From the first moment my wife discovered
she had breast cancer, there was a deafening silence from the men I know. Even
ones whose wives, mothers or girlfriends had breast cancer seemed to have
received a gag order from some Central Cancer Command and did little more than
mumble about the experience. Not one to shut up for any known reason, I started
this blog…That was four years ago – as time passed, people searching for
answers stumbled across my blog and checked out what I had to say. The
following entry appeared in June of 2016…
Targeting breast
cancer cells seems to be a major new thrust in the fight against breast cancer.
I talked about it a couple of months ago here as well as some years ago: http://breastcancerreaper.blogspot.com/2012/09/breast-cancer-research-right-now-2.html
and here: http://breastcancerreaper.blogspot.com/2016/04/breast-cancer-research-right-now.html
But how do you get
from the IDEA of targeting cancer cells to trying drugs to do it? Apparently,
you can do computer models.
Now don’t get me
wrong, I am NOT a fan of computer models. The model is only as good as the
person who inputs the raw data and the person who writes the program. Computer
models are notorious for spitting out inaccurate predictions and drawing false
conclusions – not the machine’s fault, of course. Like I said, programmers and
data entry folks. Also, the assumptions of the researcher can find their way
into the model as well; but that’s happened since forever, so it’s not a new
factor.
Here we have the
following: “Researchers have built a model to investigate the metastasis of
cancer by examining the metabolism of breast epithelial cells and look at the
role of signaling. This research may contribute to the development of cell
specific anti-cancer interventions.”
In English, then:
researchers are looking at how the
cells that typically erupt into breast cancer cells use the nutrients they get
from the body and the waste materials they give off. With that kind of a trail,
scientists can design drugs to follow the trail and destroy the cancer cells.
Sounds simple
enough – sort of like the old story of Hansel and Gretel: going out into the forest,
the smart little girl leaves an easily followed trail that her and her brother
can follow back home.
In this case, the
cancer cell leaves a trail that well-designed cancer drugs can follow. Then
they can destroy the cancer cell. The way it’s done now, is that drugs like
Taxotere (which interferes with cell division), Adriamycin (which inserts
itself into the cancer cell’s DNA so the cells can’t make new cancer cells),
and Cytoxan (which sneaks in as a harmless drug, then is converted by the
cancer cell into a toxin) – but they aren’t perfectly targeted. They kill hair
cells and T-cells that protect the body from infections.
The researchers,
programmers, and data entry people are working to reduce the amount of damage
current cancer drugs do while still maintaining the attack on cells.
So, while I won’t
CHEER this new model on, I will certainly watch to see what kinds of effective
results it produces!
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