Chemotherapy in Gynecologic Oncology — MCQs
Which of the following drugs act by inhibiting DNA replication?
Which drug is most appropriate for reducing risk of ovarian cancer in a BRCA1 positive woman not planning for children?
Point A and point B Manchester locations are important for treatment of which cancer –
A patient with a malignancy is undergoing chemotherapy. The platelet counts were reduced after the previous cycle of chemotherapy. Which of the following drugs can be used to treat this patient?
Which anticancer drug is known to inhibit spindle formation during cell division?
Leucovorin is used for side effect reduction in which anticancer drug?
What is the mechanism of action of Bevacizumab?
KEYNOTE-189 trial for pembrolizumab is done for?
Which type of tumor is most amenable to chemotherapy?
An adolescent girl with stage 1a dysgerminoma is managed by:
Chemotherapy in Gynecologic Oncology Indian Medical PG Practice Questions and MCQs
Question 1: Which of the following drugs act by inhibiting DNA replication?
- A. Mitomycin C
- B. 6-Mercaptopurine (Correct Answer)
- C. Actinomycin D
- D. Asparaginase
Explanation: ***6-Mercaptopurine*** - This drug is a **purine analog** that acts as an **antimetabolite**, directly interfering with the **synthesis of purine nucleotides** required for DNA replication. - By inhibiting enzymes like **PRPP amidotransferase** and getting incorporated into DNA as a fraudulent nucleotide, it blocks the **de novo synthesis** pathway, preventing normal DNA replication. - This represents **direct inhibition of DNA synthesis** at the nucleotide building block level. *Mitomycin C* - This agent is an **alkylating agent** that **cross-links DNA** strands, causing DNA damage that prevents strand separation. - While it does prevent DNA replication, its mechanism is through **DNA damage and structural disruption** rather than inhibition of the DNA synthesis machinery itself. - It acts by damaging already-formed DNA rather than preventing new DNA synthesis. *Actinomycin D* - Actinomycin D is an **intercalating agent** that inserts itself between DNA base pairs, primarily **inhibiting RNA synthesis** by blocking RNA polymerase movement. - While it binds to DNA, its primary therapeutic action is on **transcription (RNA synthesis)**, not direct inhibition of DNA replication. *Asparaginase* - Asparaginase is an enzyme that **depletes asparagine** from the blood, which is an essential amino acid for certain cancer cells (e.g., leukemic cells). - Its mechanism is to starve cancer cells of asparagine, leading to **inhibition of protein synthesis**, not DNA replication.
Question 2: Which drug is most appropriate for reducing risk of ovarian cancer in a BRCA1 positive woman not planning for children?
- A. Gonadotropin-releasing hormone
- B. Oral contraceptive pills (Correct Answer)
- C. Tamoxifen
- D. Progesterone IUD
Explanation: ***Oral contraceptive pills*** **Oral contraceptive pills (OCPs)** are the most appropriate pharmacological intervention for **reducing ovarian cancer risk in BRCA1/2 carriers** who do not plan to have children. - OCPs **suppress ovulation**, and this reduction in ovulatory cycles is associated with a **~50% decrease in epithelial ovarian cancer risk** in BRCA mutation carriers - The protective effect increases with **longer duration of use** (5+ years provides maximum benefit) - This is a **well-established, evidence-based strategy** supported by multiple large cohort studies and meta-analyses - OCPs are recommended by major guidelines (NCCN, ACOG) for ovarian cancer risk reduction in this population prior to risk-reducing salpingo-oophorectomy *Gonadotropin-releasing hormone* **GnRH agonists or antagonists** are not recommended for long-term ovarian cancer prevention in BRCA carriers. - Primarily used for **infertility treatments, endometriosis management**, and uterine fibroid treatment through temporary ovarian suppression - **Not established as effective** for ovarian cancer risk reduction - **Not suitable for long-term use** due to significant side effects (bone loss, menopausal symptoms) - Lack of evidence supporting their role in cancer prevention *Tamoxifen* **Tamoxifen** is a **selective estrogen receptor modulator (SERM)** used for breast cancer prevention and treatment, not ovarian cancer prevention. - Effective for **reducing breast cancer risk** in high-risk women (including BRCA