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He's also a work of science. Out in California, at the Comprehensive Cancer Center at the University of California at San Francisco, a geneticist named Katherine Rauen spent seven years teasing apart the DNA of children with CFC, to find the gene that caused it. In January of 2006, nearly 30 years after the syndrome had first been described, she published her findings. There are three billion base pairs of nucleotides in the human chromosomes, which in turn comprise about 25,000 protein-forming genes (and a lot more besides). The mutations that cause CFC only happen for certain in three genes: BRAF, MEK1, MEK2.
They sounded like newly discovered planets to me, as baffling and rarefied as genetics itself. The gene labs at the Comprehensive Cancer Center were lit like the inside of a refrigerator and cluttered with textbooks and tubes and stoppers and scales and micro-array scanners. The scientific papers the geneticists wrote — largely for one another — had titles such as Keratosis pilaris/ulerythema ophryogenes and 18p deletion: Is it possible that the LAMA1 gene is involved? The geneticists themselves bore the slightly startled air of soldiers who had just emerged from deep jungle, only to be told that the war had been over for 20 years. They were fond of unusual, non-human screensavers: a photograph of a cat, say, asleep in a tiny log-cabin cathouse.
One afternoon, I stepped into an elevator full of young geneticists leaving work for the day. It was Halloween. Two of the female geneticists in the elevator were wearing devil horns on their heads. "Going out tonight?" one of the guys ventured. The women shook their heads no. I can't say I was surprised.
It was all very interesting, but I wanted to know what had gone wrong in my son. I remember the moment Dr. Rauen told me. It was getting on toward dinner and, outside, San Francisco was washed in its standard end-of-day golden light.
"This missense mutation" — the one that causes CFC — "is one letter [nucleotide] change in the entire gene," she said. "Yup. One letter in the entire gene, which causes one amino acid to change — one amino acid, one tiny building block of the entire protein. That's what causes CFC." That brief slip had caused the snaggle of Walker's life.
"And does anyone know why that letter changes?" I asked.
"DNA replicates, but it doesn't replicate with extremely high fidelity. If it replicated and never made a mistake, we would all look the same, right? The good news and the bad news is, if it does make a mistake, it makes a mistake about once every million times. One in every one million base pairs has got a mistake in it. Now, you've got all kinds of proteins and enzymes and stuff that go back and try to find this mistake. So a lot of mistakes you never know about. But sometimes the mistake's not corrected. And when that mistake's not corrected, it causes a change in protein."
Dr. Rauen took a breath and continued. "And that protein behaviour might make our immune system better. It might make our muscles stronger. It could have beneficial effects called evolution. You know, survival of the fittest. But you can have a genetic change that makes a deleterious effect, where it causes a hole in the heart, it causes your immune system to be weak. It might be a beneficial effect, it might be a deleterious effect."
Walker was a deleterious effect. Dr. Rauen didn't put it that way, of course. Indeed, she hurried to assure me that children such as Walker would have enormous value to medicine: Though the CFC genes are found in a cancer-causing protein pathway, CFC children seem not to get cancer.
"We are going to learn so much from these kids," she said. "We are going to learn how to treat them better from knowing their genes. We are going to learn how to care for them better. We are going to learn about cancer from these children. This is a huge discovery on multiple levels."
I thanked Kate Rauen shortly after that, left her office, crossed the street and sat down on a bench to think about what she had said.
The scientific definition of evolutionary success, of a successful random mutation, is one that allows the organism to survive and reproduce. Nature alone would not have allowed Walker to survive. He was an unsuccessful random human mutation.
But Walker wasn't a product of nature alone. He was also a product of modern medical technology — drugs, a feeding tube and more drugs. If Dr. Rauen is right and children with Walker's class of syndromes help to unriddle the causes of cancer, he'll be a success — not of evolution, but of medical evolution. It was something, anyway.
I looked up then and discovered I was sitting in front of a sculpture: Regardless of History, by an English artist named Bill Woodrow. It was seven feet high and bronze — a thin tree, blighted and leafless, stunted and growing out of a rock. But growing.
For weeks after, I resented the very idea of genetics. I didn't resent Kate Rauen — her isolation of the genes associated with CFC makes the syndrome easier to diagnose, which means therapies can begin sooner. But the hype around genetics doesn't match its reality. The possibility of a genetic cure for the symptoms of CFC is generations away, even by Dr. Rauen's estimate; and no other doctor I ever met believed that the CFC gene would play much of a role in curing cancer.
"The human genome is an elegant but cryptic store of information," Roderick McInnes told me one afternoon. He's the director of genetics at the Canadian Institute for Health Research. Sickle-cell anemia, he pointed out, was the first "genetic" or molecular disease to be identified, in 1949. Nearly 60 years later, there is still no cure.
You will forgive my pride, I hope: I just didn't like the idea of my son's life reduced to a typing error in a three-billion-long chain of letters, to one dinky nucleotide. The absolutism of genetics offended me. Eventually I came across some prominent geneticists who feel the same way. Craig Venter, who helped to create the Human Genome Project, the only human whose genome has been sequenced fully, says as much in his biography, A Life Decoded. "Genes did not make us, body and mind," he writes.
At the University of Oxford, a renowned gene man named Denis Noble — the author of The Music of Life: Biology Beyond the Genome — went even further. "The social and ethical implications of understanding a human being from mere genes up are profound," he told me over the telephone from Oxford one morning — he had a fantastic accent, one of those cosmically articulate English jobs. "It does seem to me that one of the main effects to have emerged since the bottom-up appeal of genetic science is that, to the extent it unravels the human body, it dehumanizes it."
As for the mind — the strange wisp I've looked for in my boy, to only sporadic avail — Dr. Noble maintained that it had nothing to do with genes. "At the level of nerve cells and associated molecules," he said, "the mind isn't there. You can't even understand the idea of intentionality without the social networks we exist in, without communication with each other. I think we'll find that the mind lies outside the body, in the networks of social and cultural life."
He preferred the vision of "the Buddhists and the Taoists, who had this notion that the mind was not an object. It was a process."
Dr. McInnes made me see that my problem wasn't with genetics, but with the nature of genetic disease. "There's something about genetic disease and kids," he said. "It's the permanent nature of it, the emotions associated with a mutation: Once you've got it, you've got it. Other diseases, you don't have them for life. I guess it's the inexorable nature of genetic disease that makes it striking. The blueprint's been changed."
And Walker's mind? That is truly unfixable. "The brain has 20 billion neurons," Dr. McInnes said. "Each neuron makes 1,000 contacts and is touched by another 10,000. We're probably never going to understand the brain at the level of individual neurons. We'll probably have to look at it the way astrophysicists approach understanding a billion stars."
That, I find strangely comforting: Lying on my back, gazing up at the random sparkles of Walker's mind and speculating. And crying, of course. Always the fucking crying.
I keep talking to him. I don't assume he understands much, but I do it anyway. Somehow, I hope, the words will rouse him. But of course it's not Walker who needs to keep hearing me talk; it's me who needs to keep talking to Walker. I'm afraid of what will happen if I stop. I keep thinking of that scene at the end of Cormac McCarthy's The Road, when the father is dying and the boy knows it.
You said you wouldn't ever leave me.
I know. I'm sorry. You have my whole heart. You always did. You're the best guy. You always were. If I'm not here, you can still talk to me. You can talk to me and I'll talk to you. You'll see.
Will I hear you?
Yes. You will. You have to make it like talk that you imagine. And you'll hear me. You have to practise. Just don't give up. Okay?
Part 3 continued on Chapter 3…