DINO: Good news

Linda and Carolyn in Vancouver

I was lucky to have been along

According to the Tea Party, guys like John McCain are RINOs.  This translates as Republican In Name Only.  John – and many other relatively conservative public figures – acquire this designation because they are willing to compromise on occasion, to get things done.  Well, this blog is about DINOs.  These are not about Democrats In Name Only, as you might deduce.  (How about Bill Clinton in the 1990s, compromising on welfare reform and free trade?)  No, as used here, DINO is an RNA molecule that plays a crucial role in the biochemical cascade that enables the tumor-suppressor protein p53 to do its job.  In over half of all cancers, p53 is disabled.  Fooling around with the DINO (Damage Induced NOncoding) RNA, Stanford researchers have determined that p53 can be brought back from the dead and induced to do its job.  Early times, of course, but there is reason to hope.  In the immediate future many mice will die and many grant applications will be submitted, but I am optimistic.

https://www.cancer.gov/news-events/cancer-currents-blog/2016/dino-p53?cid=eb_govdel

PROFILES IN RESEARCH EXCELLENCE: Dr. Varatharasa Thiviyanathan

Linda and me, in Egypt

After chemo her hair grew back gray.  I really liked it.

Let’s get the name business over first.  Hereafter, in this essay, he will be known as Dr. T.  Some research this afternoon suggests that the name is Sri Lankan.  He received his Ph.D. from Purdue University and now works at the University of Texas Medical Center in Houston, where he has been since 1994.  He is a co-author of countless medical research papers (well, 27 since 2000).  More about his history I cannot determine.

As an aside, typing Dr. T’s full name into various search engines is laborious.  I can imagine the poor kid in grammar school, taking exams.  The other kids would be turning in their papers about the time he finished writing his name at the top of the answer sheet!

But who cares how tough his name is to spell; he is doing some great work.  Partially funded by the Rivkin Center, Dr. T is developing a novel sort of address label to deliver nanoparticles of death-dealing drugs directly to cancer cells.  His labels consist of short strands of RNA, especially constructed to zoom in on specific types of cancer cells and, binding to them, deliver their lethal load.

This line of research seems potentially fruitful to me; I have written about nanoparticles before.

However, always remember my abysmal ignorance of most things biological.  If you are curious, Google “aptamer” and go from there.  Me, I’m still tired from my recent trip.

TWO GREAT GUYS

Carolyn and Linda, with their mother

Carolyn has forwarded me this inspiring, even humbling, story of two ordinary guys using their ordinary talents to raise an extraordinary amount of money to fight ovarian cancer.  Makes me wish I were one of them.  Read it.

http://wlos.com/news/person-of-the-week/persons-of-the-week-john-zimmerman-and-taylor-sharp

Wee1: A little bit of good news.

Taking it easy,  Heron Island, Maine

2008, I think

Man, if you need any additional proof that cancer biochemistry is complicated, just Google “Wee1 cancer” and try to read the Wiki entry that pops up!

Saul Rivkin is excited about the emergence of a “new tool” for use in combating ovarian cancer – and when Saul is excited, so am I.  This useful innovation involves a “nuclear kinase” called Wee-1.  As you all know, a kinase is an enzyme that enables anabolic reactions to go by slapping phosphate groups on the substrate – thereby adding energy.  (You did know that, right?)   Well, anyway, Wee1 is in part responsible for guarding the gate between cell-cycle phase G2 and mitosis; cell-splitting, to most of us.  If the cell is too small, Wee1 won’t let it split.  (If it did split, it would croak – to use a technical term.)

It seems that there is another checkpoint in the cell cycle; escape from Gap phase 1 to Interphase depends on the activity of a molecule named TP53, which is mutated (and thus non-functional) in >85% of ovarian tumors  There exists a molecule that “inhibits” Wee1.  So, Saul’s new tool: administer this inhibitor molecule (AZD1775 for the curious), possibly together with an anti-cancer drug.  Absent functional TP53 the cycle relies on Wee1 to prevent midget cells from passing into mitosis.  Apparently they can’t survive (this is my guess), hence are “apoptosed” and ground up for use as nuclear fertilizer.  Moreover, because cancer cells are so quick to multiply, maybe baby cancer cells are unusually small.

Hell, I don’t know – all I am sure of is that Saul thinks this is a very good thing.  I suspect it’s not an earth-shattering discovery – but it helps.

Oh, you wanted to know why the thing is “Wee”.  Well, it was discovered and named in Scotland, where wee means small.  Wee1 weighs 96 kDa.  Is that small?