2804NRS · Human Pathophysiology And Pharmacology 1
Cancer
Cancer is a cell-cycle control failure. A normal cell divides only when told to and stops at checkpoints if its DNA is damaged; neoplasia is new, uncontrolled, autonomous growth that no longer obeys those controls. Two faults occur together: the accelerator sticks on (a proto-oncogene mutates to an oncogene — gain of function) and the brakes fail (a tumour-suppressor such as p53 or BRCA is lost — loss of function). This chapter covers benign vs malignant features (metastasis, not size, defines malignancy), the cell cycle and the G1/S checkpoint, the multistep carcinogenesis sequence (initiation → promotion → progression) and the four metastasis routes, the perennial grading vs staging (TNM) trap, and one cancer worked end-to-end as a cascade. In 2804NRS this is Module 4 — examined by MCQ and short-answer.
What this chapter covers
- 014.1 Neoplasia: benign vs malignant
- 024.2 The cell cycle, checkpoints & the cancer overlay
- 034.3 Carcinogenesis & the metastatic cascade
- 044.4 Grading vs staging (TNM) — the perennial trap
- 054.5 One cancer end-to-end — the SAQ cascade
Oncogene vs tumour-suppressor — gain vs loss
- +1(a) Oncogene — GAIN of function: a mutated proto-oncogene is an over-active accelerator giving the cell a constant 'divide' signal.
- +1(b) p53 = tumour-suppressor — LOSS of function: the 'guardian of the genome' normally arrests damaged cells at the G1/S checkpoint or sends them to apoptosis; losing it cuts the brakes.
- +1(c) BRCA1 = tumour-suppressor — LOSS of function: normally repairs DNA; its loss leaves damage unrepaired.
Key terms
- Neoplasia
- New, uncontrolled, autonomous cell growth not responsive to normal controls; the resulting mass is a neoplasm or tumour. Benign neoplasms stay local; malignant ones invade and metastasise.
- Metastasis
- The spread of malignant cells to distant secondary sites — by haematogenous (blood), lymphatic (to regional nodes) or transcoelomic (cavity seeding) routes. Metastasis, not size, defines malignancy.
- Oncogene
- A mutated proto-oncogene with a GAIN of function that drives uncontrolled proliferation — the accelerator stuck on.
- Tumour-suppressor gene
- A gene that normally restrains growth or repairs DNA; a LOSS of function (e.g. p53, BRCA1/2) removes that brake and permits unchecked growth.
- Grading vs staging
- Grading asks how ABNORMAL the cells look (differentiation, under the microscope); staging asks how far the cancer has SPREAD, scored by TNM (Tumour size, Node involvement, Metastasis). Staging = spread.
Cancer FAQ
What is the single feature that defines a malignant tumour?
Metastasis — the ability to spread to distant sites. A large benign tumour is still benign; a tiny malignant one is still cancer. Do not be fooled by size: it is metastasis, plus invasion and poor differentiation, that defines malignancy.
What is the difference between an oncogene and a tumour-suppressor?
An oncogene is a gain of function (the proto-oncogene was normal; the mutation jams the accelerator on). A tumour-suppressor is a loss of function (a failed brake). p53 and BRCA1/2 are tumour-suppressors — a frequent trap mislabels p53 as an oncogene. Cancer needs both faults.
What is the difference between grading and staging?
Grading is how abnormal the cells appear under the microscope (degree of differentiation, grade 1–4). Staging is how far the cancer has spread anatomically, scored by TNM — Tumour size, Node involvement, Metastasis. Memory hook: Staging = Spread; lymph-node involvement is staging (N), not grading.
What are the steps of carcinogenesis?
Initiation (a carcinogen causes an irreversible DNA mutation), promotion (the mutated cell is driven to proliferate — reversible, the slow step), and progression (further mutations make the clone invasive and able to spread). Morphologically: normal → dysplasia → carcinoma in situ → invasive.
Exam move
Anchor the whole module on one model — accelerator on (oncogene, gain), brakes off (tumour-suppressor, loss), boundaries crossed (metastasis). Memorise the benign-vs-malignant grid (metastasis is the distinguisher), the carcinogenesis sequence (initiation → promotion → progression), the four spread routes, and the grading-vs-staging distinction (appearance vs spread, TNM). Then practise running one named cancer (e.g. cervical/HPV) as a full RF → aetiology → pathophysiology → clinical cascade for the short-answer half.
