I am just back from Alaska.
Yesterday would have been Linda’s 73rd birthday. I sure do miss her. If you would like to give her a little
birthday present, please do it here:
We are closing in on an important goal.
Friday, August 31, 2018
Thursday, August 16, 2018
MEMORIAL SLOAN KETTERING
A COLD CHRISTMAS DAY
Thank God for rich people!
.
The object of today’s sermon is Memorial Sloan Kettering
Hospital and research facility, located in New York City.
Memorial Sloan Kettering (MSK) came into existence in the
late 19th century, funded in large part by one of that era’s richest
men, John Jacob Astor. (When I was a
kid, my mother would often describe somebody extremely well dressed as “being
as dressed up as Astor’s horse.) The
Sloan Kettering part arose in the mud-29th century when Alfred P.
Sloan and Charles Kettering, both General Motors big-shots, funded a cancer
research facility and attached it to Memorial Hospital.
The result: either the nation’s best, or second best (if
you’re from Houston) place to be if you have cancer.
Well, MSK has just published results of their effort to use
immunotherapy to destroy solid tumors.
Here is their press release:
Briefly, what these folks have done is to combine CAR T therapy
with a drug that acts as a checkpoint inhibitor. (And you faithful readers of this blog know
what those things are, right?). With
their usual hilarious creativity they have named this treatment as “armored
CAR”. Whatever: if it works they can
call it anything they please.
So, of course, this work is still in the mouse-model stage,
although some mention is made of human trials.
Soiunds good. The
fact that this paper is big stuff is attested to by the journal it appeared
in: Nature
Biotechnology. Get a paper into a Nature journal and you’re tenured for
sure.
Tuesday, August 14, 2018
NUTS!
Mitzi, Linda and me
A long time ago
Not what I wanted to read!
Our British brethren newly report on the genomics of ovarian
cancer. Apparently OVCA cells are a
frightful mess, harboring every kind of mutation you have ever heard of, and
maybe more. They (the Btits) have done what has become
fashionable nowadays; turned Big Data algorithms loose to look for similarities. Big Data has presented them with seven basic
patterns, and – in some cases – more than one per patient. Several of these patterns are good news, but
others are nasty.
Why I dislike this result is obvious. Immunotherapy works, it seems to me, by
recognizing fairly simple genetic problems, and then fixing them. But how go after a roiling pool of problems?
Still, every little bit of data counts.
Sunday, August 12, 2018
CLINICAL TRIAL FOR ADVANCED OVARIAN CANCER
Linda and Butch
Color coordinated
Well, here’s one I hope none of you ever need, but if you do
make sure your oncologist is aware of this:
Saturday, August 11, 2018
DISCOURAGEMENT
Probably an early anniversary
When we went to dinner, I left the hat at home
So much to learn, so little time!
In an effort to broaden my horizons, my daughter Karen has
begun to ply me with worthwhile contemporary fiction. First she introduced me to Ahab’s
Wife, which turns out to be a captivating but spectacularly implausible story, served up with some prose that I find
irritating at times, but fascinating on balance. I have nearly given up, on it twice, but here
I am – half way through – with the book next to my favorite chair and a
bookmark still in place. And smiling at me from the coffee table is
another of Karen’s suggestions – All the
light we cannot see.
The trouble is, when I am reading fiction I feel like I am
wasting time. Something deep inside me
nags: you ought to be learning more about cancer research, it insists. This has been the case for years. My usual response is to have two books going
at once, one light and frothy, and the other deep, serious and, often, really,
really dull. That’s what I am doing
now: I just started The Transformed Cell, by Stephen Rosenberg and John Barry. Rosenberg is a famous cancer researcher –
almost a demi-god in the field of immunotherapy, and Barry is a well-known and
much-published science writer.
Boy is this book anything but boring!. I don’t dare read it tonight for fear of lost
sleep; I think I will read about Ahab’s wife’s shopping trip to Boston instead.
But I did want to mention something I find very disturbing. The
Transformed Gene was written in the early 1990s. In the forward, Rosenberg relates what must
have been some of the earliest applications of immunotherapy. He writes, quoting Pasteur, I am on the verge of mysteries, and the veil
is getting thinner and thinner.
That was nearly 30 years ago.
Wednesday, August 8, 2018
GEEZ!
on our last trip
northern Mexico, probably 2009
Oh, sweet Lord in Heaven!
If You are really up there – why did you make this stuff so
complicated? Maybe we’re NOT supposed to
figure it out, but just to get awarded points for how hard we try!
This was my reaction to the “press release” cited
below. Not often in my ignorant blundering
through cancer biology have I encountered such a concentration of stuff I don’t
begin to understand. Why don’t you take
a look, if only to appreciate my dilemma?
Best as I can figure out, there is this gene called GULP1, which
somehow is important in getting rid of crap left over following apoptosis –
cell death. GULP1 can be “silenced”
epigenetically by methylation, and in a disproportionate number of cases of
ovarian cancer, it is. Whatever protein
GULP1 codes for apparently swallows the dead crap whole – hence GULP1 is
classified as an “engulfment gene”. Clever,
these people in white coats, don’t you think?
There is one thing that – other than its opaque nature –
bothers me about this “press release”
One of its principal contributors is an outfit called Insilico Medicine,
which is headquartered in Rockville, Md., but has lab facilities located all
over the place, from Belgium to Korea.
They state that they are “sourced through hackathons and competitions.” I detect a faint trace of snake oil when I
read those words, and it is amplified by the bad grammar found throughout the
article. However, this must be legit – Johns
Hopkins is another contributor.
Monday, August 6, 2018
BRAF. GOOD GOD, WHAT'S THAT?
Linda at the Otovalo market, Ecuador
Good Lord, how do they do this stuff!?
In what used to be my line of work (geology/geotectonics)
one operates thusly: First you read the
literature, talk to your buddies, and think.
From this, with luck, a clever hypothesis arises.
Next, you tests that hypothesis by first predicting a consequence:, “If
I am right then thus and such must be true.”
Finally, you go in the field in search of thus and such, which often may
be as tangible and unmistakable as a rock, a fault, or even a mountain range. If it’s not there, you’re wrong – go drink a
beer and start over.
But these molecular biologists/cancer researchers face no
such simple and straightforward task.
First of all, they are dealing with stuff far too small to actually see,,
hence must (it seems to me) grope around in the dark searching for clues. Also, the systems within which they operate
are vastly more complicated than anything I ever encountered. Geez!
Elsewhere I have stated that, if I had it to do again I
would go into cancer research. I take it
back: I’m not smart enough.
So, anyway, today I encountered another gene I’ve never
heard of. It is called BRAF, and when
functioning correctly codes for a protein
that somehow is vital for proper within-cell signaling.
Mutated BRAF may lead to cancer and birth
defects.
What can be done about it seems to be a work in progress.
Click on the link below and you will read of BRAF and OVCA,
as well as many other things. The lead
illustration alone is worth the price of admission.
Friday, August 3, 2018
EPIGENETICS GONE ROGUE
Linda and the Prince of Darkness
You all know that a mutated, non-functional BRCA1 gene places a woman at much greater risk
of breast and ovarian cancer.
Right? However, now it appears that you can have a
perfectly fine BRCA gene – and still be at increased risk of breast and/or
ovarian cancer. How? Well, some smart people in Manchester
(England) seem to have shown that BRCA1 is susceptible to epigenetic
silencing. By that is meant that an
epigenetic marker can be attached to the BRCA1 gene that prevents it being “expressed”
– giving rise to a functional protein. How
this occurs is explained, not very clearly, in this blurb
Why something like this should occur is another
question. Perhaps a more important
question.
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