Anticancer Drugs Practice Questions

Q: A 70-year-old male presented with lumps felt in the axilla. On examination, axillary lymphadenopathy was noted. Biopsy was planned with the following histopathological examination. No Reed-Sternberg cells were seen. Flow cytometry revealed CD15 and CD30 negative. Following the histopathological confirmation of the disease, the patient was started on a chemotherapy regimen. After a few days, the patient developed dysuria. Which drug could have been supplemented to prevent hemorrhagic cystitis associated with the chemotherapy?

Mesna. ***Mesna*** - **Mesna** (2-mercaptoethane sulfonate sodium) is a chemoprotective agent used to prevent **hemorrhagic cystitis** caused by **cyclophosphamide** and **ifosfamide**. - In this case, the patient with non-Hodgkin lymphoma (CD15/CD30 negative, no Reed-Sternberg cells) was likely treated with a **cyclophosphamide-containing regimen** such as **CHOP** or **R-CHOP**. - Mesna works by **detoxifying acrolein**, a nephrotoxic and urotoxic metabolite of cyclophosphamide, in the urinary tract, thereby preventing bladder mucosal damage. *Acrolein* - **Acrolein** is the **toxic metabolite** of cyclophosphamide and ifosfamide that causes damage to the bladder lining, leading to hemorrhagic cystitis. - It is not a drug but the substance that needs to be neutralized by mesna. *Dexrazoxane* - **Dexrazoxane** is a cardioprotective agent used to prevent **anthracycline-induced cardiotoxicity**, specifically from drugs like **doxorubicin**. - It chelates iron and reduces oxidative damage to cardiomyocytes but does not prevent hemorrhagic cystitis. *Amifostine* - **Amifostine** is a cytoprotective agent used to reduce **cisplatin-induced nephrotoxicity** and **xerostomia** in patients undergoing radiation therapy for head and neck cancer. - It is not indicated for the prevention of hemorrhagic cystitis.

Q: Which of the following is an alkylating agent used in cancer treatment?

Chlorambucil. ***Chlorambucil*** - **Chlorambucil** is a classic example of an **alkylating agent** used in chemotherapy. - Alkylating agents work by forming **covalent bonds** with DNA, leading to DNA damage and ultimately cell death. - It is particularly used in chronic lymphocytic leukemia and lymphomas. *Actinomycin-D* - **Actinomycin-D** is an **antibiotic** that functions as an **intercalating agent**, inhibiting RNA synthesis. - It works by inserting itself between DNA base pairs, distorting the DNA structure and preventing transcription. *5-Fluorouracil* - **5-Fluorouracil (5-FU)** is an **antimetabolite**, specifically a pyrimidine analog. - It interferes with DNA synthesis by mimicking **uracil** and inhibiting **thymidylate synthase**. *Vincristine* - **Vincristine** is a **vinca alkaloid**, a type of **microtubule inhibitor**. - It prevents the formation of the **mitotic spindle**, thereby arresting cells in metaphase and inhibiting cell division.

Q: What is the most important target of action of chlorambucil?

Lymphoid tissue. ***Lymphoid tissue*** - **Chlorambucil** is an **alkylating agent** primarily used in the treatment of various **lymphoproliferative disorders**. - Its main therapeutic effect is on rapidly proliferating cells, particularly those of **lymphoid origin**, such as in chronic lymphocytic leukemia (CLL) and other lymphomas. *Myeloid tissue* - While chlorambucil can have some effect on myeloid cells, it is not its primary or most important target; other drugs are more specifically used for **myeloproliferative disorders**. - Its use in conditions like chronic myeloid leukemia (CML) is limited and generally not first-line. *Neural tissue* - Chlorambucil is not primarily an agent targeting **neural tissue** and is not used in the treatment of neurological conditions. - It does not readily cross the **blood-brain barrier** to a significant extent, limiting its direct action on the central nervous system. *Skin* - Although some **lymphomas** can manifest with **cutaneous involvement**, chlorambucil's direct and most important target is not the skin itself but rather the underlying **lymphoid cells**. - It is not a primary treatment for general skin conditions or non-lymphomatous skin cancers.

Q: Which of the following is not a known adverse effect of tamoxifen used in breast cancer treatment?

Carcinoma in the contralateral breast. ***Carcinoma in the contralateral breast*** - Tamoxifen, a **selective estrogen receptor modulator (SERM)**, actually **reduces the risk** of new primary breast cancer in the contralateral breast. - This protective effect is one of the significant benefits of tamoxifen in high-risk women and those with a history of breast cancer. *Nausea and vomiting* - While tamoxifen is generally well-tolerated, **gastrointestinal side effects** like nausea and vomiting can occur, though typically mild compared to chemotherapy. - These side effects are often manageable and tend to diminish over time. *Endometrial carcinoma* - Tamoxifen acts as an **estrogen agonist** in the uterus, increasing the risk of **endometrial hyperplasia** and **endometrial carcinoma**. - This is a significant, well-documented adverse effect requiring regular monitoring, especially in postmenopausal women. *Cataract* - Tamoxifen has been linked to an increased risk of developing **cataracts**, particularly in long-term users. - The mechanism is not fully understood, but it is considered a known ocular side effect.

