Cancer Biology & Therapy
Cancer — A Disease of the Genome & the Cell
From driver mutations to metastasis to checkpoint blockade — eight integrating modules.
Why a course on cancer?
Cancer is the second-leading cause of death worldwide, accounting for roughly 10 million deaths each year. It is not a single disease but a family of disorders united by a common logic: the breakdown of the control circuits that keep cells faithful to a multicellular contract.
This course is structured as a top-down dissection of that breakdown — starting from the integrating Hallmarks framework (Hanahan & Weinberg), then descending through genetics, cell-cycle control, DNA repair, metabolism, the tumour microenvironment, metastasis, and ending with the therapies built to attack each vulnerability. The course pulls together material from cell signaling, metabolism, molecular biology, and pharmacology — cancer is where all of biology meets clinical reality.
Course Parts
Hallmarks of Cancer
The Hanahan-Weinberg framework: eight acquired capabilities and two enabling characteristics that distinguish malignant from normal cells.
Genetic Basis
Oncogenes, tumour-suppressor genes, the two-hit hypothesis, driver vs. passenger mutations, mutational signatures.
Cell-Cycle Dysregulation
CDKs, the Rb–E2F switch, p53 as guardian of the genome, checkpoint failure, and replication stress.
Genome Instability & DNA Repair
MMR, NER, BER, HR, NHEJ. BRCA1/2, Lynch syndrome, mutator phenotypes, microsatellite instability, synthetic-lethal targeting.
Cancer Metabolism
Warburg effect, glutaminolysis, lipogenic switch, oncometabolites (2-HG, succinate, fumarate), the Hallmark of Reprogrammed Metabolism.
Tumour Microenvironment
Hypoxia & HIF, angiogenesis (VEGF), stromal CAFs, immune evasion, PD-L1, the immunoediting framework.
Metastasis
EMT, invadopodia, intravasation/extravasation, organ tropism (Paget seed-and-soil), dormancy, premetastatic niches.
Therapy
Cytotoxic chemo, targeted kinase inhibitors, antibody therapy, immune checkpoint blockade, CAR-T, radiotherapy, drug resistance.
What you’ll learn
- Read a tumour-genomic profile and identify driver vs. passenger mutations.
- Map a kinase signalling cascade onto its therapeutic vulnerabilities.
- Explain the Warburg effect and why cancer cells are lipogenic.
- Reason about synthetic-lethal targeting (PARP-i in BRCA-mutant tumours).
- Describe immune checkpoint biology and predict response to anti-PD-1.
- Trace metastatic progression through EMT, intravasation, and organ tropism.
- Connect cell-cycle checkpoint failure to genomic instability and aneuploidy.
- Anticipate the molecular basis of acquired drug resistance.
Prerequisites
Working knowledge of cell biology, basic biochemistry, and central-dogma molecular biology. The course cross-references Cell Physiology, Molecular Biology, and Biochemistry; modules in those courses are linked at the relevant moments.