Gynecologic Oncology — MCQs

Gynecologic Oncology Indian Medical PG Practice Questions and MCQs

Question 131: What percentage of atypical endometrial hyperplasia undergoes malignant transformation?

A. 10%
B. 25% (Correct Answer)
C. 45%
D. 70%

Explanation: **Explanation:** The risk of malignant transformation in endometrial hyperplasia is primarily determined by the presence of **cellular atypia**. This concept is classically based on **Kurman’s classification**, which categorizes the risk of progression to endometrial carcinoma over a period of approximately 10–20 years. * **Correct Answer (B): 25%.** Atypical endometrial hyperplasia (specifically complex atypical hyperplasia) carries a significant risk of progression to malignancy. Studies show that approximately **25–29%** of these cases will transition to invasive adenocarcinoma if left untreated. Furthermore, in clinical practice, up to 40% of patients diagnosed with atypical hyperplasia on biopsy are found to have a coexisting "concurrent" carcinoma in the final hysterectomy specimen. **Analysis of Incorrect Options:** * **A (10%):** This is closer to the risk associated with **Complex Hyperplasia without atypia** (approx. 3–8%). * **C & D (45% & 70%):** These values are significantly higher than the established longitudinal progression rates for atypical hyperplasia. While the risk is high, it does not reach these levels unless considering specific high-risk genetic syndromes (like Lynch Syndrome) over a lifetime. **NEET-PG High-Yield Pearls:** 1. **Progression Risks (Kurman’s Criteria):** * Simple Hyperplasia (no atypia): **1%** * Complex Hyperplasia (no atypia): **3%** * Simple Atypical Hyperplasia: **8%** * Complex Atypical Hyperplasia: **29% (often rounded to 25-30%)** 2. **Management:** The gold standard treatment for atypical hyperplasia in postmenopausal women or those who have completed childbearing is **Total Laparoscopic/Abdominal Hysterectomy**. 3. **WHO 2014 Classification:** Modern pathology now simplifies this into two categories: *Hyperplasia without atypia* and *Atypical Hyperplasia/Endometrioid Intraepithelial Neoplasia (EIN)*.

Question 132: Which of the following statements regarding neoplasms of the ovary is false?

A. Stromal invasion is commonly present in ovarian tumors of borderline malignancy. (Correct Answer)
B. Lymphocytic infiltration is characteristic of dysgerminoma.
C. The presence of ascites and pleural effusion in a Brenner tumor indicates a poor prognosis.
D. Endometrioid carcinoma of the ovary may coexist with endometrial adenocarcinoma.

Explanation: **Explanation:** **1. Why Option A is the Correct (False) Statement:** The hallmark of **Borderline Ovarian Tumors (BOTs)**, also known as tumors of low malignant potential, is the **absence of destructive stromal invasion**. While these tumors exhibit features of malignancy such as cellular atypia, stratification, and increased mitotic activity, they lack the ability to invade the underlying stroma. If stromal invasion is present, the tumor is classified as a frank carcinoma rather than borderline. **2. Analysis of Other Options:** * **Option B:** Dysgerminoma is the most common germ cell tumor. Histologically, it consists of nests of large, clear cells separated by fibrous septa. These septa are characteristically **infiltrated by lymphocytes** (and sometimes granulomas), which is a key diagnostic feature. * **Option C:** Brenner tumors are usually benign. However, like fibromas, they can be associated with **Meigs’ Syndrome** (ascites and pleural effusion). In the context of benign ovarian tumors, these findings do not signify metastasis or a poor prognosis; they typically resolve after surgical removal of the tumor. * **Option D:** Approximately 15–20% of patients with **Endometrioid Ovarian Carcinoma** have a synchronous primary **Endometrial Adenocarcinoma**. This is often due to the "field effect" of the Mullerian system rather than metastasis. **Clinical Pearls for NEET-PG:** * **Psammoma bodies** are most commonly seen in Serous Cystadenocarcinoma. * **Call-Exner bodies** are pathognomonic for Granulosa Cell Tumors. * **Schiller-Duval bodies** are the hallmark of Yolk Sac Tumors (Endodermal Sinus Tumors). * **Reinke Crystals** are found in Leydig Cell Tumors. * **LDH** is the most specific tumor marker for Dysgerminoma.

