Cancer genetics

Cancer genetics for schools and colleges

Topic related resources

Our DNA is constantly mutating at a given rate. This rate can be increased or decreased depending on our exposure to mutagens (risk factors such as smoking). Cancer is an uncontrolled cell division that occurs following a series of mutations deregulating key cellular processes.

Cancer is a genetic disease, consisting of uncontrolled cell division into large, malignant tumours. There are many different types of cancers, for example: lung cancer and cancer of the blood (leukaemia). Cancers begin with the development of small benign tumours, which can develop into malignant ones, spreading to other parts of the body. Cancerous cells have lost control of their cell cycle, are immune to apoptosis (programmed cell death) and are not fixed in place meaning they can spread.

A series of mutations are required to develop cancer

Throughout our lives, we are constantly getting mutations in our DNA. Mutations are what drive adaptation and evolution, so in the long run many of these are beneficial. Whilst some mutations are beneficial, many are detrimental to our health and cause 'genetic disease'. Cancer is one such example of a genetic disease. For cancer to develop, one mutation is not enough. A series of mutations must accumulate over our lives in order for cells to become malignant. Sometimes these mutations can occur early, sometimes late, and sometimes we may never get the mutations required to develop cancer.

Cancer progression

Above is an image from the national cancer institute that illustrates the process of cancer development. Several mutations in both oncogenes and tumour suppressor genes are required for the development of cancerous, malignant tumours.

Mutations leading to cancer often occur in two different types of genes:

Proto-oncogenes

Proto-oncogenes are those which have the potential to mutate into cancer causing genes (oncogenes). In tumour cells they are mutated, or expressed in larger quantity than healthy cells. Overactive oncogenes have many functions including: speeding passage through the cell cycle uncontrollably.

Tumour suppressor genes

Tumour suppressor genes (TSGs) protect cells from damage and from becoming cancerous. For example the TSG, p53 is involved in a variety of processes including DNA repair and programmed cell death. Mutations in TSGs stop these protective functions and allow cells to become cancerous.

TSG and oncogenes

Oncogenes push the development of cancer, whereas tumour suppressor genes try to prevent cancer from developing.

For a tumour to develop into a full blown cancer, mutations must occur in both oncogenes and TSGs. Different cancer are a result of different mutations, in different oncogenes and TSGs.

 

Mutation rate

Mutations in the DNA of living cells occur at a given, stochastic rate. This is because DNA replication is not an entirely fool proof process. The rate of mutation in humans is roughly 0.32 substitutions per complete replication of the genome. The rate of mutation depends on several different risk factors.

Risk factors

The development of cancer is down to chance. We require a sequence of mutations to develop it, but whether or not this happens is pot luck! There are however some risk factors and behaviours that can increase the mutation rate of our cells, and as a result make us more likely to get the mutations responsible for cancer development. These include exposure to high levels of background radiation and smoking.

 

 Quiz

 

If you want to learn more about cancer genetics and mutations rates, take our online tutorial

 

 Creative commons logo

This work is licensed under a Creative Commons Licence.

Share this page:

Who are we?

GENIE logo

University of Leicester
genie@le.ac.uk

How can I contribute?
Glossary
Illustration of a book

Find definitions of words in bold