carriers) - **Does not reduce ovarian cancer risk** and has no protective effect against epithelial ovarian cancer - May **slightly increase endometrial cancer risk** (relative risk ~2-3) - Not indicated for ovarian cancer risk reduction *Progesterone IUD* A **levonorgestrel-releasing intrauterine device (IUD)** provides excellent contraception and manages heavy menstrual bleeding, but does not reduce ovarian cancer risk. - Acts **locally on the endometrium** with minimal systemic hormonal effects - **Does not reliably suppress ovulation** (only 5-15% of cycles are anovulatory) - **No established protective effect** against ovarian cancer - While useful for contraception and menstrual management, it lacks the ovulation suppression needed for cancer risk reduction
Question 3: Point A and point B Manchester locations are important for treatment of which cancer –
- A. Vagina
- B. Cervix (Correct Answer)
- C. Ovary
- D. Uterus
Explanation: ***Cervix*** - **Point A** and **Point B Manchester** locations are historical references used in **brachytherapy** for **cervical cancer**, defining critical dose points within the pelvis. - These points help guide the placement of radiation sources to ensure adequate tumor coverage while sparing surrounding healthy tissues. *Vagina* - While radiation therapy is used for vaginal cancer, the **Manchester system's Point A and B** are specifically defined for cervical anatomy, not primarily for vaginal tumors. - Different dosimetry systems or specific vaginal applicators are often used for vaginal brachytherapy. *Ovary* - Ovarian cancer is primarily treated with **surgery and chemotherapy**; external beam radiation is sometimes used, but brachytherapy with **Point A and B** is not a standard approach. - The anatomical location of the ovaries makes brachytherapy less suitable for delivering targeted, high-dose radiation compared to cervical cancer. *Uterus* - Endometrial (uterine) cancer treatment may involve brachytherapy, but it typically uses different applicators (e.g., **tandem and ovoids** or cylinders) and dose specifications that are distinct from the Manchester system's **Point A and B** for the cervix. - The geometry and treatment volumes for uterine brachytherapy are different due to the distinct anatomy and tumor spread patterns.
Question 4: A patient with a malignancy is undergoing chemotherapy. The platelet counts were reduced after the previous cycle of chemotherapy. Which of the following drugs can be used to treat this patient?
- A. Oprelvekin (IL-11) - stimulates platelet production (Correct Answer)
- B. Filgrastim - stimulates white blood cell production
- C. Amifostine - protects against chemotherapy toxicity
- D. Erythropoietin - stimulates red blood cell production
Explanation: ***Oprelvekin (IL-11) - stimulates platelet production*** - **Oprelvekin** is a recombinant interleukin-11 (IL-11) that directly stimulates the proliferation and maturation of **megakaryocytes**, leading to increased platelet production. - It is specifically indicated for the prevention of **severe thrombocytopenia** and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy. *Filgrastim - stimulates white blood cell production* - **Filgrastim** is a **granulocyte colony-stimulating factor (G-CSF)** that primarily acts on neutrophil precursors, promoting their proliferation and maturation. - It is used to prevent and treat **neutropenia** and reduce the incidence of febrile neutropenia, but it does not significantly affect platelet counts. *Amifostine - protects against chemotherapy toxicity* - **Amifostine** is a **cytoprotective agent** that reduces toxicities associated with chemotherapy and radiation by preferentially protecting non-malignant cells. - It does not directly stimulate blood cell production but rather acts as a **free radical scavenger** to mitigate damage from cytotoxic treatments. *Erythropoietin - stimulates red blood cell production* - **Erythropoietin** is a **hematopoietic growth factor** that specifically stimulates the production of **red blood cells** by promoting the proliferation and differentiation of erythroid progenitor cells. - It is used to treat **anemia**, particularly in patients with chronic kidney disease or those undergoing chemotherapy, but it has no role in managing thrombocytopenia.
Question 5: Which anticancer drug is known to inhibit spindle formation during cell division?
