It is important to realise that not all types of tumour are cancerous. Cancerous tumours are known as malignant tumours, non-cancerous tumours are known as benign tumours). We need to know the main characteristics of them:
Benign (non-cancerous)
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Malignant (cancerous)
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Grow to a large size very slowly
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Can also grow to a large size, but very rapidly
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The cell nucleus has a normal appearance
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The cell nucleus is often larger and darker due to an abundance of DNA
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Cells are often specialised (differentiated)
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Cells become unspecialised (de-differentiated)
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Cells produce adhesion molecules that make them stuck together so they remain within the tissue from which they arise (primary tumours)
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Cells do not produce adhesion molecules and so they tend to spread to other regions of the body (metastasis) (secondary tumours)
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Tumours are surrounded by a capsule of dense tissue so remain as a compact structure
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Tumours are not surrounded by a capsule and can therefore grow finger-like projections into surrounding tissue
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Much less likely to be life threatening but can potentially disrupt the functioning of a vital organ
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More likely to be life threatening as abnormal tumour tissue replaces normal tissue
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Tend to have localised effects on the body
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Often have systemic effects such as weight loss and fatigue
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Can usually be removed by surgery
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Removal usually involves radio/chemotherapy and also surgery
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Rarely reoccur after treatment
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More frequently reoccur after treatment
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DNA analysis of tumours has shown that cancer cells are derived from a single mutant cell. Further mutation in one of the descendent cells leads to other changes that cause subsequent cells to be different from normal cells in growth and appearance. The two main types of genes that play a role in cancer are tumour suppressor genes and oncogenes. An importance difference between oncogenes and tumour suppressor genes is that while oncogenes cause cancer as a result of the activation of proto-oncogenes, tumour suppressor genes cause cancer when they are inactivated.
Oncogenes
Most oncogenes are mutations from proto-oncogenes. Proto-oncogenes stimulate a cell to divide when growth factors attach to a protein receptor on its cell-surface membrane. This activates the genes that cause the DNA to replicate and the cell to divide. If a proto-oncogene mutates into an oncogene it can become permanently activated (switched on) for two reasons:
- The receptor protein on the cell-surface membrane can be permanently activated so that cell division is switched on even in the absence of growth factors
- The oncogene may code for a growth factor that is then produced in excessive amounts stimulating excessive cell division
The result is that cells divide too rapidly and out of control resulting in either a tumour or a cancer. A few types of cancer are caused by inherited mutations of proto-oncogenes that cause the oncogene to be activated. Most cancer-causing mutations involving oncogenes are acquired not inherited.
Tumour supressor genes
Tumour suppressor genes slow down cell division (they suppress tumours/cell division), repair mistakes in DNA, and tell cells when to die (apoptosis). They have the opposite role to proto-oncogenes. A normal tumour suppressor gene maintains normal rates of cell division which prevents tumours. If a tumour suppressor gene mutates it becomes inactive/switched off. As a result the inhibition of cell division stops and cells begin to grow out of control. The mutated cells are structurally and functionally different from normal cells. Many die but those that survive can make clones of themselves and form tumours. Some cancers are caused by inherited mutations of tumour suppressor genes but most are acquired.
Abnormal methylation of tumour suppressor genes
Abnormal DNA methylation is common in the development of a variety of tumours. The most common abnormality is hypermethylation/increased methylation. The process whereby this leads to cancer is as follows:
- Hypermethylation occurs in a specific region (a promoter region) of tumour suppressor genes
- This leads to the tumour suppressor gene being inactivated
- As a result transcription of the promoter regions of tumour suppressor genes is inhibited
- As the tumour suppressor gene normally slows the rate of cell division it's inactivation leads to increased cell division and the formation of a tumour.
Furthermore, hypomethylation/decreased methylation can occur in oncogenes where is leads it leads to their activation hence formation of tumours.
Oestrogen and breast cancer
Oestrogen plays an important role in regulating the menstrual cycle in women. The fat cells of breasts tend to produce more oestrogen after menopause. These locally [produced oestrogens appear to trigger breast cancer in postmenopausal women. Once a tumour has developed it further increases oestrogen concentration which therefore leads to increased tumour development. White blood cells that are drawn to the tumour also increase oestrogen production. Basically how this works is, if oestrogen binds to a gene that controls cell division and growth then the gene will be activated and its continued division could produce a tumour. It is also known that oestrogen causes proto-oncogenes to develop into oncogenes which leads to the development of a tumour.
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