Article — From the April 2008 issue

Contagious Cancer

The evolution of a killer

( 2 of 10 )

Under ordinary circumstances, cancer is an individuated phenomenon. Its onset is determined partly by genetics, partly by environment, partly by entropy, partly by the remorseless tick-tock of time, and (almost) never by the transmission of some tumorous essence. It arises from within (usually) rather than being imposed from without. It pinpoints single victims (usually) rather than spreading through populations. Cancer might be triggered by a carcinogenic chemical, but it isn’t itself poisoning. It might be triggered by a virus, but it isn’t fundamentally viral. Cancer differs also from heart disease and cirrhosis and the other lethal forms of physiological breakdown; uncontrolled cell reproduction, not organ dilapidation, is the problem.

Such uncontrolled reproduction begins when a single cell accumulates enough mutations to activate certain growth-promoting genes (scientists call them oncogenes) and to inactivate certain protections (tumor suppressor genes) that are built into the genetic program of every animal and plant. The cell ignores instructions to limit its self-replication, and soon it becomes many cells, all of them similarly demented, all bent on self-replication, all heedless of duty and proportion and the larger weal of the organism. That first cell is (almost always) a cell of the victim’s own body. So cancer is reinvented from scratch on a case-by-case basis, and this individuation, this personalization, may be one of the reasons that it seems so frightening and solitary. But what makes it even more solitary for its victims is the idea, secretly comforting to others, that cancer is never contagious. That idea is axiomatic, at least in the popular consciousness. Cancer is not an infectious disease. And the axiom is (usually) correct. But there are exceptions. Those exceptions point toward a broader reality that scientists have begun to explore: Cancers, like species, evolve. And one way they can evolve is toward the capacity to be transmitted between individuals.

Devil tumor isn’t the only form of cancer ever to achieve such a feat. Other cases have occurred and are still occurring. The most notable is Canine Transmissible Venereal Tumor (CTVT), also called Sticker’s sarcoma, a sexually transmitted malignancy in dogs. Again, this is not merely an infectious virus that tends to induce cancer. The tumor cells themselves are transmitted during sexual contact. CTVT is widespread (though not common) and has been claiming dogs around the world at least since a Russian veterinarian named M. A. Novinsky first noted it in 1876. The distinctively altered chromosome patterns shared by the cells of CTVT show the cancer’s lineal continuity, its identity across space and through time. Tumor cells in Dog B, Dog C, Dog D, and Dog Z are more closely related to one another than those cells are to the dogs they respectively inhabit. In other words, CTVT can be conceptualized as a single creature, a parasite (and not a species of parasite, but an individual), which has managed to spread itself out among millions of different dogs. Research by molecular geneticists suggests the tumor originated in a wolf, or maybe an East Asian dog, somewhere between 200 and 2,500 years ago, which means that CTVT is probably the oldest continuous lineage of mammal cells presently living on Earth. The dogs may be young, but the tumor is ancient.

Unlike devil tumor—now known as Devil Facial Tumor Disease, or DFTD—CTVT is generally not fatal. It can be cured with veterinary surgery or chemotherapy. In many cases, even without treatment, the dog’s immune system eventually recognizes the CTVT as alien, attacks it, and clears it away, just as our own immune systems eventually rid us of warts.

The case of the Syrian hamster is more complicated. This tumor arose around 1960, when researchers at the National Cancer Institute, in Bethesda, Maryland, performed an experiment in which they harvested a naturally occurring sarcoma from one hamster and injected those cells (as cancer scientists often do) into healthy animals. When the injected hamsters developed malignancies, more cells were harvested. Each such inoculation-and-harvest cycle is called a passage. The experiment involved a dozen such passages, and over time the tumor began to change. It had evolved. The later generations, unlike the first, represented a sort of super tumor, capable of getting from hamster to hamster without benefit of a needle. The researchers caged ten healthy hamsters together with ten cancerous hamsters and found that nine of the healthy animals acquired tumors through social contact. The hamster tumor had leapt between animals—or anyway, it had been smeared, spat, bitten, and dribbled between them. (The tenth hamster got cannibalized before it could sicken.) In a related experiment, the tumor even passed between two hamsters separated by a wire screen. The scientists had in effect created a laboratory precursor of what would eventually afflict Tasmanian devils in the wild: a Frankenstein malignancy, a leaping tumor, which could conceivably kill off not just individuals but an entire species.

's previous article for Harper's Magazine, "Darwin's Conundrum," appeared in the December 2006 issue.

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