Question 133: All of the following are recommendations for screening of Lynch syndrome in women with endometrial cancer except?

A. Evidence of microsatellite instability
B. DNA mismatch repair protein loss
C. Endometrial cancer before 60 years of age (Correct Answer)
D. First or second-degree relative with known DNA mismatch repair gene mutation

Explanation: **Explanation:** Lynch syndrome (Hereditary Non-Polyposis Colorectal Cancer - HNPCC) is the most common inherited cause of endometrial cancer. Current clinical guidelines (ACOG and SGO) recommend **universal screening** for Lynch syndrome in all women diagnosed with endometrial cancer, regardless of age. **1. Why Option C is the correct answer (The Exception):** The age threshold for screening has evolved. While older criteria (like the Bethesda criteria) used age cut-offs, modern guidelines advocate for universal screening of **all** endometrial cancer patients. If an age-based criterion were to be used in specific risk-stratification models, the traditional cut-off was **50 years**, not 60. Therefore, "Endometrial cancer before 60 years" is not a standard recommendation for initiating a Lynch syndrome workup. **2. Analysis of Incorrect Options:** * **Option A & B:** These are the primary screening modalities. Immunohistochemistry (IHC) for **DNA mismatch repair (MMR) protein loss** (MLH1, MSH2, MSH6, PMS2) or PCR for **Microsatellite Instability (MSI)** are the first-line tests performed on the tumor tissue to identify potential Lynch syndrome. * **Option D:** A known family history of a germline MMR mutation in a first or second-degree relative is a definitive indication for genetic counseling and testing, as Lynch syndrome follows an **autosomal dominant** inheritance pattern. **High-Yield Clinical Pearls for NEET-PG:** * **Lifetime Risk:** Women with Lynch syndrome have a 40–60% lifetime risk of both endometrial and colon cancer. In many cases, endometrial cancer is the **sentinel (first) cancer**. * **Screening:** Annual endometrial biopsy is recommended starting at age 30–35 for known carriers. * **Prophylaxis:** Prophylactic Total Laparoscopic Hysterectomy with Bilateral Salpingo-Oophorectomy (TLH+BSO) is recommended by age 40 or after childbearing is complete. * **Most common gene:** *MSH2* and *MLH1* are most frequently involved.

Question 134: Which of the following lymph nodes are typically NOT involved in cervical cancer?

A. Para-aortic lymph nodes
B. Obturator lymph nodes
C. Hypogastric lymph nodes
D. Femoral lymph nodes (Correct Answer)

Explanation: **Explanation:** The lymphatic drainage of the cervix follows a predictable, stepwise pattern through the pelvic and abdominal lymphatics. Understanding this hierarchy is crucial for staging and surgical management in cervical cancer. **Why Femoral Lymph Nodes are the Correct Answer:** Femoral (superficial inguinal) lymph nodes primarily drain the **vulva, lower third of the vagina, and the skin of the perineum**. They are not part of the primary or secondary lymphatic drainage pathway for the cervix. Involvement of femoral nodes in cervical cancer would be highly atypical and would only occur in cases of massive retrograde lymphatic blockage or direct extension to the lower vagina. **Analysis of Incorrect Options:** * **Obturator Lymph Nodes:** These are considered the **primary (sentinel) nodes** for cervical cancer. They are usually the first group to be involved. * **Hypogastric (Internal Iliac) Lymph Nodes:** Along with the external iliac nodes, these form the primary drainage group for the cervix. * **Para-aortic Lymph Nodes:** These represent the **secondary drainage** pathway. Cancer spreads from the pelvic nodes (common iliac) to the para-aortic nodes. Involvement of these nodes signifies Stage IIIC2 disease in the FIGO 2018 classification. **NEET-PG High-Yield Pearls:** * **Most common site of lymph node metastasis:** Obturator nodes. * **Order of Spread:** Obturator → External/Internal Iliac → Common Iliac → Para-aortic. * **FIGO 2018 Update:** The presence of lymph node metastasis now classifies the disease as **Stage IIIC** (IIIC1 for pelvic nodes, IIIC2 for para-aortic nodes). * **Ureters:** The most common cause of death in cervical cancer is uremia due to ureteric obstruction by local spread or lymphadenopathy.

