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AQA A-Level Chemistry: Cisplatin as an Anticancer Drug — mark scheme explained

Machine-verifiedchecked against the AQA A-Level Chemistry specificationlast verified 3 July 2026

The short answer

Cisplatin, a platinum(II) complex, is widely used in the treatment of various cancers due to its ability to prevent DNA replication in cancer cells. Understanding how cisplatin works and why it can have adverse effects is crucial for appreciating the balance between the benefits and risks of such drugs.

The question

Explain how cisplatin prevents DNA replication in cancer cells.

[Paraphrased for study — not reproduced from any exam paper.]

5 marks

Mark scheme, decoded

How the examiner actually awards the marks on this topic.

Gradora's own decode of the marking approach — not the exam board's published mark scheme.

How marks are awarded

For mechanism questions, marks are typically awarded for correctly describing the ligand replacement reaction and the formation of covalent bonds with DNA. For adverse effects questions, marks are given for listing and explaining specific side effects. For evaluation questions, marks are awarded for a balanced discussion of benefits and risks, considering individualized treatment plans.

What the command words demand

Explain
Provide a detailed description of the concept, including relevant principles and relationships.
List
Enumerate specific items or effects without extensive explanation.
Discuss
Examine and interpret information to draw conclusions about the topic.
Evaluate
Assess the advantages and disadvantages of a particular approach or treatment.

Model answer

A full-mark response to the question above, worked through step by step.

Timing: Allocate approximately 5-7 minutes per question to ensure you have enough time to carefully read the problem, provide detailed explanations, and check your work.

  1. Identify the structure of cisplatin.0 marks
    Cisplatin has the formula [Pt(NH 3 ) 2 Cl 2 ] and is a platinum(II) complex with two ammonia ligands and two chloride ligands.
  2. Describe the mechanism of action.2 marks
    When cisplatin enters a cancer cell, it undergoes a ligand replacement reaction where the chloride ligands are replaced by nitrogen atoms from guanine bases in the DNA.
  3. Explain the formation of covalent bonds.2 marks
    This process forms covalent bonds between platinum and the nitrogen atoms of the guanine bases, leading to the formation of intrastrand cross-links.
  4. Describe the impact on DNA replication.1 mark
    These cross-links distort the DNA double helix, making it difficult for the replication machinery to read and copy the genetic information. As a result, DNA replication is halted, which ultimately leads to cell death through apoptosis.

Final answer: Cisplatin prevents DNA replication by forming covalent bonds with nitrogen atoms on guanine bases, leading to intrastrand cross-links that distort the DNA double helix and halt replication.

Work through every step correctly and you earn all 5 marks.

Another worked example

List and explain three common adverse effects of cisplatin.

4 marks
  1. Identify the first adverse effect.2 marks
    Nephrotoxicity (kidney damage): Cisplatin can cause kidney dysfunction, which is a major concern. Regular monitoring of renal function is essential during treatment.
  2. Identify the second adverse effect.1 mark
    Neurotoxicity (nerve damage): Patients may experience peripheral neuropathy, characterized by numbness, tingling, and pain in the extremities.
  3. Identify the third adverse effect.1 mark
    Hematotoxicity (blood cell reduction): Cisplatin can reduce the production of blood cells, leading to anemia, neutropenia, and thrombocytopenia.

Final answer: 1. Nephrotoxicity (kidney damage) - Regular monitoring of renal function is essential during treatment. 2. Neurotoxicity (nerve damage) - Patients may experience peripheral neuropathy. 3. Hematotoxicity (blood cell reduction) - Cisplatin can reduce the production of blood cells, leading to anemia, neutropenia, and thrombocytopenia.

Work through every step correctly and you earn all 4 marks.

Common mistakes

  • Misunderstanding the mechanism of DNA cross-linking by cisplatin.

    Why it happens: Students may not fully grasp how covalent bonds form between platinum and nitrogen atoms on guanine bases, leading to intrastrand cross-links.

    Fix: Review the ligand replacement reaction and the formation of covalent bonds in detail. Understand that these bonds distort the DNA double helix and halt replication.

  • Failing to recognize the importance of rapidly dividing cells.

    Why it happens: Students may not appreciate why rapidly dividing cells, including both cancer and normal cells, are more susceptible to cisplatin's effects.

    Fix: Emphasize that rapidly dividing cells are more dependent on DNA replication. Cisplatin's interference with this process is particularly effective in these cells.

  • Not fully explaining the adverse effects of cisplatin.

    Why it happens: Students may list only a few side effects or provide vague descriptions, leading to incomplete answers.

    Fix: Practice listing and explaining common adverse effects such as nephrotoxicity, neurotoxicity, hematotoxicity, and gastrointestinal issues. Provide clear and concise explanations for each effect.

  • Overlooking the balance between benefits and risks in treatment decisions.

    Why it happens: Students may focus solely on the therapeutic benefits or adverse effects without considering the broader context of individualized treatment plans.

    Fix: Discuss how healthcare providers weigh the benefits and risks to determine the most appropriate treatment plan for each patient. Consider factors such as cancer type, stage, overall health, and ability to tolerate side effects.

  • Confusing cisplatin with other platinum-based drugs.

    Why it happens: Students may mix up the structures and mechanisms of different platinum-based drugs, leading to incorrect answers.

    Fix: Review the specific structure and mechanism of cisplatin. Understand that while other platinum-based drugs like carboplatin have similar mechanisms, they differ in their structures and side effect profiles.

  • Failing to explain the role of ligand replacement reactions.

    Why it happens: Students may not fully understand how chloride ligands are replaced by nitrogen atoms from guanine bases, leading to DNA cross-linking.

    Fix: Practice explaining the ligand replacement reaction step-by-step. Emphasize that this process is crucial for cisplatin's mechanism of action.

Where the marks go

The question types you’ll meet on this topic and the marks each one carries — so you know what to expect and where to focus.

Question typeWhat you’re asked to doMarks
Cisplatin Mechanism Of ActionExplain how cisplatin binds to DNA and prevents replication in cancer cells.5
Adverse EffectsList and explain three common adverse effects of cisplatin drug treatment.4
Evaluate Cisplatin UseWeigh the medical benefits of cisplatin against its risks in a balanced discussion.6
Explain Cisplatin ActionExplain why fast-dividing cells are more affected by cisplatin's DNA-binding action.5
Describe Reaction MechanismExplain how cisplatin undergoes ligand replacement to form covalent bonds with DNA.4
Total across these question types24

Question types and mark tariffs are Gradora’s guidance based on how this topic is typically examined — not the board’s official paper structure.

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