BABS2202 Chap.3 Molecular Mechanisms of Cancer
Molecular Mechanisms of Cancer
Cancer is not a single broken switch. It is an evolving cell population in which changes to growth signalling, cell-cycle restraint, genome maintenance, death responses, tissue interaction and resource acquisition combine over time. Oncogenic alterations can create or amplify positive signals; loss of tumour-suppressive functions can remove brakes, repair or checkpoint responses.
These categories describe functional consequences rather than implying that every oncogene is normally bad or every tumour suppressor performs the same job.
The chapter begins the stated Lectures 7–22 Final Exam range. Its central reasoning move is to connect molecular alteration to selective advantage without skipping intermediate steps.
A constitutively active receptor may sustain pathway output without ligand, but the relevant phenotype depends on cell type, network feedback and which downstream branches remain intact. Loss of a damage checkpoint may permit division with lesions, while failure of apoptosis may preserve altered clones. Genomic instability increases variation on which selection can act.
Invasion and metastasis add further requirements: altered adhesion, matrix remodelling, motility, survival away from the original niche and colonisation of another tissue.
What this chapter covers
- 01
Proto-oncogenes and oncogenes: normal growth functions altered by increased, constitutive or misplaced activity
- 02
Tumour suppressors as restraints, damage responders, repair functions or death-promoting systems
- 03
Checkpoint bypass and genome instability as sources of heritable variation
- 04
Clonal evolution, heterogeneity and selection imposed by tissue environment or treatment
- 05
Evasion of death, altered metabolism, angiogenic support and immune interactions
- 06
Adhesion change, matrix remodelling, migration, invasion and metastatic colonisation
- 07
Targeted-treatment logic, resistance mechanisms and the distinction between growth arrest and regression
Why pathway suppression may not shrink a tumour
- +1Target suppression shows the drug reaches and inhibits the chosen pathway; stable volume indicates reduced net expansion.
- +1Regression additionally requires cell loss, so arrest without apoptosis can produce stable disease rather than shrinkage.
- +1A second alteration may protect survival even after the proliferative signal is removed, or resistant subclones may persist.
- +1Compare each single treatment with a rational death-sensitising combination and measure pathway output, cycling and apoptosis over time.
Key terms
- Oncogene
- An altered or inappropriately active gene whose function can promote cancer-relevant cell behaviour, often through increased or constitutive activity.
- Tumour suppressor
- A gene whose ordinary function restrains cancer-relevant processes, preserves genome integrity or promotes removal of damaged cells; loss can create selective advantage.
- Driver alteration
- A heritable change that contributes to the growth, survival or spread of a tumour-cell clone, rather than merely accompanying it.
- Clonal evolution
- Change in tumour composition as heritable variants arise and clones with context-dependent advantages expand.
- Metastasis
- Spread and successful establishment of cancer cells at a site discontinuous from the primary tumour, requiring multiple biological steps.
- Synthetic lethality
- A relationship in which loss or inhibition of either of two functions alone is tolerated but their combined loss is lethal, creating a possible selective treatment strategy.
Molecular Mechanisms of Cancer FAQ
Does one mutation cause cancer?
A single alteration can strongly change behaviour, but clinically important cancer usually reflects accumulated and interacting changes plus selection in a tissue environment. Distinguish initiation of a phenotype from the full requirements for sustained growth, survival, immune escape, invasion and treatment resistance.
Are oncogenes abnormal genes that healthy cells do not have?
Usually the healthy cell has a normal proto-oncogene with a legitimate role in growth, survival or differentiation. Mutation, amplification, rearrangement or inappropriate expression can convert its regulated activity into an oncogenic input. State the altered regulation or activity rather than describing the normal gene as inherently cancerous.
Why are tumours heterogeneous?
Altered cells continue to acquire or select heritable variation. Different local environments and therapies favour different traits. The resulting subclones can differ in pathway dependence, antigen expression, metabolism, invasion and drug sensitivity, so a sample from one location or time may not represent the entire tumour.
How does a targeted therapy differ from a non-specific poison?
A targeted strategy exploits a molecular dependency or vulnerability enriched in tumour cells. Selectivity is relative, not absolute, because normal cells can share the target. Demonstrate target engagement, connect it to the phenotype and compare effects in relevant normal and tumour contexts.
Exam move
Organise cancer around functional capabilities rather than a list of named genes. For each alteration, write its normal role, the direction of change, the first pathway consequence, the cell behaviour and the selective advantage. Then add one likely resistance route. Practise explaining why biochemical target engagement, reduced proliferation and tumour regression are different claims requiring different measurements.
Because this chapter begins the current Final Exam lecture range, rehearse both short pathway diagnoses and essay outlines that connect molecular mechanisms to evolution, tissue context and therapeutic response.
Working through Molecular Mechanisms of Cancer in BABS2202? Sia is AskSia’s AI Biology tutor — ask any BABS2202 Molecular Mechanisms of Cancer question and get a clear, step-by-step explanation grounded in how BABS2202 is taught and assessed. Read this chapter free, then take your hardest questions to Sia.