Q: Imatinib primarily acts by inhibiting which specific target?

BCR–ABL tyrosine kinase. ***BCR–ABL tyrosine kinase*** - Imatinib mesylate is a **specific inhibitor** of the **BCR–ABL tyrosine kinase**, which is the constitutively active oncoprotein found in **chronic myeloid leukemia (CML)**. - Its action involves binding to the ATP-binding site of the kinase domain, thus preventing the **phosphorylation** of downstream substrates required for cell proliferation and survival. *Tyrosine Kinase* - While Imatinib is a **tyrosine kinase inhibitor**, this option is too general as there are many different tyrosine kinases. - The question asks for the **specific target** of Imatinib, which is the BCR-ABL fusion protein's tyrosine kinase activity. *PDGFR* - Imatinib does inhibit **PDGFR (Platelet-Derived Growth Factor Receptor)** tyrosine kinases, which is relevant in some other conditions like gastrointestinal stromal tumors. - However, its primary and most historically significant target, especially in the context of CML that this class of question usually refers to, is the **BCR-ABL fusion protein**. *None of the options* - This option is incorrect because **BCR–ABL tyrosine kinase** is the correct and specific target. - Imatinib's designation as a **tyrosine kinase inhibitor** is due to its action on this specific enzyme.

Q: Which of the following drugs is MOST classically associated with hypomagnesemia?

Cisplatin. ***Cisplatin*** - **Cisplatin** is a platinum-based chemotherapy drug **most classically and severely** associated with **hypomagnesemia** due to **direct renal tubular damage** - Causes significant **magnesium wasting** in the urine through damage to the distal convoluted tubule - This **renal magnesium loss** is a common and often **dose-limiting side effect** of cisplatin therapy - Can persist for **months to years** after treatment and may be **irreversible** *Valproate* - **Valproate** is primarily associated with hepatotoxicity, hyperammonemia, pancreatitis, and teratogenicity - **Not associated** with hypomagnesemia - Its mechanism involves enhancing GABAergic transmission with limited direct renal effects on electrolyte balance *Foscarnet* - **Foscarnet** is an antiviral agent that can cause multiple electrolyte abnormalities including hypocalcemia, hypomagnesemia, and hypokalemia - However, it is **more characteristically associated with hypocalcemia** rather than hypomagnesemia - Works by inhibiting viral DNA polymerase and can chelate divalent cations *Cetuximab* - **Cetuximab**, an EGFR inhibitor, does cause **hypomagnesemia** through increased renal excretion of magnesium (occurs in 10-15% of patients) - However, **cisplatin** is the **more classic and severe** cause due to: - Direct nephrotoxic tubular damage (vs. EGFR-mediated mechanism) - Higher incidence and severity of hypomagnesemia - Longer duration and potential irreversibility - More established in medical literature as the prototypical drug causing this side effect

Q: Bleomycin toxicity affects which organ predominantly?

Lungs. ***Lungs*** - **Bleomycin** is well-known for causing **pulmonary fibrosis**, an irreversible scarring of the lungs, as its most significant and dose-limiting toxicity. - This toxicity is thought to be due to an inability of the lungs to adequately inactivate bleomycin, leading to oxidative damage. *Bone marrow* - While many chemotherapeutic agents cause **bone marrow suppression**, bleomycin is notable for causing **minimal myelosuppression** compared to other cytotoxic drugs. - Therefore, bone marrow is not the predominantly affected organ for toxicity with bleomycin. *Liver* - **Hepatotoxicity** (liver damage) can occur with some chemotherapy agents, but it is **not a primary or prominent toxicity associated with bleomycin**. - Other drugs are much more frequently associated with liver damage. *RBC* - Bleomycin does not directly target **red blood cells (RBCs)** for toxicity. - While severe bone marrow suppression from other drugs can lead to anemia, bleomycin's effect on RBCs is indirect and not its predominant toxicity profile.

Q: Hand foot syndrome is an adverse effect of what?

5-Fluorouracil. ***5-Fluorouracil*** - **Hand-foot syndrome** (**palmar-plantar erythrodysesthesia**) is a common and dose-limiting side effect of 5-Fluorouracil and its prodrug, capecitabine. - It presents with **redness**, **swelling**, **pain**, and **desquamation** of the palms and soles. *Bleomycin* - The primary dose-limiting toxicity of bleomycin is **pulmonary fibrosis**, not hand-foot syndrome. - Other common toxicities include **hyperpigmentation** of the skin and mucocutaneous reactions, but not typically severe palmar-plantar changes. *Etoposide* - Etoposide is associated with adverse effects like **myelosuppression** (leukopenia, thrombocytopenia) and **alopecia**. - While skin reactions can occur, **hand-foot syndrome** is not a characteristic or common side effect of etoposide. *Actinomycin D* - Actinomycin D (dactinomycin) is known for causing **myelosuppression**, **nausea**, **vomiting**, and **mucositis**. - It can also cause **radiation recall phenomenon**, but not typically hand-foot syndrome as a primary or common adverse effect.

