Explain how cancers are a result of uncontrolled cell division and list factors that can increase the chances of cancerous growth

How is it caused? (In context to Mitosis)

Cancer is caused by mutations and abnormalities to genes which inflict excessive cell replications. The two major contributors of cause are oncogenes and Tumour suppressor genes.

• Onconogenes
  Onconogenes are the “engines” of cell division. In their normal cellular version they are proto-oncongenes.  Oncogenes code for specific protein to be produced which are involved in important intracellular signalling pathways which control aspects of the cells behaviour. A mutation in an onconogene can either give rise to the production of this protein and enhance the activity of the cell, or it can decrease the production of the protein which can decrease the activity of the cell.
  
  Growth stimulatory signal proteins are examples of these proteins for which are coded for by an onconogene. When produced normally, a growth stimulator or “factor” will trigger the cell to divide by binding to a specialized receptor glycoprotein which forms the upper part of the fluid mosaic model of a cell membrane. This then induces relay proteins to form to reach the nucleus to trigger the DNA inside it to replicate. This then goes through a normal cycle of mitosis and the cell replicates.
  
  However if the onconogene is mutated two possible outcomes can happen:
  Firstly the proteins can deregulate the pathways between cells so that the receptor protein is mutated. If the receptor protein is mutated, it can no longer respond to the growth factors so triggers relay proteins to be produced which go on and cause the DNA and the cell to replicate. This is all done in the absence of the growth factor so reproduction is continuous and has no limits.
  Secondly an abnormal onconogene can inflict many growth factors to be produced in excessive amounts. This causes the receptor protein to be continually bound to a growth factor so replication rate is very fast.
  
  Both of these result in a formation of a lump of cells where growth has been excessive. This lump is called an adenoma. It can grow larger and invade surrounding tissue. Some cells may even break off and be transported from the body in the blood stream if it is malignant. If it is benign, the growth is sealed by non-cancerous local specialized cells and white blood cells.
  
  
• Tumour Suppressor Genes
  Tumour suppressor genes are the “breaks” on cell division. This form of cancer explains certain types of cancer which are heredity and most members of the family have similar types of cancer present. This would be a coincidence if it was due to the mutated oncongenes in every single case. Unlike oncongenes, tumour suppressor genes slow or stop cell division if it is know to be faulty or mutated. Just before DNA replication when growth factors “switch on” and become active to trigger cell division is an important regulatory point. Oncongenes encourage this part of the cycle, Tumour Suppressor cells prevent it. So instead of having to destroy thousands of mutated cells which can cause damage, it is easier and safer to kill the parent faulty cell to prevent extensive replication of mutated cells. So if a cell suffers DNA damage, the level of TSGene is increased. Once it is repaired these levels will drop to normal again.
  In some cases, damage to a Tumour Suppressor gene can be the cause of cancers. When a mutated cell has not been repaired it can replicate extensively and form an adenoma. Therefore it replicates very quickly because of the increasing number of cancerous replicating cells. Usually, this is the more dangerous form of cancer and in most cases is malignant due to the higher amount of cells.
  Examples of Tumour Suppressor genes include the P53 gene (“guardian of the genome”) and Rb which is important in preventing the development of retinoblastoma in children.
  
• Lack of apoptosis
  Apoptosis is when a cell “commits suicide”. When a tumour suppressor gene is not sufficient to repair the cell, apoptosis occurs and kills it as to not replicate. Apoptosis is very important and happens frequently e.g. in a developing foetus, apoptosis occurs between their fingers to ensure they are free to move and only attached to the hand, not other fingers. Apoptosis is triggered by the gene P53. If this is lacking or mutated not only will it cause faulty cells to replicate (see above) but will not be able to destroy them when they do replicate.

What factors increase the chances of developing cancer? (Carcinogenic factors)

• Smoking – This is the biggest risk factor causing 30% of all cancers. It damages the lungs and causes dangerous chemicals such as Carbon Monoxide.
• Age – as someone ages, genes will suffer damage just through day-to-day living
• Alcohol consumption - Excessive alcohol consumption plays a role in mouth, throat, oesophagus and liver cancers.
• Chemicals present in the combustion of fuel i.e. coal.
• Heredity – Chances are much more likely of developing cancer if a family member has already had it due to inherited genes.
• Sun/UV Exposure – Causes damage to epidermis of skin so it is more vulnerable.
• Diet – poor diet (high animal fat content) can cause malnutrition and poor health of body increasing the chances of cancer.
• Exercise – Not exercising can again cause poor health of the body, poor circulation etc increases the chances of cancer.
• Occupation - if exposed to radiation, asbestos, silicon, dusts, etc.
• Medication - radiation and/or drugs for one cancer can cause later cancers.