- A. Busulfan
- B. Vinca alkaloids (Correct Answer)
- C. 5-FU
- D. Methotrexate
Explanation: ***Vinca alkaloids*** - **Vinca alkaloids**, such as **vincristine** and **vinblastine**, bind to **tubulin** and prevent its polymerization into microtubules. - This action effectively **inhibits the formation of the mitotic spindle**, leading to metaphase arrest and ultimately cell death. *Busulfan* - **Busulfan** is an **alkylating agent** that **cross-links DNA**, thereby interfering with DNA replication and transcription. - Its primary mechanism is **DNA damage**, not direct inhibition of spindle formation. *5-FU* - **5-fluorouracil (5-FU)** is an **antimetabolite** that inhibits **thymidylate synthase**, thereby impairing DNA synthesis and repair. - It acts by **mimicking pyrimidine bases** and incorporating into DNA and RNA, leading to cellular dysfunction. *Methotrexate* - **Methotrexate** is an **antifolate** drug that inhibits **dihydrofolate reductase**, an enzyme crucial for the synthesis of purines and pyrimidines. - This enzyme inhibition leads to **impaired DNA and RNA synthesis**, impacting rapidly dividing cells.
Question 6: Leucovorin is used for side effect reduction in which anticancer drug?
- A. Cisplatin
- B. 5-FU
- C. Adriamycin
- D. Methotrexate (Correct Answer)
Explanation: ***Methotrexate*** - **Leucovorin rescue** is a critical adjunct therapy for **methotrexate** to prevent severe toxicity. - Methotrexate is a **folate antagonist**, and leucovorin (folinic acid) provides a reduced folate form that bypasses the blocked enzyme, restoring normal cellular function and protecting healthy cells. - This is true **"rescue therapy"** - leucovorin protects normal cells from methotrexate toxicity. *Cisplatin* - **Cisplatin** is a platinum-based chemotherapy drug primarily associated with **nephrotoxicity** and **ototoxicity**. - Its side effects are managed with **hydration, amifostine**, and antiemetics, not leucovorin. *5-FU* - **5-FU (5-fluorouracil)** is a pyrimidine analog that can cause severe **myelosuppression** and **gastrointestinal toxicity**. - While leucovorin is used WITH 5-FU (e.g., in colorectal cancer regimens), it serves to **enhance/potentiate** 5-FU's cytotoxic effect through biochemical modulation, NOT to rescue from toxicity. - This is the key distinction: leucovorin + 5-FU = **potentiation**; leucovorin + methotrexate = **rescue**. *Adriamycin* - **Adriamycin (doxorubicin)** is an **anthracycline antibiotic** known for causing **cardiotoxicity** and **myelosuppression**. - **Dexrazoxane** is used to prevent Adriamycin-induced cardiotoxicity, not leucovorin.
Question 7: What is the mechanism of action of Bevacizumab?
- A. Anti VEGF antibody (Correct Answer)
- B. Histone deacetylase inhibitor
- C. HER2 neu inhibitor
- D. Proteasome inhibitor
Explanation: ***Anti VEGF antibody*** - **Bevacizumab** is a **monoclonal antibody** that specifically targets and binds to vascular endothelial growth factor (VEGF). - By inhibiting VEGF, bevacizumab prevents the formation of new blood vessels (**angiogenesis**) that tumors need to grow and metastasize. *Histone deacetylase inhibitor* - **Histone deacetylase (HDAC) inhibitors** influence gene expression by modifying chromatin structure, leading to cell cycle arrest and apoptosis in cancer cells. - They are used in certain hematologic malignancies and solid tumors but do not directly interfere with angiogenesis. *Proteasome inhibitor* - **Proteasome inhibitors** like bortezomib block the action of proteasomes, leading to an accumulation of ubiquitinated proteins and induction of apoptosis in cancer cells. - This mechanism is distinct from blocking new blood vessel formation. *HER2 neu inhibitor* - **HER2 neu inhibitors** (e.g., trastuzumab) specifically target the HER2/neu receptor, which is overexpressed in certain breast and gastric cancers. - Their action primarily involves blocking growth signals transmitted through this receptor, not inhibiting VEGF or angiogenesis.
Question 8: KEYNOTE-189 trial for pembrolizumab is done for?
