AMED3001 Cancer
Cancer Aetiology & Carcinogens
Week 5 opens Module 2 with what causes cancer. It splits causation into hereditary, familial and sporadic, catalogues the hereditary cancer syndromes, then classifies carcinogens as physical, chemical or biological and shows how each damages DNA — building to the initiation-promotion-progression model. Carcinogen classification and DNA-damage mechanisms are core MCQ and short-answer material in the mid-semester quiz and the final (50%, confirm on Canvas).
What this chapter covers
- 01Aetiology and the causation split: hereditary 5-10%, familial 10-20%, sporadic 70-80%; ~80-90% of cancers driven by somatic mutation
- 02Hereditary cancer syndromes: BRCA1/2 (breast/ovarian), Lynch (mismatch-repair genes), FAP (APC), Li-Fraumeni (TP53)
- 03Physical carcinogens: ionizing radiation → single- and double-strand breaks; UV → pyrimidine dimers (CPDs, 6-4 photoproducts)
- 04Chemical carcinogens: polycyclic aromatic hydrocarbons, alkylating agents, aflatoxin (activated by liver CYP450), asbestos → mesothelioma
- 05IARC classification: Group 1 (carcinogenic), 2A (probable), 2B (possible), 3 (not classifiable)
- 06Biological carcinogens: viruses (HPV, HBV/HCV, EBV), bacteria (H. pylori), flukes (Opisthorchis, Schistosoma)
- 07Multistep carcinogenesis: initiation → promotion → progression; mutations accumulate with dose and exposure
Classify the carcinogens and name their DNA-damage mechanism
- +2Physical carcinogens — examples: ionizing radiation (X-rays/gamma) and ultraviolet (UV) light. Mechanism: ionizing radiation causes single- and double-strand DNA breaks (directly and via water-derived radicals); UV creates pyrimidine dimers (CPDs) between adjacent pyrimidines that mispair during replication.
- +2Chemical carcinogens — examples: polycyclic aromatic hydrocarbons in tobacco smoke and aflatoxin. Mechanism: many require metabolic activation by liver CYP450 enzymes to become reactive, then form DNA adducts (e.g. aflatoxin binds guanine) that cause mutation.
- +1Biological carcinogens — examples: HPV (cervical/oropharyngeal cancer) and Helicobacter pylori (gastric cancer). Mechanism: viral genome integration and expression of viral oncoproteins, and/or chronic inflammation with reactive-oxygen-species DNA damage and immune suppression.
Key terms
- Aetiology
- The cause of a disease; cancer aetiology divides into hereditary (5-10%), familial (10-20%) and sporadic (70-80%) origins, with the great majority driven by somatic mutation.
- Carcinogen
- Any agent whose exposure increases the incidence of malignant neoplasia (IARC definition); may be physical, chemical or biological, natural or human-made.
- IARC groups
- The International Agency for Research on Cancer classification of carcinogenicity: Group 1 (carcinogenic to humans), 2A (probably), 2B (possibly), 3 (not classifiable).
- Pyrimidine dimer
- A UV-induced covalent lesion (cyclobutane pyrimidine dimer or 6-4 photoproduct) between adjacent pyrimidines that distorts DNA and causes replication errors.
- Initiation-promotion-progression
- The multistep model of carcinogenesis: an initiating mutation, then promotion (clonal expansion) and progression (accumulation of further changes) to malignancy.
- Germline vs somatic mutation
- A germline mutation is inherited and present in every cell, predisposing offspring; a somatic mutation arises in non-germ cells from exposures and is not inherited, and causes about 80-90% of cancers.
Cancer Aetiology & Carcinogens FAQ
What is the hereditary/familial/sporadic split of cancer causation?
Roughly 5-10% hereditary (a known inherited germline mutation), 10-20% familial (runs in families with an unknown genetic cause and gene-environment interaction) and 70-80% sporadic (chance somatic events). Knowing these proportions with one example each is a common short answer.
How does UV light cause mutations?
UV creates pyrimidine dimers — cyclobutane pyrimidine dimers and 6-4 photoproducts — between adjacent pyrimidines. These distort the helix, and error-prone bypass during replication inserts the wrong base, producing mutations. Ionizing radiation, by contrast, causes strand breaks.
Which viruses and bacteria are cancer-causing?
Examples include HPV (cervical, oropharyngeal, anal), hepatitis B and C (hepatocellular carcinoma), EBV (lymphomas), and the bacterium Helicobacter pylori (gastric cancer). They act through genome integration/viral oncoproteins or chronic inflammation.
Can AI help me learn carcinogens for AMED3001?
Yes — Sia can drill the physical/chemical/biological classification, pair each carcinogen with its DNA-damage mechanism and IARC group, and check your short-answer wording; it teaches the method and checks your reasoning, not your graded work.
Exam move
Build a three-column table — physical, chemical, biological — with two examples and the exact DNA-damage mechanism for each, because that is the shape of the likely short-answer and the source of MCQ traps (carcinogen paired with the wrong lesion). Memorise the hereditary/familial/sporadic split and the four hereditary syndromes with their genes. Ask Sia to quiz carcinogen-to-mechanism pairings and the IARC groups; keep this warm for the mid-semester quiz and the final, and confirm details on Canvas.
Working through Cancer Aetiology & Carcinogens in AMED3001? Sia is AskSia’s AI Biology tutor — ask any AMED3001 Cancer Aetiology & Carcinogens question and get a clear, step-by-step explanation grounded in how AMED3001 is taught and assessed. Read this chapter free, then take your hardest questions to Sia.
