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?