- A. Nivolumab with chemo given for NSCLC
- B. Only Pembrolizumab for NSCLC
- C. Pembrolizumab with chemo given for NSCLC (Correct Answer)
- D. Only nivolumab for NSCLC
Explanation: ***Pembrolizumab with chemo given for NSCLC*** - The **KEYNOTE-189 trial** investigated the efficacy of **pembrolizumab** in combination with chemotherapy as first-line treatment for **metastatic nonsquamous non-small cell lung cancer (NSCLC)**. - This trial demonstrated significant improvements in overall survival and progression-free survival, leading to the approval of pembrolizumab in this setting. *Nivolumab with chemo given for NSCLC* - **Nivolumab** is another PD-1 inhibitor, but studies specifically combining nivolumab with chemotherapy for NSCLC (e.g., CheckMate 227) are distinct from KEYNOTE-189. - While both drugs are used in NSCLC, their pivotal trials and specific combination regimens differ. *Only Pembrolizumab for NSCLC* - Although pembrolizumab monotherapy is approved for certain NSCLC patients with high PD-L1 expression, the **KEYNOTE-189 trial specifically focused on a combination approach** with chemotherapy. - Other KEYNOTE trials, like KEYNOTE-024, evaluated pembrolizumab monotherapy in NSCLC. *Only nivolumab for NSCLC* - **Nivolumab monotherapy** has been studied and approved for NSCLC, particularly in the second-line setting or for patients with high PD-L1 expression, but this was not the focus of the KEYNOTE-189 trial. - Trials like CheckMate 017 and 057 investigated nivolumab as a single agent in NSCLC.
Question 9: Which type of tumor is most amenable to chemotherapy?
- A. Choriocarcinoma (Correct Answer)
- B. Embryonal rhabdomyosarcoma
- C. Hepatocellular carcinoma
- D. Thyroid carcinoma
Explanation: ***Choriocarcinoma*** - **Choriocarcinoma** is highly sensitive to chemotherapy, often achieving **cure rates greater than 90%** even in metastatic settings, especially when treated with combination regimens such as EMA-CO. - Its rapid growth rate and high mitotic index make it particularly susceptible to **cytotoxic agents** that target rapidly dividing cells. *Embryonal rhabdomyosarcoma* - While treatable with chemotherapy, **rhabdomyosarcoma**, especially the embryonal subtype, typically requires a combination of **surgery, chemotherapy, and radiation**, and its response to chemotherapy alone is not as uniformly curative as choriocarcinoma. - The efficacy of chemotherapy is often dependent on the tumor's stage, location, and the completeness of surgical resection. *Hepatocellular carcinoma* - **Hepatocellular carcinoma (HCC)** is notoriously resistant to traditional systemic chemotherapy, with limited response rates and often requiring targeted therapies like sorafenib or lenvatinib. - Its management is primarily based on **surgical resection, liver transplantation**, or locoregional therapies such as **transarterial chemoembolization (TACE)** or radiofrequency ablation (RFA). *Thyroid carcinoma* - Most types of thyroid carcinoma, especially **differentiated thyroid cancers (papillary and follicular)**, are managed primarily with **surgery and radioactive iodine (RAI)** therapy, showing limited responsiveness to conventional chemotherapy. - Anaplastic thyroid carcinoma, while aggressive, also typically responds poorly to standard chemotherapy regimens, often requiring multimodal treatment.
Question 10: An adolescent girl with stage 1a dysgerminoma is managed by:
- A. Chemotherapy
- B. Bilateral salpingo-oophorectomy alone
- C. Total abdominal hysterectomy with unilateral salpingo-oophorectomy
- D. Unilateral salpingo-oophorectomy alone (Correct Answer)
Explanation: ***Unilateral salpingo-oophorectomy alone*** - For **stage 1a dysgerminoma**, which is confined to one ovary, **fertility-sparing surgery** with unilateral salpingo-oophorectomy is the standard treatment, especially in young patients. - This approach aims to preserve reproductive function while effectively treating the localized tumor, given the **high radiosensitivity** and **chemosensitivity** of dysgerminomas. *Chemotherapy* - While dysgerminomas are sensitive to chemotherapy, it is typically reserved for **advanced stages** (stage 1c or higher), **recurrent disease**, or cases with **residual disease** after surgery. - It is not the primary treatment for **stage 1a disease** when complete surgical resection is achievable, especially when fertility preservation is desired. *Bilateral salpingo-oophorectomy alone* - This procedure would remove both ovaries and fallopian tubes, leading to **sterility and premature menopause**. - It is an **over-treatment** for stage 1a dysgerminoma, as the disease is localized to one ovary, and it is not fertility-sparing. *Total abdominal hysterectomy with unilateral salpingo-oophorectomy* - This extensive surgery involves the removal of the uterus and one ovary/fallopian tube, rendering the patient **infertile**. - It is an **overly aggressive** approach for stage 1a dysgerminoma in an adolescent girl, as the uterus is not involved, and fertility preservation is a crucial consideration.
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