Linda and Raelyn Joyce
Borrego Springs, 2009
Now let’s see if I’ve got this straight. There is a gene named p53 (sounds like a WWII
fighter plane) that is sometimes referred to as the “Angel of Death”. This gene “codes for” a protein that tells
badly damaged cells to go ahead and die.
To illustrate the depth of my learning, I could have said that “P53
initiates apoptosis”, but of course I would never show off like that. Anyway, cancer cells certainly are “badly
damaged”, but p53 lets them go on their way, multiplying and causing trouble. Why?
Well, apparently cancer cells defend themselves in one of two ways: they
either disable the p53 gene (mutation) – I may have cause and effect a little
screwed up here, but never mind; - or they disable the p53 protein by attaching
another big biochemical blob – MDM2 - to it. Thus, two ways to fight cancer, both involving
p53: P53 has long been known as a key
player in the cancer game; Science magazine named it “Molecule of the Year” way
back in 1993, and interest in it has been intense ever since. So why is there still cancer? As with so many other promising avenues in
cancer research, initial euphoria gives way to “Well, hell, it’s a lot more
complicated that I thought.”
An attempt has been made to insert healthy p53 genes into
cancerous cells, so far to no avail, although efforts to do so continue. A more promising approach has been to attack that
portion of cancers (I gather it’s large) enabled to prosper by virtue of the MDM2-p53
protein union, this by administering a drug that delivers a small molecule that will pry
the two apart. (How in heaven’s name do
they do stuff like that?). An
experimental drug doing this has cured one type of cancer in mice,
completely and without any fuss. (Of
course, one of the researchers is quoted as saying “If we just wanted to cure
cancer in mice we would have been out of a job 30 years ago”). Small
scale “efficacy” trials in humans currently are under way. There are three big drug companies competing
to get the best drug on the market first: Merck, Roche, and Sanofi. Curiously, there is another, much smaller,
company that is leading the race: Cellceutrix, with their drug Kevetrin. Reader comments to the NYTimes article I am
paraphrasing (http://nyti.ms/XZS1PB)
include two from people associated with Celleutrix, expressing outrage that
their little company was ignored in the article. Expect Pfizer or Novartis or the like to buy out Celleutrix and thus get in the
game, making a few multi-millionaire biochemists as a bi-product. By God, if they can cure cancer – any cancer,
let alone a whole bunch of them – they deserve their reward.
Because, you see, this type of clinical treatment supposedly
is independent of cancer type or origin; it should work equally well with many
cancer types, common and uncommon – ovarian, alas, not mentioned. Back during the Nixon administration the Feds
initiated a “war on cancer”, visualized as a medical version of
the moon-landing program. It failed, not
least because cancer was found to be so disparate – there isn’t a “cancer”;
rather, there are a whole host of cancers, each with its own
characteristics. Now, maybe there is hope for
a general cure, after all - and p53 may be our White Knight.
By the way, the book “The
Emperor of All Maladies: A biography of cancer” has a very readable – if at
times horrifying – history of cancer
treatment. Read it only if you have a
strong stomach.
This blog comes to you indirectly from Dick Ingwall, who did
not write it but fed me the information (again, http://nyti.ms/XZS1PB). Dick deserves to be co-author on many of my
blogs, but he is too modest to allow it. Or maybe he simply is protecting his scientific integrity.
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