Question 135: Features considered under Reid colposcopic index are all except?

A. Margin
B. Color
C. Vessels
D. Floor (Correct Answer)

Explanation: The **Reid Colposcopic Index (RCI)** is a standardized scoring system used to predict the histological severity of cervical intraepithelial neoplasia (CIN) based on colposcopic findings. It assigns a score of 0, 1, or 2 to four specific criteria. ### Why "Floor" is the Correct Answer The **Floor** of a lesion is not a component of the Reid Colposcopic Index. While the characteristics of the base of an ulcer or lesion are important in general surgical pathology, they are not part of this specific scoring system used to grade cervical dysplasia. ### Explanation of Incorrect Options (Components of RCI) The RCI evaluates the following four features: 1. **Margin (A):** Evaluates the border and surface. Faint, feathered, or geographic borders score 0; sharp, straight borders score 1; and "peeling" or "rolled" edges score 2. 2. **Color (B):** Assesses the shade of acetowhite change. Shiny, translucent white scores 0; intermediate/dull white scores 1; and distinct, "oyster-gray" or thick opaque white scores 2. 3. **Vessels (C):** Evaluates vascular patterns. Fine punctation or mosaicism scores 0; absent vessels score 1; and coarse punctation or coarse mosaicism scores 2. 4. **Iodine Staining:** (Not listed in options but the 4th component). Mahogany brown staining (Schiller negative) scores 0; variegated/speckled staining scores 1; and mustard yellow (Schiller positive) scores 2. ### High-Yield Clinical Pearls for NEET-PG * **Total Score:** The RCI ranges from **0 to 8**. * **Interpretation:** * **0–2:** Likely Low-grade (CIN 1). * **3–5:** Intermediate (CIN 1 or 2). * **6–8:** Likely High-grade (CIN 2 or 3). * **Swede Score:** A similar system that includes a 5th parameter—**Lesion Size**. * **Atypical Vessels:** The presence of irregular, "comma-shaped," or "corkscrew" vessels is highly suggestive of invasive carcinoma rather than just CIN.

Question 136: Which of the following ovarian tumors cause masculinization?

A. Gynandroblastoma and Arrhenoblastoma (Correct Answer)
B. Gynandroblastoma
C. Arrhenoblastoma and Gonadoblastoma
D. Gynandroblastoma, Arrhenoblastoma, and Gonadoblastoma

Explanation: **Explanation:** The correct answer is **A: Gynandroblastoma and Arrhenoblastoma**. **1. Why Option A is Correct:** Masculinization (virilization) in ovarian tumors is caused by the excessive production of androgens (primarily testosterone). * **Arrhenoblastoma (Sertoli-Leydig Cell Tumor):** This is the most common virilizing ovarian tumor. It contains Leydig cells that secrete testosterone, leading to hirsutism, clitoromegaly, and deepening of the voice. * **Gynandroblastoma:** This is an extremely rare sex cord-stromal tumor that contains both male (Sertoli-Leydig) and female (Granulosa-Theca) cell components. Because it contains androgen-secreting elements, it frequently causes masculinization. **2. Why Other Options are Incorrect:** * **Gonadoblastoma (Options C & D):** While gonadoblastomas occur in dysgenetic gonads (like in Swyer syndrome) and are associated with a Y chromosome, the tumor itself is usually **hormonally inert**. Any virilization seen in these patients is typically due to the underlying gonadal dysgenesis or the presence of a co-existing malignant germ cell tumor (like a Dysgerminoma), rather than the gonadoblastoma itself producing androgens. * **Option B:** This is incomplete as it omits Arrhenoblastoma, the classic cause of virilization. **NEET-PG High-Yield Pearls:** * **Most common virilizing tumor:** Sertoli-Leydig Cell Tumor (Arrhenoblastoma). * **Tumor Marker:** Sertoli-Leydig tumors often show elevated **Testosterone** levels with low/normal DHEAS (DHEAS is an adrenal marker). * **Reinke’s Crystals:** Pathognomonic histological finding in **Hilus cell tumors** (another rare virilizing tumor). * **Meigs’ Syndrome:** Triad of Benign Ovarian Fibroma, Ascites, and Pleural Effusion.

