.

Non-epithelial ovarian tumor markers

Tumor	Marker	Clue
Dysgerminoma	LDH	Most common malignant germ cell tumor
Yolk sac (endodermal sinus) tumor	AFP	Aggressive; Schiller-Duval bodies
Choriocarcinoma	β-hCG	Early hematogenous spread
Granulosa cell tumor	Inhibin, estrogen	Precocious puberty or postmenopausal bleeding via endometrial stimulation

Germ cell tumors affect girls and young women; adult granulosa cell tumors peak around menopause (the juvenile form causes precocious puberty).

Vulvar, vaginal, and breast evaluation

Vulvar squamous cell carcinoma affects postmenopausal women and arises from HPV or from lichen sclerosus (thin, white, itchy skin treated with high-potency topical steroids). It presents as pruritus, a plaque, or an ulcer. Any persistent or suspicious vulvar lesion warrants biopsy, not repeated empiric creams.

Vaginal clear-cell adenocarcinoma is the classic tumor of in-utero diethylstilbestrol (DES) exposure, along with cervical clear-cell adenocarcinoma. Most other vaginal cancers are squamous.

Breast mass: triple assessment. A dominant or suspicious mass is worked up with clinical exam, imaging (mammography and/or ultrasound; ultrasound first in women under 30), and biopsy (core needle)—not watchful waiting. A new hard, fixed, or irregular mass always needs tissue diagnosis. Average-risk screening mammography now begins at age 40.

A negative mammogram does not exclude cancer: biopsy any persistent dominant or suspicious mass.