Book Review: “Transhuman”, by Ben Bova

Today it’s back to basics – in the sense that this blog started as a way for me to recommend books to friends who like to read the same sorts of things that I do, but it quickly diverged from that. But today I want to discuss the last novel I read: “Transhuman”, by Ben Bova.

THERE WILL BE SPOILERS BELOW. Consider yourself warned.

I have read other novels by Bova, most notably for today’s review “Brothers”, which is also about the quest for scientifically-induced immortality. I am not a huge fan, but have enjoyed his novels and never had any major issues with one. Until now.

The plot of “Transhuman” is this: The main character, Luke Abramson, is a brilliant “cellular” biologist (first red flag there) whose 10-year-old granddaughter, Angela, has been diagnosed with a rare and incurable form of brain cancer. She is going to die, and soon – except that Luke thinks he can cure her. The cure: he’s going to give her telomerase inhibitors.

Sidebar for the non-biologists in the mix: Telomeres are the sequences at the very ends of chromosomes, which, for reasons that aren’t important here, get shorter every time a cell replicates its DNA and divides. This leads to gradual shortening of the chromosomes, and it one of the ways in which cells are limited in how many times they can replicate before exiting the cell cycle (a process called “senescence”). Telomerase is a cellular enzyme that extends the lengths of telomeres, and which tends to be present at low levels in cells that aren’t supposed to be dividing (most cells most of the time), and at high levels in cells that are (for example, stem cells that renew tissues like the skin and the lining of the gut). Cancer cells also tend to (inappropriately) express high levels of telomerase, and this is one of the factors that makes them immortal.

Telomerase inhibitors are a reasonable approach to cancer treatment. So reasonable, in fact, that it’s been tried. More than once. That second article is 12 years old, and this novel is one year old. So the idea was already a decade old or more by the time Bova wrote his novel – in the year 2014, the year in which the novel is set, this would not be a brilliant idea that no one had ever tried before. We’ve tried it…a lot. This is one of several problems that come down to the same thing: it feels like Bova didn’t do his homework when writing this novel.

The story proceeds – Luke kidnaps his granddaughter from imminent hospice care to give her his treatment, accompanied by her oncologist, and takes her on a cross-country trip, fleeing from the FBI and the clutches of a powerful multinational biotechnology company who wants his work for their very own. He soon finds that he’s too old to successfully evade capture, and decides to try his other pet telomerase theory: if you could turn ON telomerase in your cells, you could reverse the process of aging.

Another sidebar: one of the hypotheses about what causes aging involves senescence, the process I mentioned above, whereby cells are leaving the cell cycle. Aged tissues have far more senescent cells than young tissues, and there’s some data from mice that inhibiting senescence does slow down aging. Again, none of this is recent information, though.

This is where the science begins to leave the rails: you might be able to PREVENT aging with telomerase, but you almost certainly couldn’t reverse it. I suppose you could hypothesize that you’re replacing senescent cells with new ones from cells that are now dividing. My problem with that explanation is twofold: first, telomerase activity wouldn’t drive cells to divide more, which is what you’d need to replace senescent cells. It would just allow the ones that were still dividing to do so longer – prevention, not cure. Second, the data that actually exist don’t back up this idea.

Also, as I alluded to above, telomeres are ONE method cells use to determine cellular age. One of at least three I’m aware of. Here’s another. Telomeres aren’t the be-all and end-all of aging.

Unsurprisingly (this being a science fiction novel), the cancer treatment works. Angela’s tumors disappear. Unfortunately, she develops progeria (premature aging), which was a predictable side-effect, but, of course, Luke has a plan to fix that (see above). And, as long as he’s at it, he and another “cellular” biologist friend (former student, in fact) are going to fix another of Angela’s problems for her. It seems she carries only one copy of the p53 gene, which, of course, is why she has cancer in the first place. Luke explains that, due to this mutation in p53, her immune system can’t destroy cancer cells like a normal person’s would, and that’s why she has cancer in the first place.

Jeez, where to start? Okay, p53. The p53 protein is very important in cancer development, as the protein itself regulates a LOT of processes that are necessary for cellular monitoring and control of incipient cancer. It is involved in DNA repair, cell-cycle arrest, senescence, programmed cell death…and, yes, immune function. Both copies of p53 are mutated in something like half of all cancers. The function of p53 is central to cancer prevention.

However, we KNOW what happens when you’re born with only one functional copy of p53, as Angela is described in the novel. The disorder that results is, yes, a cancer-predisposition disease. Specifically, Li-Fraumeni Syndrome (LFS), which is well-known, and if Bova had been doing his homework, he should have mentioned it. By name. Yes, a small percentage of people with LFS get childhood brain tumors. But the usual presentation is early-adulthood tumors, most often breast cancer. Also, the clinical presentation, as with pretty much all inherited “cancer mutations,” is dominant – she inherited the mutation from a parent, who would ALSO have the disorder. Unless it’s a new mutation. Which isn’t uncommon in this disorder. My problem is that if you’re going to be this specific about your science, you need to do your homework, and not to mention all of this while going on repeatedly about p53 mutation is sloppy work.

Finally, they apparently just flip a new copy of p53 into Angela’s genome. In a world where this would be possible, wouldn’t you think they could target their telomerase inhibitors to the tumors, and not give the child progeria?

Yes, this is a rant. Each of the above problems, by itself, I would overlook. But when a writer is specific enough about extant science to mention two proteins by name (p53 and telomerase), they should also know that: the “miracle treatment” they’re hypothesizing has been tested already, that you’d probably want to target your telomerase inhibitors, and if you could do a whole-body transformation of a human to get p53 into her cells, you could probably target your inhibitors to the brain tumors, and that the specific, inherited, cancer-causing mutation you’ve given to one of your characters is already known and has known consequences. You can’t both use the real science AND ignore the real science.

Successful science-fiction novels are either much more specific, or much more vague.

Okay, rant over. I don’t recommend this one, obviously.

ETA: Oh, forgot to mention: “cellular” biologist is a red flag because nobody calls themselves a “cellular” biologist anymore. “Cell biologist”, and “cell biology”, please.


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