top of page
Search
  • Ayah

Mutations and Cancer: A Despicable Yet Fascinating Relationship

Cancer is the uncontrollable growth and division of cells; this occurs as a result of a mutation occurring in the genes that code for the regulation of mitosis. If these genes mutate (due to a change in the base sequence) and undergo transcription, the mRNA produced will carry the incorrect genetic code from the faulty DNA it was transcribed from. This mRNA then travels out of the cell and into the cytoplasm to a ribosome, here, translation will occur but due to the mutation in the original base sequence of DNA, this mRNA will be translated by tRNA into a non-functioning protein. As this non-functioning protein would have controlled the rate of mitosis if it were not faulty, the cell is left to undergo mitosis without any form of control. This results in the uncontrollable growth and division of cells which causes tumours (clusters of cells growing out of control) to develop.


These tumours can be classified as either benign or malignant. Unlike benign tumours malignant tumours are cancerous. Malignant tumours are invasive and have a rapid rate of growth. These tumours do not produce adhesion molecules causing metastasis to occur. Metastasis is the spread of cancer from one site of the body to other sites. During this process, parts of the tumour will be dislodged and spread to other organs and tissue in the body via the bloodstream. Once cancer has spread it can become very difficult for doctors to determine where exactly the tumour they have to remove is located since there is more than one invaded site. Since malignant tumours are not encapsulated, they can grow projections into adjacent tissue to form their own blood supply. This feature contributes to the uncontrollable spread of malignant tumours.



Stages of tumour development (image credits: ResearchGate)

The development of a malignant tumour is due to a gene mutation in either the proto-oncogenes and/or the tumour suppressor gene.


Proto-oncogenes are genes that responsible for synthesising proteins that are involved in cell growth, division, and apoptosis. When a mutation occurs (deletion, substitution, duplication, etc.) in the proto-oncogene, the DNA base sequence is altered, and the gene becomes an oncogene. When oncogenes are translated onco-proteins are formed. Onco-proteins are the cause of cancer in this case; these proteins induce cell division and proliferation, and inhibit apoptosis. The cell then continuously grows and replicates but since apoptosis is inhibited, eventually, the cell will have produced a mass of undifferentiated cells, forming a malignant tumour. This tumour will continue to grow and divide, if unencapsulated, eventually, metastasis will occur. Metastatic cancer is also known as stage 4 cancer, as it has spread far into the body and is very difficult to treat. Most cancer patients die as a result of metastatic cancer, in fact, metastatic cancer accounts for approximately 90% of cancer deaths.

The rate of tumour growth expressed through the ‘Power Law’ model (Image credits: Archive ouverte HAL)

Tumour suppressor genes supress the growth and development of tumours. When translated, these genes produce proteins that slow down cell division and cause apoptosis if any DNA copying errors during DNA replication are detected. Tumour suppressor genes also help repair DNA that has been damaged by mutagens. If a mutation occurs in the tumour suppressor gene, such as P53, the gene becomes inactive and can no longer synthesise the proteins required to halt the cell cycle at the G1 checkpoint in order to repair DNA before it is replicated. As a result, mutated cells begin dividing at an exponential rate as they have not been identified nor destroyed. This rapid division leads to the rapid build-up of mutations as the absence of the tumour suppressor genes means that the damaged DNA cannot be repaired. As the mutant cells continue to divide and replicate, tumours are formed, very often these tumours will be cancerous.


82 views0 comments

Comments


bottom of page