Risk Factors & Cancer (AQA A-Level Biology): Revision Notes
Risk Factors & Cancer
Understanding cancer risk factors
Cancer develops through complex interactions between our genes and environment. Risk factors are conditions or behaviours that increase the likelihood of developing cancer, though they do not guarantee it will occur.
Understanding risk factors helps us make informed decisions about our health and lifestyle choices. While we cannot control all risk factors, recognising which ones we can influence empowers us to reduce our overall cancer risk.
Risk factors fall into two main categories:
- Non-modifiable factors
- Modifiable lifestyle factors
Non-modifiable factors - beyond our control:
- Age: Cancer risk increases with age as mutations accumulate over time
- Genetic factors: Inherited gene variants that predispose individuals to cancer
Modifiable lifestyle factors - within our control:
- Smoking: The most preventable cause of cancer
- Diet: High-fat, low-fibre diets increase risk; diets rich in fruit and vegetables reduce risk
- Obesity: Being overweight increases cancer risk
- Physical activity: Regular exercise reduces risk for several cancer types
- Sunlight exposure: UV radiation increases skin cancer risk
How hormones can trigger cancer development
Oestrogen provides a clear example of how normal biological processes can lead to cancer when disrupted. Oestrogen functions by binding to specific genes and promoting their transcription. When these target genes control cell division and growth, continued oestrogen exposure can drive excessive cell proliferation.
How Oestrogen Triggers Cancer Development:
Step 1: Oestrogen binds to specific target genes in breast tissue
Step 2: This binding promotes transcription of genes that control cell division
Step 3: Continued oestrogen exposure leads to excessive cell proliferation
Step 4: Normal proto-oncogenes become activated oncogenes
Result: Uncontrolled cell growth and tumour formation
In breast tissue, oestrogen can cause proto-oncogenes to develop into oncogenes. Proto-oncogenes are normal genes that regulate cell division, but when mutated or overactivated, they become oncogenes that promote uncontrolled cell growth and tumour formation.
Smoking and cancer: the evidence
Historical context and epidemiological studies
Tobacco smoking represents one of the clearest examples of how scientific evidence established a causal link between lifestyle factors and cancer. Initially introduced to Britain in the 16th century, smoking was considered harmless until the mid-20th century.
Critical Epidemiological Findings:
The evidence against smoking is overwhelming and mathematically clear. These studies provided the foundation for understanding smoking as a major cancer risk factor.
Epidemiological studies revealed striking patterns:
- Regular smokers face three times higher risk of premature death compared to non-smokers
- Risk correlates directly with consumption: heavier smokers die earlier on average
- A person smoking 25 cigarettes daily has 25 times greater lung cancer risk than non-smokers
- Long-term smoking duration increases risk more significantly than daily amount
- Smokers who quit experience risk reduction over 10-15 years, approaching non-smoker levels
Experimental evidence
While epidemiological data showed correlations, experimental studies in the 1960s provided crucial evidence for causation. Scientists conducted controlled experiments using laboratory animals.
Experimental Design: Dogs and Cigarette Smoke
Method: Researchers exposed dogs to cigarette smoke through different methods - some inhaled filtered smoke while others received unfiltered exposure.
Results:
- Dogs breathing unfiltered smoke: developed pulmonary disease and early lung cancer signs
- Dogs inhaling filtered smoke: remained healthy
Conclusion: This provided direct experimental evidence for smoking's harmful effects
Further experiments analysed tobacco smoke components chemically. Each constituent was tested individually for its ability to damage epithelial cells and cause genetic mutations. These studies identified carcinogens - cancer-causing chemicals in tobacco tar.
Benzopyrene emerged as a key carcinogen. Laboratory studies showed it becomes absorbed by epithelial cells, converts to a derivative form, then binds to DNA and causes mutations. When scientists mutated genes at the same specific points where benzopyrene caused damage, this led to uncontrolled cell division and tumour growth.
The two-hit hypothesis
The two-hit hypothesis explains why cancer risk increases with age and why some cancers show inherited patterns.
Understanding the Two-Hit Mechanism:
This hypothesis is fundamental to cancer biology as it explains the relationship between age, inheritance, and cancer development. Unlike other genes, tumour suppressors need both copies to be damaged before problems occur.
Tumour suppressor genes normally prevent excessive cell division. Unlike proto-oncogenes, which require only one mutated copy to cause problems, tumour suppressor genes need both alleles to be mutated before losing their protective function.
This explains several important observations:
- Cancer risk increases with age because it takes time for both alleles to accumulate mutations
- Some individuals inherit one mutated allele, requiring only one additional mutation to develop cancer
- These inherited cases often develop cancer earlier than sporadic cases
- Multiple mutations must occur for most cancers to develop
Cancer treatment approaches
Modern cancer treatments target the molecular mechanisms underlying tumour development:
Gene therapy approaches include introducing functional tumour suppressor genes into rapidly dividing cancer cells to restore normal growth control.
Targeted drug therapy focuses on developing medicines that specifically destroy protein receptors on cancer cell membranes, disrupting the signals that promote uncontrolled division.
Key Points to Remember:
- Risk factors include both modifiable lifestyle choices (smoking, diet, exercise) and non-modifiable factors (age, genetics)
- Proto-oncogenes become oncogenes when activated inappropriately, leading to excessive cell division
- Scientific evidence for cancer causation requires both epidemiological studies (showing correlations) and experimental studies (demonstrating mechanisms)
- The two-hit hypothesis explains why tumour suppressor genes need both alleles mutated and why cancer risk increases with age
- Carcinogens like benzopyrene directly damage DNA and cause the specific mutations that lead to cancer development