David Quammen discusses contagious cancer — like the variant killing off the Tasmanian Devil:
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.
Sadly, “the phenomenon of transmissible tumors isn’t confined to canines, Tasmanian devils, and Syrian hamsters”:
There have been human cases, too. Forty years ago a team of physicians led by Edward F. Scanlon reported, in the journal Cancer, that they had “decided to transplant small pieces of tumor from a cancer patient into a healthy donor, on a well informed volunteer basis, in the hope of gaining a little better understanding of cancer immunity,” which they thought might help in treating the patient. The patient was a fifty-year-old woman with advanced melanoma; the “donor” was her healthy eighty-year-old mother, who had agreed to receive a bit of the tumor by surgical transplant. One day after the transplant procedure, the daughter died suddenly from a perforated bowel. Scanlon’s report neglects to explain why the experiment wasn’t promptly terminated — why they didn’t dive back in surgically to undo what had been done to the mother. Instead, three weeks were allowed to pass, at which point the mother had developed a tumor indistinguishable from her daughter’s. Now it was too late for surgery. This cancer moved fast. It metastasized, and the mother died about fifteen months later, with tumors in her lungs, ribs, lymph nodes, and diaphragm.
The case of the daughter–mother transplant and the case of the Syrian hamsters have one common element: the original sources of the tumor and the recipients were genetically very similar. If the genome of one individual closely resembles the genome of another (as children resemble their parents, and as inbred animals resemble one another), the immune system of a recipient may not detect the foreignness of transplanted cells. The hamsters were highly inbred (intentionally, for experimental control) and therefore not very individuated from one another as far as their immune systems could discern. The mother and daughter were also genetically similar — as similar as two people can be without being identical twins. Lack of normal immune response, because of such closeness, goes some way toward explaining why those tumors survived transference between individuals.
Low immune response also figures in two other situations in which tumor transmission is known to occur: pregnancy and organ transplant. A mother sometimes passes cancer cells to her fetus in the womb. And a transplanted organ sometimes carries tiny tumors into the recipient, vitiating the benefits of receiving a life-saving liver or kidney from someone else. Cases of both kinds are very rare, and they involve some inherent or arranged compatibility between the original victim of the tumor and the secondary victim, plus an immune system that is either compromised (by immuno-suppressive drugs, in the organ recipient) or immature (in the fetus).
Other cases are less easily explained. In 1986, two researchers from the National Institutes of Health reported that a laboratory worker, a healthy nineteen-year-old woman, had accidentally jabbed herself with a syringe carrying colon-cancer cells; a colonic tumor grew in her hand, but she was rescued by surgery. More recently, a fifty-three-year-old surgeon cut his left palm while removing a malignancy from a patient’s abdomen, and five months later he found himself with a palm tumor, one that genetically matched the patient’s tumor. His immune system responded, creating an inflammation around the tumor, but the response was insufficient and the tumor kept growing. Why? How? It wasn’t supposed to be able to do that. Again, though, surgery delivered a full cure. And then there’s Henri Vadon. He was a medical student in the 1920s who poked his left hand with a syringe after drawing liquid from the mastectomy wound of a woman being treated for breast cancer. Vadon, too, developed a hand tumor. Three years later, he died of metastasized cancer because neither the surgical techniques of his era nor his own immune system could save him.
There are a couple reasons why cancer doesn’t normally spread to other individuals:
“Cells are very effete. Very susceptible to dying in the outside world.” They dry out, they wither, they don’t remain viable when they’re naked and alone. Bacteria can form spores. Viruses in their capsules can lie dormant. But cells from a metazoan? No. They’re not packaged for transit.
And that’s only one of two major constraints, Weinberg said. The second is that if cancer cells do pass from one body to another, they are instantly recognized as foreign and eliminated by the immune system. Each cell of any sort bears on its exterior a set of protuberant proteins that declare its identity; they might be thought of as its travel papers. These proteins are called antigens and are produced uniquely in each individual by the MHC (major histocompatibility complex) genes. If the travel papers of a cell are unacceptable (because the cell is an invader from some other body), the T cells (one type of immunological police cell) will attack and obliterate it. If the invader cell shows no papers at all, another kind of police cell (called NK cells) will bust it. Only if the antigens on the cell surface have been “downregulated” discreetly but not eliminated altogether can a foreign cell elude the immune system of a host. That’s what Canine Transmissible Venereal Tumor seems to have done: downregulated its antigens. It shows fake travel papers — blurry, faded, but just good enough to get by.