Linda at Oxford
It is hard to just sit down
and write when you don’t feel like it.
I have something important to write about, but I can’t summon so much as
a drop of either inspiration or enthusiasm. The problem probably stems from the weather; it is cool and
sunny today, and something inside me keeps saying: “Get your butt outside and
get some exercise!” And I would,
but it also is blowing hard. If I could drive to a deep wash somewhere and walk I probably would be sheltered –
but it has been raining lately, and I don’t trust a sandy wash after a
rain. So, weather wimp that I seem
to have become, I will stay inside and write another blog.
Dick Ingwall again has
alerted me to an important article in the NYTimes. It appears that two research teams have simultaneously reported
on an investigation of the genomes of certain cancer patients, specificially those with
melanoma. They sequenced the
so-called “dark matter” of DNA, which is a cute reference to the roughly 98% of
DNA which does NOT code for a
protein (are not “genes”, sensu strictu.) They found a mutation of a particular
sequence that codes for a regulartory molecule: something that tells a gene
when to turn on and when to turn off.
In 70% of the 70 melanomas
studied, the same short region of “dark matter” was mutated. Interestingly, the identical mutation
was found in examples of liver and bladder cancer. A separate study also published found that some people for whom melanoma
“runs in the family” (poor devils) INHERITED this mutation. So, this little DNA mistake is a nasty
brute, worthy of further study.
If I get this right, the
mutation is responsible for the proliferation of telomerase in the tumor
cells. You remember telomeres and
telomerase from previous blogs. Telomeres
are the protective stuff at the end of chromosomes that prevents premature
cell death. Telomerase is an
enzyme that rebuilds the telomere string – in stem cells and, regrettably,
cancer cells as well. If the
cancer cells didn’t have telomerase handy they would die normally after a few
divisions, not spread without limit, to the detriment of the organism. So far it has not proven possible to
attack cancer by going after its telomerase. However, efforts are underway – and progress is being made,
I certainly hope.
This is an interesting
article to which I have not done the least justice. You can read it yourself at: http://nyti.ms/WpggGy. .
It also is possible to read the abstracts of the two scientific papers
referred to in the Times story, by using Google Scholar. You can even get the articles
themselves; for $20 per, but - unless you majored in biochemistry - don't bother.
I am going to go back through
this blog and find all the times telomeres have come up. I will report, in a Comment. I think we’re on to something.
This just in! The NCI Cancer Bulletin, which I have mined repeatedly for blog ideas, has ceased publication. Why? BUDGET PROBLEMS! If there is one Federal agency that should never have a budget problem it is NCI. I would be willing to pay for the NCI Bulletin. Well, depending on the price, of course. I will still have plenty to write about - st least as long as Dick Ingwall continues to subscribe to the NYTimes.
ReplyDeleteBut there is a silver lining. The NCI Cancer Bulletin has an Archive, which is easy to use and will find you any articles published (by them) since 2004. You can get to it by simply Googling "NCI Cancer Bulletin Archive".
DeleteInteresting. Time for a little gene therapy, if we could just figure out how to target the cancer cells! I have faith that some day they will figure out how to do this.
ReplyDelete