5.1.65 · The Mitotic Cell Cycle
How Tumours Form — Cambridge AS & A Level Biology 9700 Revision Notes & Topical Questions
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Lesson summary
5.1.6 How Tumours Form — CAMBRIDGE AS & A LEVEL BIOLOGY 9700 — REVISION NOTES notes: Explain how mutations in proto-oncogenes and tumour suppressor genes disrupt the cell cycle to form tumours, and distinguish benign and malignant tumours.
- Normal control
- Several mutations
- Common events
- Fate of mutated cells
- Cancer-causing mutations
- Both together
Section 1 of 10Uncontrolled cell division
Tumour
Tumour an irregular mass of cells formed by uncontrolled mitosis.
Normal control
- Normal control checkpoints and signals from other cells balance cell division and cell death.
Escape
- Escape a tumour forms when a cell escapes these controls, divides repeatedly and passes its abnormal characteristics to its daughters,
- forming a clone.
Several mutations
- Several mutations tumour formation almost always needs several mutations in the same cell line, which is why cancer is more common in older people.
Mutation
- Mutation a change in any gene, and one that causes cancer is called an oncogene.
Section 2 of 10Why most mutations do not cause cancer
Common events
- Common events mutations are common and usually do not lead to cancer.
Fate of mutated cells
- Fate of mutated cells most die early or are destroyed by the immune system, and since most cells are easily replaced there is no harm.
Cancer-causing mutations
- Cancer-causing mutations they avoid early death and destruction by the immune system, so the mutation passes to all the cell's descendants.
Section 3 of 10Genes that control the cell cycle
| Feature | Proto-oncogene / oncogene | Tumour suppressor gene |
|---|---|---|
| Normal role | Codes for proteins that stimulate the cell cycle in a controlled way, such as growth factor receptors, signalling proteins and cyclins | Codes for proteins that slow or stop the cycle, repair DNA or trigger apoptosis if damage cannot be repaired |
| Effect of mutation | The gene becomes an oncogene that is permanently active, so the cell gets a continual signal to divide | The gene is inactivated, which removes the brake |
| Copies needed | One mutated copy is enough (dominant at cell level) | Both alleles must be lost or mutated (recessive at cell level) |
| Example | RAS | TP53 (p53), mutated in more than half of human cancers, and BRCA1 |
| Analogy | Stuck accelerator | Failed brakes |
- Both together
- a cell with both problems divides rapidly and fails to repair DNA, which raises the rate of further mutation.
Section 4 of 10Causes of the mutations
Inherited
- Inherited for example an inherited faulty BRCA1 allele increases the risk of breast cancer.
Carcinogens
- Carcinogens agents that may cause cancer, such as ultraviolet light, ionising radiation (X-rays), tar in tobacco smoke and aflatoxins.
- A carcinogenic agent is one that causes cancer.
Viruses
- Viruses oncoviruses such as HPV cause cancer and so are carcinogens.
- (HPV causes cervical cancer)
Chance
- Chance mistakes occur during DNA replication.
Lifestyle
- Lifestyle smoking and diet can raise the risk.
Section 5 of 10Benign and malignant tumours
| Feature | Benign tumour | Malignant tumour (cancer) |
|---|---|---|
| Growth | Slow | Rapid |
| Boundary | Often enclosed in a capsule; well defined | Irregular; invades surrounding tissue |
| Cells | Resemble normal cells (differentiated) | Undifferentiated, abnormal shapes, large nuclei |
| Spread | Does not spread to other organs (for example warts) | Spreads by metastasis via blood or lymph |
| Danger | Usually not life-threatening unless pressing on organs | Life-threatening; can block the intestines, lungs or blood vessels |
Section 6 of 10Metastasis
1
Malignant cells lose adhesion to their neighbours.
2
They secrete enzymes that digest the surrounding matrix.
3
They break off and enter blood vessels and lymph.
4
They settle in other tissues and form secondary tumours.
Angiogenesis
- Angiogenesis tumours stimulate new blood vessels to supply their large mass of cells.
Danger
- Danger metastasis is hard to detect, locate and remove.
Section 7 of 10Treatment and prevention
Treatment
- Treatment surgery, radiotherapy, chemotherapy and targeted therapies that block growth-factor receptors.
- Many treatments damage DNA or block the spindle in dividing cells,
- so they also affect healthy dividing cells and cause side effects.
- (hair follicles, gut lining, bone marrow)
- so they also affect healthy dividing cells and cause side effects.
Prevention
- Prevention avoid mutagens, vaccinate against HPV, and screen to find tumours early.
- (not smoking, protecting skin from UV)
Cancer data
- Cancer data incidence rises steeply in older age groups, consistent with the need for several mutations,
- and lung cancer is more common in smokers with risk falling after quitting.
Relative risk
- Relative risk the rate in the exposed group divided by the rate in the unexposed group.
Section 8 of 10More from the specification
1
The Eukaryotic Cell Cycle and Interphase
- The cell cycle comprises interphase (G1 growth phase, S phase for DNA replication,
- and G2 phase for organelle duplication) followed by mitotic cell division (M phase) and cytokinesis.
2
Chromosome Structure and Sister Chromatids
- Following DNA replication in S phase, each chromosome consists of two genetically identical sister chromatids held together at the centromere until separated during anaphase.
3
Role of Telomeres in Mitotic Aging
- Telomeres are repetitive non-coding DNA sequences at chromosome ends that protect essential genes from degradation during successive replication cycles in adult somatic tissues.
4
Oncogenesis and Tumour Formation
- Uncontrolled mitotic division triggered by mutations in proto-oncogenes or tumour suppressor genes bypasses cell cycle checkpoints,
- leading to an abnormal mass of cells called a tumour.
5
Asexual reproduction
- Reproduction from one parent giving genetically identical offspring.
6
Chromatid
- One of the two identical copies of a replicated chromosome.
7
Telomere
- Repetitive non-coding DNA at the ends of a chromosome that prevents loss of genes during replication.
8
Interphase
- The stage when the cell grows and DNA is replicated.
9
Chromosome
- A thread-like structure of DNA carrying genes.
10
Organism
- A living thing, such as a plant or an animal.
11
Genetically identical
- Having the same alleles
12
Sister chromatids
- The two identical DNA copies of a replicated chromosome joined at the centromere.
13
Multicellular organism
- An organism made of more than one cell.
Section 9 of 10Key terms
| Term | Meaning |
|---|---|
| Tumour | Mass of cells formed by uncontrolled division. |
| Proto-oncogene | Normal gene that stimulates cell division. |
| Oncogene | Mutated proto-oncogene that is permanently active. |
| Tumour suppressor gene | Gene whose product slows division, repairs DNA or triggers apoptosis. |
| Metastasis | Spread of cancer cells to other parts of the body. |
| Carcinogen | Agent that increases the chance of cancer. |
| Malignant | Cancerous; invasive and able to spread. |
| Benign | Non-cancerous; does not spread. |
Section 10 of 10Exam technique
1
Saying proto-oncogenes cause cancer — only the mutated oncogene does.
2
Mixing up the two gene types — oncogenes act like an accelerator and tumour suppressors like a brake.
3
Stating that all tumours are cancerous — benign tumours do not metastasise.
4
Stating that cancer is caused by a single mutation.
Marked practiceQuizzes for this lesson
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