5.07 Cancers
Control of the Cell Cycle
- Cell Division Control:
- Governed by genes within each cell.
- Ensures mitosis occurs only when needed.
- Regulation Mechanism:
- Signals from neighbouring cells:
- Direct whether a cell divides or does not divide.
- Signals from neighbouring cells:
- Consequences of Faulty Control:
- Under-Division:
- Growth failure.
- Delayed wound healing.
- Over-Division:
- Uncontrolled growth → Tumour formation (Cancer).
- Under-Division:
Key Concepts:
- Tumours: Result of uncontrolled cell division due to failed regulation.
- Signals: Communication between cells ensures proper timing of division.
Cancer Overview
- Cancer Statistics:
- High-Income Countries: Cancer causes ~1 in 4 deaths.
- Global Impact: Accounts for ~1 in 6 deaths worldwide (approx. 9.6 million in 2018).
- Second leading cause of death after cardiovascular diseases.
Causes and Characteristics of Cancer
- Uncontrolled Mitosis:
- Cancer results from uncontrolled cell division due to mutations in genes controlling cell growth.
- Tumour Formation: Cancerous cells divide rapidly, forming an abnormal mass of cells called a tumour.
- Tumour Types:
- Benign Tumours: Do not spread from their origin (e.g., warts).
- Malignant Tumours: Invasive; spread to other tissues and can cause severe damage.
- Metastasis: Process by which malignant cells travel via blood or lymphatic system, forming secondary tumours in other body parts.
Genetic Changes in Cancer Cells
- Mutations:
- Changes in genes controlling cell division; a cancer-causing mutation is called an oncogene.
- Oncogenes develop when mutations disrupt normal cell cycle regulation, allowing cells to escape normal control mechanisms.
- Carcinogens:
- Substances that cause cancer (e.g., UV light, tobacco tar, asbestos, X-rays).
- Carcinogens cause mutations that may lead to cancer development.
Progression of Cancer Development
1.Oncogene Activation:
- Mutation or exposure to carcinogens transforms normal genes into oncogenes.
2.Unregulated Division:
- Cancer cells do not respond to normal growth signals and continue dividing.
3.Immune Evasion:
- Cancerous cells evade destruction by the immune system.
4.Rapid Cell Division:
- Cancer cells undergo continuous mitosis, forming larger tumours.
5.Tumour Growth:
- Tumours develop their own blood supply to obtain nutrients and continue growing.
6.Metastasis:
- Cancer cells spread to other tissues, creating secondary tumours.
Comparison Between Benign and Malignant Tumor Stages
| Feature | Benign Tumors | Malignant Tumors |
|---|---|---|
| Oncogene Activation | Activation leads to controlled growth without invasive properties. | Activation drives uncontrolled growth and invasive capabilities. |
| Cell Division Regulation | Regulated by normal growth signals, maintaining controlled proliferation. | Unregulated division ignores normal growth controls, leading to rapid and unchecked cell proliferation. |
| Immune Evasion | Minimal or no mechanisms to evade the immune system. | Develops sophisticated strategies to avoid immune detection and destruction. |
| Cell Division Rate | Steady and consistent, contributing to gradual tumor growth. | Rapid and continuous, resulting in aggressive tumor expansion. |
| Tumor Growth Mechanism | Localized expansion without the need for new blood vessels (angiogenesis). | Induces angiogenesis to support sustained and expansive growth. |
| Metastasis | Does not spread to other parts of the body; remains localized. | Capable of invading surrounding tissues and spreading to distant organs (metastasis). |
| Encapsulation | Often encapsulated by a fibrous capsule, preventing invasion. | Typically non-encapsulated, facilitating invasion into surrounding tissues. |
| Recurrence Risk | Low likelihood of recurrence after removal. | High likelihood of recurrence and spread after initial treatment. |
| Impact on Body | Generally less harmful unless located in critical areas causing pressure effects. | Highly detrimental due to potential to disrupt vital organs and systems through invasion and metastasis. |
| Growth Limitation | Growth confined by surrounding structures and available space. | Growth continues despite spatial constraints due to invasive behavior and angiogenesis. |
Cancer Cell Characteristics
- Structural Changes:
- Cancer cells often display abnormal shapes and structures compared to healthy cells.
