Wednesday, September 17, 2014


Enjoying herself, in a small town at the top of Norway.
Back in the day I used to pay a lot of attention to my science citation score.  To all you unfortunate enough not to have played the academic game, a “science citation score” is the number of times that your work has been cited in the scientific literature.  The higher your score, so goes the thinking, the more important you are, or can pretend to be – in your own field, of course.  Whatever its actual meaning, a good SCS is a useful lever to pry a promotion or a sabbatical leave out of a college administration.  For a brief, glorious half decade or so I was #3, according to this measure.  Ted Irving and Rob van der Voo were ahead of me – Ted was untouchable; Rob usually within reach.  But I was #3, which, I thought, was pretty darned good.  Being the competitive sort, every few weeks I would go to the library and check the new “Science Citation Index” record.  Each time I did I would get a jolt: “my God, I’m  #2 and I’m even pushing Ted”.  But then I would remember Melinda Beck.  It happened that both Melinda and I were recorded under “M. Beck”.  After I went through the titles of the cited papers and subtracted Melinda I would find myself back at #3, and that sometimes by the skin of my teeth.  Now, of course, I must have dropped completely off the charts.  I haven’t checked, and I’m not going to.    However, I may still claim one honor: I suspect that I have written more papers that have never been cited by anyone, than anyone else in my field.
All this by way of introducing Melinda Beck.  Among other things, she is a science writer for the Wall Street Journal.  She is the author of an informative article in the Wall Street Journal, titled “It’s Time to Rethink Early Detection”.  Read it yourself at:
So, what is Melinda on about?  A short summary of a fairly lengthy article follows. You can think of her essay as reporting on a new set of skirmishes in the “early-detection: is it useful?” wars.  We have been reading a lot about this altercation lately.  It applies particularly to breast and prostate cancer, but has application across the board.
The fundamental proposition here is that early detection may catch some truly dangerous cancers, but also potentially nets schools of conditions, conventionally called cancer, that will never develop into anything bad, or will do so slowly that they can be ignored if the patient has reached  a certain age.  Medical folks can never resist an acronym: they call these things “indolent lesions of epithelial origin”, or IDLE for short.  Some of these medical folks argue that so many IDLE’s are detected, and then fussed over, that periodic screening does more harm than good.
Now, I think this reasoning is wrong, because I lost a wife to a cancer that, if detected in stage 1, might have been cured.  However, the other side has some good points.
For one thing, they call for more research on ways to determine with reasonable certainty if a newly-detected baby lesion will develop into a dangerous cancer, or into an IDLE.  That’s obvious.  They also present lots of numerical evidence to the effect that “over-diagnosis” leads to “over-treatment”, and then inevitably into unnecessary expense and anxiety.  They also call for more genetic counseling and more public education in general, which would be hard to argue against.  Moreover they point out, correctly, that some cancers are so aggressive and lethal that they will never be detected in time, absent a very short screening period.  They argue persuasively.  I am still unconvinced.
One thing seems obvious, though.  If the situation in the screening/IDLE situation is really this complicated, and the consequences of guessing wrong so dire, choice should be left entirely to the patient.   If the patient has access to and understands the facts, and if his or her doctor also is keeping up with the times and thus can give useful advice, then the patient obviously should make the decision. Government, the Health Care Establishment, Organized Religion, and Writers of Blogs - all should butt out. This sort of thinking appeals to my small government, laissez-faire, liberal (in the original sense of the word) soul.

