20.5 - Gene Expression And Cancer Flashcards
What is cancer, and how does it arise?
Cancer is a group of diseases caused by damage to genes regulating mitosis and the cell cycle. This leads to unrestrained cell growth, resulting in a group of abnormal cells called a tumour that expands in size.
Why is cancer considered both destructive and potentially avoidable?
Cancer is common and destructive but can be avoidable and successfully treatable if diagnosed early enough.
What is the difference between benign and malignant tumours?
Benign tumours are non-cancerous, while malignant tumours are cancerous.
What are the main characteristics of benign and malignant tumours?
- Growth size: Both can grow large.
- Growth speed: Benign grows slowly; malignant grows rapidly.
- Nucleus appearance: Benign nuclei are relatively normal; malignant nuclei are larger and darker due to abundant DNA.
- Cell differentiation: Benign cells are well-differentiated; malignant cells are de-differentiated.
- Adhesion: Benign cells produce adhesion molecules and remain within tissue (primary tumours); malignant cells lack adhesion molecules, leading to metastasis and secondary tumours.
- Structure: Benign tumours are surrounded by a capsule and remain compact; malignant tumours lack capsules and grow finger-like projections into surrounding tissue.
- Life threat: Benign is less likely to be life-threatening but can disrupt vital organs; malignant is more likely to be life-threatening as it replaces normal tissue.
- Effects: Benign has localised effects; malignant often causes systemic effects like weight loss and fatigue.
- Treatment: Benign is usually removed via surgery alone; malignant requires surgery and often radiotherapy/chemotherapy.
- Recurrence: Benign rarely recurs after treatment; malignant frequently recurs.
How do cancer cells arise genetically?
Cancer cells usually arise from a single mutant cell where uncontrolled mitosis occurs. Subsequent mutations in descendant cells cause differences in growth and appearance.
What are the two main types of genes involved in cancer?
Tumour suppressor genes and oncogenes.
What are oncogenes, and how do they form?
Oncogenes are mutated proto-oncogenes. Proto-oncogenes normally stimulate cell division when growth factors bind to receptors, but mutations can permanently activate oncogenes.
How can oncogenes become permanently activated?
1) The receptor protein on the cell-surface membrane may become permanently activated, leading to cell division even without growth factors.
2) The oncogene may code for excessive growth factor production, causing uncontrolled division.
What is the result of oncogene activation?
Cells divide uncontrollably, leading to tumour formation. Most mutations in proto-oncogenes are acquired rather than inherited.
What is the role of tumour suppressor genes?
Tumour suppressor genes slow down cell division, repair DNA mistakes, and trigger apoptosis (programmed cell death).
What happens if tumour suppressor genes are mutated?
Mutations inactivate tumour suppressor genes, stopping them from inhibiting cell division. Cells grow uncontrollably, forming tumours.
Name examples of tumour suppressor genes and their roles in cancer.
Examples include TP53, BRCA1, and BRCA2. Mutations in TP53, which codes for the p53 protein, prevent apoptosis, leading to cancer. Acquired TP53 mutations are common in cancers like lung and breast cancer.
What is the difference between oncogene and tumour suppressor gene mutations?
Oncogenes cause cancer when activated, while tumour suppressor genes cause cancer when inactivated.
How does hypermethylation of tumour suppressor genes lead to cancer?
1) Hypermethylation occurs in the promoter region of tumour suppressor genes.
2) The gene becomes inactivated, silencing transcription.
3) Inactivation stops the gene from slowing cell division, leading to tumour formation.
Give an example of hypermethylation’s role in cancer.
Hypermethylation of the BRCA1 tumour suppressor gene can lead to breast cancer.
