Download P53 genes HW - St Paul`s School Intranet

Mutations, mitosis and cancer
Around 11 million people per year are diagnosed with cancer, half of them over the age of 65 and the
majority in MEDCs. Cancer is multifactorial, meaning that a number of things affect a person’s
likelihood of contracting the disease. The major risk factors include AGE, GENETICS and LIFESTYLE.
Age is a factor mainly because cancer is about probability; the longer you live the more likely you are
to get it. Since people in MEDCs live longer and don’t die of infectious diseases very often, they are
more likely to suffer from cancer; it doesn’t necessarily follow that living in a rich country causes
cancer, only that you have to die of something.
There are a very large number of genes associated with cancer. Remember that these genes don’t
exist to make you ill. Problems usually arise following a mutation which affects their normal
function.
CDK2 (chromosome 9)
One of a number of proteins which control cell division. The CDK2 protein switches on DNA
replication and stimulates cells to initiate mitosis.
p53 (chromosome 17)
Produces a protein which acts as a “transcription factor”, switching on a number of other genes. One
of these is p21. Some people inherit a defective p53 allele from one of their parents, so each cell has
only one working copy. Accidental damage to this copy (during replication or due to ionising
radiation or chemical carcinogens) may result in a change in the cell’s behaviour.
p21 (chromosome 6)
The p21 protein interacts with the CDK2 protein and switches it off. As long as p21 protein is
present, DNA replication and mitosis will be blocked. p21 will be active during interphase to prevent
the replication of DNA and to allow the cell time to grow and develop normally.
Questions:
1. Produce a flow chart showing how a p53 mutation might cause uncontrolled cell division.
2. p53 is a “transcription factor”. Outline what happens in transcription and why this results in
protein synthesis.
3. What do you think a cell with inactive p21 would look like?
4. Suggest why a p53 mutation is likely to increase the chance of further mutations.
5. What are the differences between benign and malignant tumours?
6. Anti-cancer drugs (chemotherapies) kill any cells involved in cell division. Why do they work,
and why do they have unpleasant side effects?
L8th | Cell Division Cycle & Cancer HW