Question 137: Which of the following human papillomavirus (HPV) types is most commonly associated with carcinoma of the cervix?

A. HPV 16 (Correct Answer)
B. HPV 18
C. HPV 33
D. HPV 35

Explanation: **Explanation:** **Correct Option: A (HPV 16)** Human Papillomavirus (HPV) is the primary etiological agent for cervical cancer. While over 15 high-risk HPV types are identified, **HPV 16** is the most oncogenic and prevalent. It is responsible for approximately **50-60%** of all cases of squamous cell carcinoma of the cervix globally. Its high oncogenicity is attributed to the E6 and E7 oncoproteins, which degrade the p53 and pRb tumor suppressor proteins, respectively, leading to uncontrolled cell cycle progression. **Incorrect Options:** * **B. HPV 18:** This is the second most common high-risk type, accounting for about 10-15% of cases. Notably, HPV 18 has a stronger association with **adenocarcinoma** of the cervix than HPV 16. * **C & D. HPV 33 and 35:** These are also classified as high-risk HPV types (along with 31, 45, 52, and 58), but they are significantly less common than types 16 and 18. Together, HPV 16 and 18 account for over 70% of all cervical cancer cases worldwide. **High-Yield Clinical Pearls for NEET-PG:** * **Most common type overall:** HPV 16 (Squamous cell carcinoma). * **Most common type in Adenocarcinoma:** HPV 18. * **Low-risk types:** HPV 6 and 11 (associated with Condyloma acuminatum/genital warts). * **Vaccination:** The Quadrivalent vaccine (Gardasil) covers types 6, 11, 16, and 18. The Nonavalent vaccine adds types 31, 33, 45, 52, and 58. * **Screening:** The primary screening tool is the Pap smear (cytology) or HPV DNA testing, starting at age 21 or 25-30 depending on guidelines.

Question 138: Carcinoma of the cervix is caused by which of the following viruses?

A. Herpes simplex virus type 1
B. Papillomavirus (Correct Answer)
C. Epstein-Barr virus
D. Adenovirus

Explanation: **Explanation:** **Human Papillomavirus (HPV)** is the primary causative agent of cervical carcinoma. It is a double-stranded DNA virus that infects the basal layer of the cervical epithelium. The oncogenic potential lies in the integration of viral DNA into the host genome, leading to the overexpression of oncoproteins **E6 and E7**. E6 degrades the **p53** tumor suppressor protein, while E7 inactivates the **Retinoblastoma (Rb)** protein, resulting in uncontrolled cell proliferation and malignant transformation. **Analysis of Incorrect Options:** * **A. Herpes Simplex Virus Type 1 (HSV-1):** Primarily causes orofacial lesions (cold sores). While HSV-2 was once investigated as a co-factor, it is not the primary cause of cervical cancer. * **C. Epstein-Barr Virus (EBV):** Associated with Burkitt lymphoma, Nasopharyngeal carcinoma, and Hodgkin lymphoma, but not cervical cancer. * **D. Adenovirus:** Typically causes respiratory infections, conjunctivitis, and gastroenteritis; it has no established link to human cervical malignancy. **High-Yield Clinical Pearls for NEET-PG:** * **High-risk HPV types:** 16 and 18 are responsible for ~70% of cervical cancers worldwide (Type 16 is the most common). * **Low-risk HPV types:** 6 and 11 cause genital warts (Condyloma acuminata) but rarely lead to cancer. * **Screening:** The Papanicolaou (Pap) smear identifies cytological changes (koilocytes), while HPV DNA testing detects the virus itself. * **Vaccination:** The Quadrivalent vaccine (Gardasil) targets types 6, 11, 16, and 18; the Nonavalent vaccine covers five additional high-risk types.

Question 139: What are the most common types of human papillomavirus (HPV) causing cervical cancer?