Monday, September 15, 2014


Mt. St. Helens, a few years ago.
If that tree is vertical, then the concrete pillar is snuzzling up to her.
The link above will lead you to an interesting and very informative article in the New Yorker Magazine.  It is written by a journalist who specializes in medicine and biology.  It is easy to understand.  Like all New Yorker articles it is over-long; it says in 23 pages what the Economist would say in two, and The Week might stuff into two terse paragraphs.  But read it anyway.  You will be glad you did.
I am sure that New Yorker authors are paid by the word.
The main point here seems to be that there is a new way to deal with cancer.  Mainly, of course, we try to avoid it entirely.  We stop smoking.  We have our fallopian tubes removed.  We avoid asbestos.  We stay thin.  We eat “right” (whatever that is.)  We try to avoid having a family history of cancer.  (Well, that is impossible, of course, but it would help if we could.)  But sometimes we get cancer, anyway.  Then what to do?
Well, heretofore our only recourse in that event is to kill the cancer cells.  We cut them out, poison them with chemo drugs, blast them with X-rays, and pray.  According to this article there is another route: we can teach the damned cancer cells to behave themselves.  We can persuade (trick? force?) them to grow up and behave like normal cells.  There are several drugs in clinical trial or on the market that attempt to do just that, with encouraging results.
I am going to quote from the article.  The author was once a practicing physician, specializing in blood diseases and oncology.  The states that”
“In medical school we were taught that, although cancer comes in many forms, it has one immutable characteristic: it is composed of immature cells”.
 I underlined the word “immature” in the previous sentence because it is the cornerstone of this sort of therapy: the drugs being developed force the cancer cells to “mature”.  How they do it is interesting and complicated: I will let you puzzle it out for yourselves.  However: here is a hint.  Molecules responsible for cancerous behavior can do so because they have a certain precise shape, enabling them to glom onto other cells and shut them down, activate them, or otherwise change their behavior.  If we humans can devise other molecules with precisely the right shape to glom onto these bad actors and immobilize them before they do their damage, then – game over!  I have been gloomy lately (about cancer, that is); this article has cheered me up. 
Joanne Ingwall alerted me to this essay.  She and Dick keep me busy – for which I am very grateful.
Finally, I have recently engaged in an email exchange with a former graduate student and valued colleague, who told me that he enjoys the pictures I put in my blog.  When I thanked him and mentioned the text he said, in effect “Oh?  Is there text?”  Well, I mostly made that up, but it serves my purpose - I know many of you enjoy the picture, then say "Oh, what is he on about this time?" and cut to Facebook.  I can't really blame you, but - please read this one.  It's good.

Friday, September 12, 2014


Artist's Point
Quite a while ago.
Also in a recent NY Times was news of another front in the dogs vs. ovarian cancer war.  You should read it; it is informative, encouraging, and even a bit amusing.
It appears beyond question that some dogs, properly trained, can detect the presence of some cancers with astounding accuracy.  With regard to ovarian cancer, one reason for pessimism is the stage at which the dog could sniff out the offending growth.  Can they detect them at Stage 1, or even sooner?  If so, hooray!  But maybe not.  Scientists at U. Pennsylvania are using dogs to isolate the precise chemicals that - to the dog – indicate the presence of cancer.  Then, these same scientists hope to construct a “mechanical nose” that will, in effect, go the dog one better.  More power to them.  However, in the meantime, covering their bets, so to speak, they are honing the abilities of their canine machines: maybe even breeding good sniffers.  A warm, furry detection device with a wagging tail would beat a metal gadget, any day.
Another problem that may arise is that the dogs will detect chemicals that may be common to several different kinds of cancer.  This leaves the clinician with a big problem: where to look? 
I blogged previously about dogs and ovarian cancer*.
Ha!  Spell (& grammar) Check doesn’t know that “blogged” is a verb.  The language evolves!

Thursday, September 11, 2014


With unknown baby, in unknown venue.
Wow!  Dick Ingwall has opened the digital horn of plenty and dumped a load of interesting cancer news onto my computer.  I will deal with a little of it here, then come back to it in a day or two.
The first bit is both gratifying and provocative.  Dr. Mary-Claire King, of the University of Washington, has been awarded the Lasker Prize, which is an enormously prestigious award for contributions to medical science.  It appears that Dr. King was the first person to recognize that a mutation of the BRCA1 gene is associated with a greatly increased risk of breast cancer (and, as it later appeared, ovarian cancer was well).  In her acceptance address she called for universal testing of women for this, and presumably other related, genetic anomalies.  We have pondered that possibility before.  The argument "for” is simple; it would save women’s’ lives, as mutation-carriers  could gthen be monitored more carefully and treated, if necessary, when the cancer is small.  The argument “against” is twofold: cost, and quality of life.  Eventually, I fervently hope, technology will reduce the cost of genetic testing to a manageable level.  However, it will remain true that such universal testing will reduce the quality of life for a substantial number of people; those women who are positive for the mutation but never develop the disease (and that would be most of them), and – of course – their families and friends.  This seems to boil down to a simple choice: is it better to scare the moderate hell out of 100 women and save one life, or leave everyone in blissful ignorance and lose that life?  To me the answer is obvious.  What do you think?
However, several things seem indisputable.  First of all, we need more access to genetic counseling.  Also, the organization called FORCE* is definitely on to something.
*I blogged about FORCE previously:
and several times thereafter.

