Gene Expression & Cancer
This lesson covers:
- The differences between benign and malignant tumours
- Differences between tumour cells and normal cells
- How mutations can cause uncontrolled cell growth
- The role of abnormal methylation in cancer
- How oestrogen may contribute to some breast cancers
Benign and malignant tumours
Unrestrained cell division results in the creation of a mass of cells.
These masses of cells are known as tumours:
- Primary tumours - The original abnormal growths that develop where a cancer first begins.
- Secondary tumours - These are formed when primary tumours spread to other regions of the body via metastasis.
Not all tumours are cancerous. They fall into two categories: benign and malignant tumours.
| Benign tumours | Malignant tumours | |
|---|---|---|
| Growth pace | Grow slowly | Multiply quickly |
| Cellular appearance | Usually look like normal cells | Often have an abnormal, DNA-rich appearance |
| Cellular specialisation | Retain their specific functions | Lose their specialised functions |
| Adhesion | Have binding molecules that keep them in place | Lack binding molecules, allowing them to spread |
| Tumour containment | Encased in a dense layer, forming a distinct mass | Not encased, spreading irregularly into surrounding tissue |
| Threat level | Generally not life-threatening, but can impact organ function | Highly dangerous, can replace healthy tissue |
| Surgical outcomes | Often effectively treated with surgery | May need surgery, chemotherapy, and radiotherapy |
Differences between tumour cells and normal cells
Tumour cells exhibit several distinctive features compared to normal cells.
Some key features of tumour cells include:
- They have an irregular shape and large, dark nuclei.
- They may have extra nuclei.
- Their protein production is altered.
- They display different surface antigens.
- They divide uncontrollably through mitosis.
- They do not respond appropriately to growth signals.
How mutations can cause uncontrolled cell growth
Cancer originates when mutations occur in genes that regulate cell division, leading to cells dividing without control.
There are two primary types of gene involved in this process: tumour suppressor genes and proto-oncogenes.
- Tumour suppressor genes
- Tumour suppressor genes regulate cell division, repair DNA, and initiate apoptosis to prevent tumour formation.
- Mutations can deactivate these genes.
- This prevents them from producing proteins that normally regulate cell division, DNA repair, and apoptosis, leading to uncontrolled cell growth and cancer.
- Proto-oncogenes
- Proto-oncogenes stimulate cell division when growth factors bind to the cell's receptors, activating DNA replication.
- Mutations or excessive growth factor production can amplify the function of proto-oncogenes.
- This causes them to promote excessive DNA replication and cell division.
- Once mutated, proto-oncogenes are known as oncogenes.
The role of abnormal methylation in cancer
Methylation is the addition of methyl groups to DNA, affecting gene expression. This process determines whether genes are active or silent.
Hypermethylation means more methylation is occurring than normal, while hypomethylation means less methylation is occurring.
These abnormal patterns of methylation can play a significant role in cancer development:
- Hypermethylation of tumour suppressor genes prevents them from being active.
- This stops the production of proteins that would normally inhibit cell division, and cells divide unchecked to form tumours.
- Hypomethylation of proto-oncogenes leads to their activation as oncogenes.
- This activation promotes excessive cell division and tumour growth, especially as some oncogenes code for growth factors that stimulate further cell division.
Oestrogen may contribute to some breast cancers
Increased levels of oestrogen over time can elevate the risk of breast cancer.
Possible explanations for this include:
- Oestrogen can stimulate breast cell division by activating genes that control transcription, leading to tumour development.
- Oestrogen may encourage the replication of already cancerous cells.
- Oestrogen may directly cause mutations in the DNA of breast cells.
Although the exact mechanisms remain unclear, reducing oestrogen exposure might lower the risk of breast cancer for some women. There is a higher risk of breast cancer in postmenopausal women because they have higher levels of oestrogen production in fat cells within breast tissue.