- Immune cells, such as white blood cells, attempt to target and kill cancer cells but are not always successful.
Clinical Implications
- Telomerase and Cancer:
- Research Focus: Inhibiting telomerase (an enzyme that prevents telomere shortening) in cancer cells may limit their ability to replicate indefinitely.
- Rationale: Without telomerase activity, telomeres shorten with each division, eventually leading to cell death.
Question
Why is research focused on inactivating telomerase in cancer cells?
Answer: Inactivating telomerase may cause telomeres to shorten over time in cancer cells, leading to eventual cell death and potentially limiting cancer progression.
Practise Questions
Question 1
Explain how the cell cycle is regulated and the consequences of faulty regulation. (6 marks)
Mark Scheme:
- The cell cycle is regulated by genes within each cell, which ensure mitosis occurs only when necessary. (1 mark)
- Signals from neighbouring cells communicate whether a cell should divide or remain inactive. (1 mark)
- Under-division can result in growth failure or delayed wound healing. (1 mark)
- Over-division leads to uncontrolled cell proliferation, resulting in tumour formation. (1 mark)
- Benign tumours remain localized and do not invade other tissues, whereas malignant tumours are invasive and can metastasize. (1 mark)
- Faulty regulation of the cell cycle is often caused by mutations in genes that control cell division, such as oncogenes. (1 mark)
Question 2
Describe the differences between benign and malignant tumours. (6 marks)
Mark Scheme:
- Benign tumours grow slowly and remain localized, while malignant tumours grow rapidly and invade other tissues. (1 mark)
- Benign tumours are often encapsulated by a fibrous capsule, preventing invasion, whereas malignant tumours are non-encapsulated. (1 mark)
- Benign tumours do not metastasize, but malignant tumours can spread via blood or lymphatic systems. (1 mark)
- Benign tumours are less harmful unless located in critical areas, while malignant tumours disrupt vital organs and systems. (1 mark)
- Malignant tumours induce angiogenesis (formation of new blood vessels) to sustain growth, whereas benign tumours do not. (1 mark)
- After removal, benign tumours have a low recurrence risk, while malignant tumours are more likely to recur. (1 mark)
Question 3
What is metastasis, and how does it contribute to cancer progression? (5 marks)
Mark Scheme:
- Metastasis is the process by which cancer cells spread from their original site to other parts of the body. (1 mark)
- Cancer cells travel through the bloodstream or lymphatic system, establishing secondary tumours. (1 mark)
- This enables cancer to invade distant organs, disrupting their normal functions. (1 mark)
- Metastasis increases the severity of cancer, making it harder to treat and more likely to cause death. (1 mark)
- Malignant tumours often exhibit rapid division and evasion of immune system detection, facilitating metastasis. (1 mark)
Question 4
Explain the role of mutations and carcinogens in cancer development. (5 marks)
Mark Scheme:
- Mutations in genes controlling cell division (oncogenes) can lead to uncontrolled cell proliferation. (1 mark)
- Oncogenes allow cells to bypass normal growth signals and divide continuously. (1 mark)
- Carcinogens, such as UV light, tobacco tar, and X-rays, cause mutations in DNA, increasing cancer risk. (1 mark)
- Mutations may also impair tumour suppressor genes, which normally prevent uncontrolled division. (1 mark)
- Accumulation of genetic changes allows cancer cells to evade growth control mechanisms and form tumours. (1 mark)
Question 5
How do cancer cells differ from normal cells in their structure and behavior? (6 marks)
Mark Scheme:
- Cancer cells often display abnormal shapes and structures compared to healthy cells. (1 mark)
- They divide uncontrollably, ignoring normal growth signals. (1 mark)
- Cancer cells evade the immune system, resisting destruction by white blood cells. (1 mark)
