Tumour Suppressor Genes and Oncogenes

⏱️ 30 mins read 📖 Genetics 🎯 MLA Relevance: High

Cancer arises from genetic alterations in oncogenes (gain of function) and tumour suppressor genes (loss of function); Knudson's two-hit hypothesis explains retinoblastoma and other hereditary cancers.

📌 Learning Objectives

Describe the underlying mechanism of Tumour Suppressor Genes and Oncogenes.
Identify the key clinical features and complications of Tumour Suppressor Genes and Oncogenes.
Outline the appropriate investigations and management of Tumour Suppressor Genes and Oncogenes.
Discuss the implications for patients and families of Tumour Suppressor Genes and Oncogenes.

📋 Overview

Oncogenes (e.g. RAS, MYC, BCR-ABL) drive proliferation when constitutively activated. Tumour suppressors (e.g. TP53, RB1, APC, BRCA1) normally restrain growth and require biallelic loss in cancers.

🔬 Basic Science

Oncogenes (e.g. RAS, MYC, BCR-ABL) drive proliferation when constitutively activated. Tumour suppressors (e.g. TP53, RB1, APC, BRCA1) normally restrain growth and require biallelic loss in cancers.

🏥 Clinical Relevance

Targeted therapies inhibit specific oncogenic drivers (e.g. imatinib for BCR-ABL).

🧪 Investigations

Investigation depends on clinical context: relevant blood tests, imaging, and specific genetic or histopathological tests as appropriate. Refer to specialist services where indicated.

💊 Management

Management is condition-specific and typically multidisciplinary, combining medical therapy, surgical intervention where appropriate, supportive care, and family/genetic counselling.

Revision Resources – expand the sections below for high-yield notes, exam pearls, key facts and further reading.

🎯 MLA High-Yield Notes & Quick Revision ⌄

Common SBA themes: recognising the underlying mechanism, identifying classic clinical features, and choosing the first-line investigation or management step. Watch for inheritance pattern and characteristic associations.

oncogene tumour suppressor tp53 knudson two-hit hypothesis

Oncogenes act dominantly (gain of function); only one mutated allele is needed.
Tumour suppressor genes typically require biallelic inactivation (Knudson's two-hit).
TP53 is the most commonly mutated gene in human cancers ('guardian of the genome').
Retinoblastoma is the classical Knudson model.
Targeted therapies exploit oncogene addiction (e.g. imatinib for BCR-ABL).

⭐ Exam Pearls ⌄

⭐ High Yield

Oncogenes act dominantly (gain of function); only one mutated allele is needed.

Tumour suppressor genes typically require biallelic inactivation (Knudson's two-hit).

TP53 is the most commonly mutated gene in human cancers ('guardian of the genome').

Retinoblastoma is the classical Knudson model.

Targeted therapies exploit oncogene addiction (e.g. imatinib for BCR-ABL).

💡 Clinical Pearl

Oncogene: Targeted therapies inhibit specific oncogenic drivers (e.g. imatinib for BCR-ABL).

⚠️ Exam Tip — Common Mistakes

Confusing the mechanism of Tumour Suppressor Genes and Oncogenes with related conditions.

Missing classic clinical features of Tumour Suppressor Genes and Oncogenes in SBA stems.

Failing to consider Tumour Suppressor Genes and Oncogenes in the differential diagnosis.

🔑 Key Facts ⌄

Oncogenes act dominantly (gain of function); only one mutated allele is needed.

Tumour suppressor genes typically require biallelic inactivation (Knudson's two-hit).

TP53 is the most commonly mutated gene in human cancers ('guardian of the genome').

Retinoblastoma is the classical Knudson model.

Targeted therapies exploit oncogene addiction (e.g. imatinib for BCR-ABL).

🔗 Related Topics ⌄

📚 References ⌄

GMC MLA Content Map
NICE Clinical Knowledge Summaries
BMJ Best Practice

Further Resources

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