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How a 6,000-Year-Old Dog Cancer Spread Around the World

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In clams and mussels, where a fatal leukemia-like cancer has been observed in at least 15 different species, the cancer cells jettison themselves into the seawater, where other filter-feeding bivalves pick them up. Michael Metzger, a biologist at the Pacific Northwest Research Institute, discovered how clam cancers jump from one animal to another. He believes transmissible cancers, particularly in invertebrates, which have less developed immune systems, will turn out to be much more common than anyone thought. “A lot of the reason we didn’t see it in the past is we weren’t looking for it,” says Metzger. “Transmissible cancer really blurs the lines between infection, infestation, metastasis, but evolution doesn’t care about classifications. It’s just whatever works. And spreading cells from one animal to another works.”

It works less well in vertebrates, which are better at sussing out and rejecting foreign cells, than, say, clams. But even in humans, a few rare documented cases of transmissible cancer do exist. They involve scenarios where people’s immune systems were suppressed or undeveloped—organ transplant recipients who acquired cancer from the donor’s diseased tissue and fetuses acquiring cancer from their mother’s cells passed through the placenta. These are extreme examples, says Metzger, and while there’s no evidence any human cancers have yet developed broader transmissibility, it’s not impossible to imagine. “We don’t bite each other’s faces or filter-feed ocean water,” he says. “But we do have sex. So there are possibilities for transmission.”

If scientists ever have to grapple with a human patient-hopping cancer, understanding CTVT’s genetic evolution will be an invaluable asset. But for now, the genetic map has more to teach them about how to treat the cancers people already have.

According to Baez-Ortega’s analysis, CTVT cells are riddled with mutations, with an average of 38,000 per tumor sample. By contrast, most human cancers have only about 100. But, they discovered, for a long, long time these mutations have just been occurring randomly in dogs. After the first few mutations that turned those cells cancerous millenia ago, evolution stopped selecting for additional changes that would make the cancer dominate its host.

That means that with thousands of years to optimize their fitness, CTVT cells haven’t gotten more aggressive. In fact, the opposite happened. Today, most cases of CTVT can be cured with a single dose of chemotherapy. Evolution actually tamed the cancer. “The best strategy for this tumor turned out not to behave like a tumor at all, but like a parasite,” says Baez-Ortega. “And since dogs don’t seem to be affected by it much, you don’t see the cancer trying to get better, because it’s already good enough. If it does as little harm to the dogs as possible, it can survive indefinitely.”

This lends support to a clever new strategy for treating cancer, called adaptive therapy, which exposes tumors to medication intermittently, rather than in a constant barrage. The idea is to prevent the small subsets of cancer cells with genetic changes that render them resistant to drugs from taking over tumors and turning them into an unstoppable force.

Rather than killing a tumor, adaptive therapy researchers want to keep it alive but small, mild, and stable. A half-dozen clinical trials employing this dosing strategy with existing cancer drugs are already underway in the US. Baez-Ortega says what they found in CTVT is that given enough time, evolution can already do that. Like the dogs whose body it inhabits, the cancer has been domesticated.

“The cancer will never be fitter than it is right now,” says Baez-Ortega. At some point, this strategy may spell trouble for CTVT, since it won’t have enough genome left to adapt to changes further down the road. But that’s in evolutionary time: Tens, even hundreds of thousands of years from now, says Baez-Ortega. “I think it will outlive us all, and probably our children as well.”


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