How can we find "cancer genes"?

14 January 2013


Cracking Cancer DNA

Chris, Kat,

If a cancer is the result of random mutations in my DNA, how can they "crack entire genetic code" of (a) cancer?

From linked article.     "The scientists found the DNA code for a skin cancer called melanoma contained more than 30,000 errors almost entirely caused by too much sun exposure." "Although many of these mutations will be harmless, some will trigger cancer."
"Most of the time the mutations will land in innocent parts of the genome, but some will hit the right targets for cancer."

Do common cancers mutate the same way coincidently in every person so that cancer is like a lottery where 48, 56, 20, 19, 40 is meaningless but 67, 50, 26, 10, 40 always means "Congratulations you just won lung cancer type X!"

Do we inherit mutations (67, --, 26, 10, 40) from our parents/cline and 1 cell in our body just happens to roll that 50 - the required trigger to activate the inherited cancer genes? Is that the explanation for "inherited" cancers?

Is cancer a set of newly mutated genes that do "cancerous" things, or is it always a ruining of "good" genes so that they can't do their good jobs - like ensuring cell-death.

Or more pictorially, Did the mutation render useless the apoptotic executioner, or did the mutation create a new "super" gene that overwhelmed the executioner? Or are both possible?

And because this new super-gene is not inheritable - because it didn't happen in the egg or sperm cell - it can't be passed on, but only randomly appears again in some other person?


Answered by Dr Julie Sharp from Cancer Research UK

Julie - When scientists are trying to crack the code of a particular cancer, they look at all the different genes from an individual's healthy cells and then their cancer cells, and they make comparisons between them. This gives them a huge map of all the different genes that are faulty in that particular cancer. They then have to sift through all of these information because there are many, many different faulty genes, but some of them will be the really important genes, the ones that are really causing and driving the cancer, helping it to grow and spread. Some of the faults are just picked up because the cell's in disarray, there are things going wrong, and some of them aren't really, really important.

So, the thing they have to do is then to, from this great amount of information they've discovered, actually work out which are the key driving faults, which are the you know, really important ones. And there isn't just one combination of gene faults and bingo! You've got cancer. There are lots of different possible combinations of gene faults. You can have a number of faults before your cells develop cancer. But there are genes that are commonly faulty in a particular cancer, so for example, the gene BRAF is quite often faulty in melanoma skin cancer, but then it will be faulty along with different other genes and those range of genes will differ between different people.

The genes that lead to cancer when they're faulty, it's stopping them from doing their normal function and some of these genes will normally be involved in things like helping cells to grow and develop. That means when they're faulty, cells will start growing and developing out of control. And in other cases, genes are linked to processes that would normally protect us from cancer. So they're the checks and balances in the cell, when they're faulty, that just means those safeguards aren't there and things can develop out of control.

And finally, there's a real spectrum of different types of faults that lead to cancer. So, we know that a minority of cases, people will inherit this really high risk genes that are passed on through families, and that means you're at greater risk of developing cancer - that's the genes like the BRCA genes. They don't mean you will get cancer, but you have a much greater chance of developing the disease. Most cases of cancer are caused by the faults that we develop through our lifetime, just through the ageing process, through wear and tear in the cell, and through the effect of lifestyle.

So, whether we've smoked, whether we've laid out in the sun and got sunburn, all of those things play a part. What we're gradually finding out more about is that there are also some genes that are passed on through families that have a smaller effect on our risk and so, it's really a spectrum. In most cases, it's what we've done during our lifetime, but there will be things that have been passed on through our families that will have had an effect.

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