Tuesday, September 9, 2014


Chiricahua National Monument
mid 1980s
Ten top take-aways from the Ovarian Cancer Research Symposium, held at Seattle University and sponsored by the Marsha Rivkin Center for Ovarian Cancer Research.
I attended the first sessions, but my brain screamed “maximum overload” at the end of the day, so I came home a day early.  I will puzzle over the Abstract volume at leisure, and if I find something earth-shaking – that I can understand - I will get back to you.  In the meantime: 
1)      Demographics:  Of the 300 participants, about 65% were white Anglo-Saxon/European types, 35% were Asian, and <1% were something else.  One of the presenters was an African-American woman.
2)      More Demographics:    Well more than half of the audience consisted of women, but most of the presenters were men.
3)      Asian presenters were reasonably easy to understand if they were Chinese, but essentially incomprehensible if they were from India.  This ran completely contrary to my expectations.
4)      An outsider such as myself may know what many biochemical/cancer biology terms mean, but when they are strung together and spit at you rapidly, forget it.
5)      Cancer people serve better lunches than geology people, and they furnish breakfast to boot.  This despite the fact that most cancer people are M.D.s, hence can afford to buy their own food.
6)      Cancer people are kind to old folks, and even stop to talk to them.  Rock people simply trample then into the dust.
7)      The most important person at any symposium, by far, is the audio-visual technician.
8)      Tenure-track (or tenured) cancer people give oral presentations; their graduate students present posters after dinner, when nobody wants to learn more science.
9)      There are a whole lot of bright young cancer people, not to mention wise and experienced old ducks, all apparently working diligently on curing ovarian cancer.  Why haven’t we made more progress?
10)   Dr. Saul Rivkin is, indisputably, a very great man.  A this conference he chaired a session and gave a talk.  By force of will and determination he brought this organization and this conference, into being, raised upwards of $14 million for ovarian cancer research, and has arranged for most of it to be given to bright young people with clever, frequently innovative, ideas.  On the side he took care of cancer patients at Swedish Hospital for about 45 years.  He is nearly as old as I am, and still working every day for the cause.  More power to you, Saul!

Sunday, September 7, 2014


At a quilt store in St. Charles, Missouri
I’m off to Seattle, to attend the annual ovarian cancer symposium, organized by the Marsha Rivkin Center for Ovarian Cancer Research, and presided over by my buddy, Dr. Saul Rivkin.  I intend to listen faithfully and diligently to every talk (well, most of them, anyway) and try to wrap my elderly, physical-sciencey brain around as much as possible.  I definitely will not ask any questions.
My nametag reads “Dr. Myrl Beck, Ph.D. -   just below which  I am described as “Student”.  That should confuse ‘em.
So, while I am gone, I toss you this to feed your inner biologist.  It is a pretty sharp essay, and if you’d read Epigenetics, by Nessa Carey like I told you to do you would immediately catch this guy’s drift.  Otherwise, it will take some effort – but, what the heck, mental effort keeps the mind young and supple.  Right?

Saturday, September 6, 2014

PROGRAMMED DEATH: To cancer cells, that is.

Guess where
Do you remember our old friend PD-1?  Probably not; I last wrote about it on June 6th of last year.  It has the catchy name “Programmed Death Receptor 1”, and it has something important to do with the immune system.  Anyway, it is back in the news, big-time.  Both the Wall Street Journal and the NY Times  have stories featuring this important little bio- molecule.  Several drugs based on PD-1 are newly on the market, or soon will be.  They are aimed principally at advanced melanoma, but by implication this type of therapy may apply to other forms of cancer.  However, the two articles are more concerned with how much a course of treatment will cost (astronomical) than how it works.  Here is what I guess is going on:  1) these drugs feature something called a “monoclonal antibody”, which is designed to glom onto receptors on various kinds of guardian cells of the immune system; 2) This prevents PD-1 from killing off these friendly cells, which; 3) attack the cancer and kill it dead!  I may be all wet here, but two things are certain: PD-1 is a hot commodity in the pharma world, and it costs a lot to use.  This is another example of a very intractable problem confronting society: we can (potentially) cure many diseases, including some forms of cancer, but can we afford it? 
Oh, by the way….  I remember puzzling somewhere about why so many new drugs end with “mab”.  Now, finally, I know – mab stands for monoclonal antibody, as any fool should have been able to guess,  (not)