The Cellular Basis of Cancer and Treatment | OCR A-Level Biology B (Advancing Biology) (H422)
The Cellular Basis of Cancer and Treatment
- 85 questions
- 6 subtopics
- Biology content, examined on all three papers
- Component 01, Component 02 and Component 03
The Cellular Basis of Cancer and Treatment is examined in all three written papers — the specification states that Components 01, 02 and 03 can each assess content from any of the five modules, so nothing is confined to one paper.
It covers risk factors for non-communicable disease, cell cycle control and tumour formation, proto-oncogenes and tumour suppressor genes, epidemiological evidence, screening and genetic testing, methods used to detect cancer and treating patients with cancer.
Sample questions from The Cellular Basis of Cancer and Treatment
Answer each one closed book first, then open the answer.
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Risk factors for non-communicable disease
Define the term carcinogen.
Show the answer
A carcinogen is any agent that increases the risk of cancer developing, usually by causing mutations in DNA. -
Risk factors for non-communicable disease
Why can an epidemiological study never prove on its own that a risk factor causes a disease?
Show the answer
It can only show a correlation between exposure and disease, and a confounding variable linked to both could be the real cause. -
Cell cycle control and tumour formation
What is checked at the spindle assembly checkpoint during metaphase?
Show the answer
That every chromosome is correctly attached to spindle fibres from both poles, so the chromatids will be separated evenly. -
Cell cycle control and tumour formation
Explain why a benign tumour can still be life-threatening.
Show the answer
It can press on surrounding tissue or block a vessel or duct as it grows, which is particularly dangerous in a confined space such as the skull. -
Proto-oncogenes and tumour suppressor genes
What is the normal role of the Ras protein in a cell?
Show the answer
Ras sits on the inside of the cell surface membrane and relays the signal from an activated growth factor receptor to the nucleus, switching itself off afterwards by hydrolysing its bound GTP to GDP. -
Proto-oncogenes and tumour suppressor genes
Explain why both alleles of a tumour suppressor gene must be inactivated before cancer can develop.
Show the answer
The mutation is a loss of function, so a single working allele still produces enough functional protein to restrain the cell cycle. -
Epidemiological evidence, screening and genetic testing
Why is processed meat linked more strongly to bowel cancer than fresh meat?
Show the answer
Processed meat is preserved with nitrites, which can be converted in the gut into N-nitroso compounds that are carcinogenic to the colon lining. -
Epidemiological evidence, screening and genetic testing
Why is a false negative screening result dangerous?
Show the answer
The patient is falsely reassured, so they may ignore later symptoms and the cancer is diagnosed at a more advanced and less treatable stage.
The 6 subtopics
One subtopic is one session. Work down the list.
| Subtopic | What it covers | Questions |
|---|---|---|
| Risk factors for non-communicable disease | Recall questions on non-communicable disease and its risk factors, why cancer rises with age, heredity, carcinogens, ultraviolet and ionising radiation, cancer-causing viruses, air pollution and asthma, and epidemiology, dose-response relationships, and cohort and case-control studies. | 14 |
| Cell cycle control and tumour formation | Recall questions on the stages of the cell cycle, the G1 and spindle assembly checkpoints, cyclins and cyclin-dependent kinases, apoptosis of damaged cells, tumours and contact inhibition, benign and malignant tumours, metastasis and angiogenesis. | 14 |
| Proto-oncogenes and tumour suppressor genes | Recall questions on proto-oncogenes and oncogenes, the proteins they code for and how they are activated, the Ras and Myc proteins, tumour suppressor genes and why both alleles must be lost, p53 and p21 at the G1 checkpoint, and silencing by promoter methylation. | 15 |
| Epidemiological evidence, screening and genetic testing | Recall questions on the epidemiological evidence linking smoking to lung cancer, diet and bowel cancer, BRCA1 and breast cancer risk, screening and its false positives, false negatives and overdiagnosis, its economic costs, HNPCC testing, and the ethics of genetic testing. | 16 |
| Methods used to detect cancer | Recall questions on detecting cancer by chest X-ray, mammography, CT, MRI, ultrasound and PET scans, their advantages and drawbacks, why a biopsy is still needed, and tumour markers in blood tests. | 14 |
| Treating patients with cancer | Recall questions on when surgery is appropriate, how cytotoxic chemotherapy works and its side effects, targeted radiotherapy, monoclonal antibodies, hormone-related treatment for breast and prostate cancer, and complementary and alternative therapies. | 12 |
How the guide is worked
Answering a question from memory stores it far better than reading the answer again. The guide runs that as a fixed procedure on one subtopic at a time, about twenty minutes a session.
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Step 1 · Closed book
Cover the answers. Work through one subtopic and write down what you can. Leave blanks where you have nothing.
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Step 2 · Open book
Go back to the top. Read each printed answer and write it out in full, including the ones you had right.
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Step 3 · Closed book again
Same questions, same order, from memory. The gap between pass one and pass three is the session result.
Read the full method, the return schedule and the research behind it.
Nearby topics
OCR A-Level Biology B (Advancing Biology) Active Recall Guide
Every topic, not just this one. 2,895 questions with their answers.