Q: What is the mechanism of action of fulvestrant?

Selective estrogen receptor downregulator. ***Selective estrogen receptor downregulator*** - Fulvestrant is classified as a **selective estrogen receptor downregulator (SERD)**. It binds to the estrogen receptor (ER) and promotes its degradation. - This effectively reduces the total number of ERs in the cell nucleus, leading to a profound anti-estrogenic effect without agonist activity. *Selective estrogen agonist* - An estrogen agonist would **activate estrogen receptors**, mimicking the effects of estrogen, which is not the therapeutic goal of fulvestrant in hormone-sensitive cancers. - Such a drug would promote tumor growth in estrogen-sensitive breast cancers. *Selective estrogen receptor modulator* - A selective estrogen receptor modulator (SERM) exhibits **tissue-specific agonist and antagonist effects** (e.g., tamoxifen acts as an antagonist in breast tissue but an agonist in bone). - Fulvestrant, in contrast, is a pure antagonist with no agonist activity and causes receptor degradation. *Selective estrogen receptor upregulator* - An upregulator would **increase the number of estrogen receptors**, potentially making cancer cells more sensitive to estrogen and promoting growth. - This mechanism is contrary to the therapeutic action of fulvestrant, which aims to reduce ER signaling.

Q: Which GnRH agonist is approved for advanced prostate cancer?

Goserelin. ***Goserelin*** - **Goserelin** is a **gonadotropin-releasing hormone (GnRH) agonist** approved for the treatment of **advanced prostate cancer**. - It works by initially stimulating, then desensitizing, the pituitary gland to GnRH, leading to a profound decrease in **luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)**, which in turn reduces **testosterone production**. - This sustained suppression of testosterone is effective in managing hormone-sensitive prostate cancer. *Abarelix* - **Abarelix** is a **GnRH antagonist** (not an agonist), which directly blocks GnRH receptors. - While it was approved for advanced prostate cancer, it works through a different mechanism (antagonism vs agonism) and was later withdrawn from the market. - It is not a GnRH agonist. *Cetrorelix* - **Cetrorelix** is a **GnRH antagonist** (not an agonist) primarily used in **assisted reproductive technology (ART)** to prevent premature ovulation. - It is not approved for the treatment of prostate cancer. *Ganirelix* - **Ganirelix** is a **GnRH antagonist** (not an agonist) also used in **assisted reproductive technology (ART)** to prevent premature LH surges. - It is not approved for the treatment of prostate cancer.

Question 1

A 70-year-old male presented with lumps felt in the axilla. On examination, axillary lymphadenopathy was noted. Biopsy was planned with the following histopathological examination. No Reed-Sternberg cells were seen. Flow cytometry revealed CD15 and CD30 negative. Following the histopathological confirmation of the disease, the patient was started on a chemotherapy regimen. After a few days, the patient developed dysuria. Which drug could have been supplemented to prevent hemorrhagic cystitis associated with the chemotherapy?

Accepted Answer

Mesna

Answer

Acrolein

Answer

Dexrazoxane

Answer

Amifostine

Question 2

Which of the following is an alkylating agent used in cancer treatment?

Accepted Answer

Chlorambucil

Answer

Actinomycin-D

Answer

5-Fluorouracil

Answer

Vincristine

Question 3

What is the most important target of action of chlorambucil?

Accepted Answer

Lymphoid tissue

Answer

Myeloid tissue

Answer

Neural tissue

Answer

Skin

Question 4

Which of the following is not a known adverse effect of tamoxifen used in breast cancer treatment?

Accepted Answer

Carcinoma in the contralateral breast

Answer

Nausea and vomiting

Answer

Endometrial carcinoma

Answer

Cataract

Question 5

Imatinib primarily acts by inhibiting which specific target?

Accepted Answer

BCR–ABL tyrosine kinase

Answer

Tyrosine Kinase

Answer

PDGFR

Answer

None of the options

Question 6

Which of the following drugs is MOST classically associated with hypomagnesemia?

Accepted Answer

Cisplatin

Answer

Valproate

Answer

Foscarnet

Answer

Cetuximab

Question 7

Bleomycin toxicity affects which organ predominantly?

Accepted Answer

Lungs

Answer

Bone marrow

Answer

Liver

Answer

RBC

Question 8

Hand foot syndrome is an adverse effect of what?

Accepted Answer

5-Fluorouracil

Answer

Bleomycin

Answer

Etoposide

Answer

Actinomycin D

Question 9

What is the mechanism of action of fulvestrant?

Accepted Answer

Selective estrogen receptor downregulator

Answer

Selective estrogen agonist

Answer

Selective estrogen receptor modulator

Answer

Selective estrogen receptor upregulator

Question 10

Which GnRH agonist is approved for advanced prostate cancer?

Accepted Answer

Goserelin

Answer

Abarelix

Answer

Cetrorelix

Answer

Ganirelix

Anticancer Drugs — MCQs

Anticancer Drugs — MCQs

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