A. 16 and 18 (Correct Answer)
B. 1 and 33
C. 6 and 11
D. 2 and 14

Explanation: **Explanation:** Cervical cancer is primarily caused by persistent infection with **High-Risk Human Papillomavirus (hrHPV)**. Among the various oncogenic strains, **HPV 16 and 18** are the most significant, accounting for approximately **70% of all cervical cancer cases** worldwide. HPV 16 is the most common (linked to squamous cell carcinoma), while HPV 18 has a higher association with adenocarcinoma. These strains produce E6 and E7 oncoproteins, which inhibit the tumor suppressor proteins p53 and pRb, respectively, leading to uncontrolled cell proliferation. **Analysis of Options:** * **Option A (Correct):** HPV 16 and 18 are the primary high-risk types responsible for the majority of cervical malignancies. * **Option B:** While HPV 33 is a high-risk type, HPV 1 is associated with benign cutaneous warts (verruca plantaris). * **Option C:** HPV 6 and 11 are **Low-Risk types**. They cause approximately 90% of genital warts (Condyloma acuminata) and recurrent respiratory papillomatosis, but they do not typically cause cancer. * **Option D:** HPV 2 is associated with common skin warts (verruca vulgaris); HPV 14 is not a major clinical subtype in this context. **High-Yield Clinical Pearls for NEET-PG:** * **Most common HPV type in Cervical Cancer:** HPV 16. * **Most common HPV type in Adenocarcinoma:** HPV 18. * **HPV Vaccines:** The Quadrivalent vaccine (Gardasil) targets 6, 11, 16, and 18. The Nonavalent vaccine adds 31, 33, 45, 52, and 58. * **Screening:** The primary screening tool is the Pap smear (cytology) and hrHPV DNA testing. The transformation zone is the most common site for cervical carcinogenesis.

Question 140: All of the following statements are true for melanoma of the vulva EXCEPT?

A. It is the second most common vulvar cancer.
B. The most common site is the labia majora. (Correct Answer)
C. It may arise from a junctional nevus.
D. It has a poor prognosis.

Explanation: **Explanation:** Vulvar melanoma is a rare but aggressive malignancy, accounting for approximately 5–10% of all vulvar cancers. **Why Option B is the Correct Answer (The Exception):** The most common site for vulvar melanoma is the **clitoris or the labia minora**, not the labia majora. Unlike squamous cell carcinoma (SCC) of the vulva, which frequently involves the labia majora, melanomas have a predilection for the mucosal surfaces and midline structures of the vulva. **Analysis of Other Options:** * **Option A:** Squamous cell carcinoma is the most common vulvar cancer (approx. 90%), making **melanoma the second most common** primary vulvar malignancy. * **Option C:** While many arise de novo, vulvar melanomas can develop from pre-existing **junctional nevi**. Any pigmented lesion on the vulva in a postmenopausal woman should be viewed with suspicion and biopsied. * **Option D:** It has a **poor prognosis** compared to SCC. This is due to its high propensity for early hematogenous and lymphatic spread. The most important prognostic factor is the depth of invasion (Breslow’s thickness). **High-Yield Clinical Pearls for NEET-PG:** * **Staging:** Unlike SCC, which uses FIGO staging, vulvar melanoma is often staged using the **AJM/TNM system** (similar to cutaneous melanoma) or the **Breslow/Clark scale**. * **Appearance:** Often presents as a pigmented, raised, or ulcerated lesion (ABCDE criteria apply). * **Treatment:** Radical local excision with adequate margins (1–2 cm) is the primary treatment. Routine radical vulvectomy is no longer the standard. * **Sentinel Lymph Node Biopsy (SLNB):** Recommended for lesions >1 mm in thickness to assess nodal status.

Practice by Chapter

Cervical Cancer

Practice Questions

Endometrial Cancer

Practice Questions

Ovarian Cancer

Practice Questions

Vulvar and Vaginal Cancer

Practice Questions

Gestational Trophoblastic Disease

Practice Questions

Screening for Gynecologic Cancers

Practice Questions

Principles of Gynecologic Oncology Surgery

Practice Questions

Radiation Therapy in Gynecologic Malignancies

Practice Questions

Chemotherapy in Gynecologic Oncology

Practice Questions

Palliative Care in Gynecologic Oncology

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free