• Question: Would it be possible to cure/prevent cancerous tumours by genteically mutating the cancer gene to introduce a Hayflick limit? Presumably, if this were possible, cancerous tumours would be significantly reduced in size?

    Asked by christiancox to Fiona, Jane, Joanna, Michelle, William on 18 Jun 2010 in Categories: .
    • Photo: Joanna Brooks

      Joanna Brooks answered on 16 Jun 2010:

      Wow you are super clever. Introducing a ‘hayflick limit’ means introducing a limit on the number of times a cell is able to divide. So yes, in theory it would be possible to introduce a hayflick to cure or prevent cancers in this way because if you stop the cancer dividing you can stop it from spreading.

    • Photo: Michelle Murphy

      Michelle Murphy answered on 16 Jun 2010:

      great question however all cell types divide at different rates just think of all the dust in your room being mostly dead skin and how many times your cells need to divide to replace that. Most of the time we can regulate this naturally as you know when it gets out of control we get cancer. There are so many causes for cancer and for skin cancer alone there can be any 1 or combination of 30,000 changes to a persons genes simularly 23,000 changes could cause lung cancer so it would be very difficult to target a gene. Death by cance has reduced by 11% in the last 10 years so scientists and doctors are doing something right and hopefully it will continue to decrease. Great question, thanks.

    • Photo: Fiona Randall

      Fiona Randall answered on 18 Jun 2010:

      Hi, that is a nice idea! All tumours are different and have different factors influencing their growth so finding one gene in all tumours would be difficult, however, you never know!

    • Photo: William Davies

      William Davies answered on 18 Jun 2010:

      The Hayflick limit is the number of times a normal cell can divide. Cancer cells are different, because they already have a mutation which causes them to go beyond the Hayflick limit, and divide indefinitely. This mutation can either disrupt a so-called tumour suppressor gene (which normally kills the cell when it starts dividing uncontrollably) or activate a so-called oncogene (which normally causes cells to divide). Our best hope for gene therapy is to restore the function of the tumour suppressor genes, or to reduce the activity of mutated oncogenes

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