Cancer Biology

26 questions • 2 tests • tap a section to begin

Welcome! This is the Cancer Biology module — the molecular basis of cancer (oncogenes, tumour suppressors) and how tumours develop and spread.

How the tests are arranged

  • Test 1 (12.1) — Molecular Basis of Cancer
  • Test 2 (12.2) — Cancer Development & Progression

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12.1 Molecular Basis of Cancer — Test 1
Q1. The p53 protein is associated with which of the following?✓ Tumour suppression
Q2. The p53 protein is often called the:✓ 'Guardian of the genome'
Q3. A proto-oncogene is best described as:✓ A normal gene that promotes growth and can become an oncogene if mutated
Q4. An oncogene is best defined as:✓ A dominantly acting, mutated gene that confers a growth/survival advantage on the cell
Q5. The mutation that converts a proto-oncogene into an oncogene is typically a:✓ Gain-of-function mutation
Q6. All of the following can activate a proto-oncogene into an oncogene EXCEPT:✓ Deletion of its enhancer
Q7. A tumour-suppressor gene is best described as:✓ A gene whose loss-of-function (both alleles) contributes to cancer
Q8. In cervical cancer, the human papillomavirus (HPV) oncoproteins act such that:✓ E6 inactivates p53 and E7 inactivates pRb
Q9. Which of the following is NOT a recognised hallmark of cancer?✓ Halted (suppressed) angiogenesis
Q10. The MDM2 protein promotes degradation of p53, while p19ARF inhibits MDM2. Based on these roles, MDM2 and p19ARF act respectively as:✓ An oncogene and a tumour suppressor
Q11. The retinoblastoma (Rb) protein normally restrains the cell cycle. Loss of functional Rb leads to:✓ Unregulated entry into S phase (uncontrolled proliferation)
Q12. The tyrosine-kinase inhibitor used to treat chronic myeloid leukaemia (CML), which is driven by the BCR-ABL fusion protein, is:✓ Imatinib
12.2 Cancer Development & Progression — Test 2
Q13. Metastasis is best defined as:✓ The spread of cancer cells from the primary site to distant sites
Q14. Angiogenesis refers to:✓ The formation of new blood vessels
Q15. Tumour angiogenesis is most directly driven by the over-expression of:✓ VEGF (vascular endothelial growth factor)
Q16. The genetic variation that allows clonal expansion and tumour heterogeneity arises largely from:✓ Genome instability (an increased mutation rate)
Q17. Arrange the stages of tumour development in the correct order: (I) Metastasis, (II) Progression, (III) Promotion, (IV) Initiation.✓ IV → III → II → I
Q18. In the TNM cancer-staging system, the letters T, N and M refer respectively to:✓ Tumour size, lymph-Node involvement, Metastasis
Q19. Tumours are generally classified on the basis of:✓ The tissue / cell type of origin
Q20. A carcinoma is a malignant tumour arising from:✓ Epithelial tissue
Q21. A sarcoma is a malignant tumour arising from:✓ Mesodermal (connective) tissue
Q22. Liver cancer (hepatocellular carcinoma) can be caused by:✓ Both viruses (e.g., hepatitis B/C) and chemical carcinogens (e.g., aflatoxin)
Q23. A key step that allows cancer cells to become immortal is:✓ Reactivation of telomerase
Q24. Compared with a normal cell, a transformed (cancerous) cell in culture typically shows:✓ Cellular immortality and loss of contact inhibition
Q25. A distinguishing property of malignant (versus merely transformed) cells is their ability to:✓ Grow unattached to the extracellular matrix (anchorage independence)
Q26. The form of programmed cell death triggered when normal epithelial cells detach from the extracellular matrix is called:✓ Anoikis