- They can undergo angiogenesis, forming new blood vessels to supply nutrients for rapid growth. (1 mark)
- Cancer cells can metastasize, spreading to other tissues, unlike normal cells. (1 mark)
- They often exhibit high telomerase activity, preventing telomere shortening and enabling indefinite division. (1 mark)
Question 6
What is the significance of telomerase in cancer cells, and why is it a target for cancer therapy? (5 marks)
Mark Scheme:
- Telomerase prevents telomere shortening, allowing cancer cells to divide indefinitely. (1 mark)
- This enables tumour growth and contributes to cancer progression. (1 mark)
- Inhibiting telomerase could cause telomeres in cancer cells to shorten over time, leading to cell death. (1 mark)
- Telomerase inhibitors are being researched as potential cancer treatments to limit tumour growth. (1 mark)
- Targeting telomerase could selectively affect cancer cells without harming most normal cells, which lack telomerase activity. (1 mark)
Question 7
Outline the steps in cancer development from oncogene activation to metastasis. (6 marks)
Mark Scheme:
- Oncogene activation: Mutations or exposure to carcinogens transform normal genes into oncogenes. (1 mark)
- Unregulated division: Cancer cells bypass growth signals and divide continuously. (1 mark)
- Immune evasion: Cancer cells evade detection and destruction by the immune system. (1 mark)
- Rapid cell division: Cancer cells undergo continuous mitosis, forming larger tumours. (1 mark)
- Tumour growth: Tumours develop their own blood supply via angiogenesis to sustain growth. (1 mark)
- Metastasis: Cancer cells spread through the bloodstream or lymphatic system, forming secondary tumours in distant tissues. (1 mark)
Question 8
Discuss the clinical implications of targeting telomerase in cancer treatment. (5 marks)
Mark Scheme:
- Telomerase inhibition could lead to telomere shortening in cancer cells, limiting their ability to divide indefinitely. (1 mark)
- This approach may induce apoptosis (programmed cell death) in cancer cells. (1 mark)
- Telomerase inhibitors could selectively target cancer cells, as most normal cells lack significant telomerase activity. (1 mark)
- However, therapies must balance telomerase inhibition to avoid unintended effects on stem cells, which rely on telomerase. (1 mark)
- Research on telomerase offers promising strategies for slowing cancer progression and reducing tumour recurrence. (1 mark)
Question 9
Why is uncontrolled mitosis a hallmark of cancer, and how does it contribute to tumour formation? (5 marks)
Mark Scheme:
- Uncontrolled mitosis occurs when mutations disrupt regulation of the cell cycle. (1 mark)
- Cancer cells bypass checkpoints, dividing continuously without responding to normal growth signals. (1 mark)
- This leads to rapid accumulation of cells, forming an abnormal mass known as a tumour. (1 mark)
- Tumours grow aggressively, invading surrounding tissues and disrupting normal organ function. (1 mark)
- In malignant tumours, uncontrolled mitosis facilitates metastasis, spreading cancer to distant parts of the body. (1 mark)
Question 10
What is angiogenesis, and why is it important for tumour progression? (4 marks)
Mark Scheme:
- Angiogenesis is the process of forming new blood vessels. (1 mark)
- It provides tumours with a nutrient and oxygen supply, enabling rapid growth. (1 mark)
- Angiogenesis allows tumours to overcome spatial constraints and expand further. (1 mark)
- It is a target for cancer therapy, as inhibiting angiogenesis can starve tumours and limit their progression. (1 mark)
Quizzes
Test 1
1. What governs the control of cell division?
2. What is a consequence of under-division in the cell cycle?
3. What is metastasis?
4. What differentiates malignant tumours from benign tumours?
5. What is an oncogene?
6. What are carcinogens?
7. How do cancer cells differ structurally from normal cells?
8. Why do cancer cells form their own blood supply?
9. How do carcinogens lead to cancer?
10. Why is research focused on inactivating telomerase in cancer cells?
Correct Answers: 0%