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Cancer Genetics: Oncogenes & Tumour Suppressors — MRCP Part 1 Exam Classics

TL;DR

Cancer genetics is a high-yield MRCP Part 1 topic that repeatedly tests whether you can distinguish oncogenes from tumour suppressor genes. The exam focuses on mechanisms (gain vs loss of function), inheritance patterns, and classic gene–cancer associations. Mastering these principles prevents common traps and secures straightforward marks.


Why this topic matters in MRCP Part 1

Cancer genetics underpins questions across oncology, haematology, endocrinology, and even general medicine. MRCP Part 1 rarely asks for laboratory techniques or experimental pathways; instead, it tests whether you understand how genetic alterations drive malignant transformation and how those mechanisms translate into clinical patterns.

Most candidates lose marks not because the topic is obscure, but because they confuse oncogenes with tumour suppressor genes, particularly when inheritance and allele number are tested together.

For the wider exam framework, see the official MRCP(UK) examination overview:https://www.mrcpuk.org/mrcpuk-examinations/part-1


Scope of cancer genetics you are expected to know

For MRCP Part 1, the examinable scope is deliberately limited and principle-based:

  • Definitions and core differences

  • Gain-of-function vs loss-of-function mutations

  • One-hit vs two-hit models

  • Key examples and their associated malignancies

  • Basic cell-cycle checkpoints and DNA repair concepts

You are not expected to memorise detailed signalling cascades or molecular assays.


Oncogenes vs tumour suppressor genes: the essential contrasts

1. Mechanism of action

  • Oncogenes: Gain of function. A proto-oncogene becomes constitutively active.

  • Tumour suppressor genes: Loss of function. Normal growth-inhibitory control is removed.

2. Number of alleles required

  • Oncogenes: One mutated allele is sufficient to drive abnormal proliferation.

  • Tumour suppressor genes: Both alleles must be inactivated (Knudson’s two-hit hypothesis).

3. Inheritance pattern

  • Oncogenes: Typically sporadic mutations.

  • Tumour suppressor genes: Often inherited in an autosomal dominant pattern, but with recessive behaviour at the cellular level.

4. Normal physiological role

  • Oncogenes: Promote cell growth, division, or survival.

  • Tumour suppressors: Restrain the cell cycle, repair DNA, or trigger apoptosis.


High-yield comparison table

Feature

Oncogenes

Tumour suppressor genes

Normal role

Stimulate controlled growth

Inhibit growth / repair DNA

Mutation effect

Gain of function

Loss of function

Alleles needed

One

Two

Typical inheritance

Sporadic

Often inherited (AD clinically)

Classic examples

RAS, MYC

TP53, RB1, APC

This table alone accounts for a large proportion of MRCP Part 1 genetics marks.

The five most tested cancer genetics subtopics

  1. RAS oncogene activation Constitutive signalling independent of growth factors.

  2. TP53 (“guardian of the genome”)Causes G1/S arrest and promotes DNA repair or apoptosis after damage.

  3. RB gene and cell-cycle control Loss leads to unchecked transition from G1 to S phase.

  4. APC gene and colorectal cancer Dysregulation of β-catenin signalling and adenoma formation.

  5. BRCA1/BRCA2 and DNA repair Defective homologous recombination with increased breast and ovarian cancer risk.

These topics frequently appear as single best answer (SBA) questions.


Medical student revising cancer genetics concepts for MRCP Part 1 examination.

Mini-case (MRCP-style SBA)

Question: A 30-year-old man has a family history of early-onset colorectal cancer. Genetic testing reveals a germline mutation in a gene responsible for regulating β-catenin levels. Which statement best explains how cancer develops in this condition?

Correct answer: Both alleles of a tumour suppressor gene must be inactivated.

Explanation: This describes an APC mutation. Although the condition is inherited in an autosomal dominant manner, malignant transformation requires a second somatic hit. MRCP Part 1 commonly tests this distinction between clinical inheritance and cellular behaviour.

For structured practice on similar questions, use a dedicated MRCP question bank such as:https://www.passmedicine.com/mrcporhttps://www.onexamination.com/mrcp-part-1


Five common exam traps to avoid

  • Assuming autosomal dominant inheritance means one mutated allele is sufficient at the cellular level

  • Confusing oncogenes and tumour suppressors based only on cancer association

  • Forgetting that TP53 primarily causes cell-cycle arrest before apoptosis

  • Mixing up DNA repair genes with checkpoint regulators

  • Over-interpreting molecular detail not required by the question stem


Practical study-tip checklist

  • Classify the gene first: oncogene or tumour suppressor

  • Decide whether the mutation causes gain or loss of function

  • Ask how many alleles must be affected

  • Link each gene to one classic cancer association

  • Practise timed SBAs to reinforce pattern recognition

Short, repeated revision is far more effective than reading advanced molecular texts.


FAQs (People Also Ask)

What is the key difference between oncogenes and tumour suppressor genes?

Oncogenes act through gain of function and require only one mutated allele, whereas tumour suppressor genes require loss of both alleles.

Are tumour suppressor gene disorders autosomal recessive?

Clinically they appear autosomal dominant, but at the cellular level both alleles must be inactivated.

Is detailed molecular genetics examined in MRCP Part 1?

No. The exam focuses on mechanisms, inheritance patterns, and classic associations.

How frequently is cancer genetics tested in MRCP Part 1?

It appears regularly, often integrated into oncology and general medicine questions.


Ready to start?

Consolidate this topic by answering timed SBAs and reviewing explanations. Use the MRCP Part 1 overview to place cancer genetics within your wider revision plan, and reinforce learning through targeted practice in the question bank or structured lectures.


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