Two days ago, an intriguing story began circulating on the web. In a new paper, a UC Berkeley biologist suggested that cancers—ravenously reproducing, endowed with radically different DNA from normal human cell—are actually a new parasitic species. Because such massive genetic rearrangement is reminiscent of how new species sometimes form, it could be said that cancers were doing just that. Some site picked up the story and ran it at face value: new species are a catchy idea, and cancer is always an interesting topic.
But to anyone who's studied evolutionary biology or recognized the name of the lead researcher, it was a bizarre reminder of both how easy it is take scientific papers at face value and how quickly we forget.
To understand the researcher's claim for yourself, it helps to remember that "species" is just a word made up by humans to help us better understand the world. For centuries it meant a group of organisms that resembled each other, and when Carolus Linnaeus published his taxonomy of species in 1735, he was working from appearance. Today, we know that DNA can tell us quite a bit more about how organisms are related to each other. Now that we can clearly see the genetic variation between members of a species, though, we can also see how slight the overall genetic difference from another group can sometimes be. So one of the best definitions is empirical: a species, as defined by Ernst Mayr, is a group of organisms that can mate and have offspring with each other. Anything they can't reproduce with is, for the purposes of biologists who study evolution, another species.
The definition is problematic when it comes to organisms like bacteria that reproduce asexually, of course, so biologists will sometimes call a group of bacteria that share more than 98% of their DNA phylotypes instead of species. But what this all underscores is that "species" is really a semantic concept. It's useful for biologists who want to trace the evolution of different groups of organisms, but efforts to cure cancer don't have anything to do with the concept of species, and wouldn't be improved by such designations. Calling a cancer a new species is just philosophical wordplay. It's fine as a reminder that scientific definitions aren't fixed, but as a contribution to the discussion of cancer biology, it probably doesn't have much meaning.
As for the second revelation, the lead researcher, Peter Duesberg, is indeed a professor at UC Berkeley. And no one will dispute that he has done groundbreaking work in his career. But a moment Googling reveals what sites that picked up the story overlooked: Duesberg is one of the most prominent HIV denialists in the world. His claim that drug use causes AIDS and that HIV is a harmless virus, first published in 1987, has made him a scientific pariah. Some consider his theories to be behind the deaths of hundreds of thousands of people in South Africa, who were denied medication by a government sympathetic to his ideas. He has been working with almost no funding and in isolation from the rest of the molecular biology community for decades now.
Duesberg's story is fascinating, and you can learn more about his claims and his career since then in a DISCOVER profile from a few years back. For those interested in how controversial ideas are handled in science, it's a must-read. Duesberg also carries out a separate thread of research on how errors in chromosome replication contribute to cancer. And it's a fascinating area, deserving of much more attention that it's received so far. While the focus of most cancer research is mutations in individual genes, Duesberg and others have begun exploring the strange multiplication of entire chromosomes in cancer cells. In a Scientific American piece explaining this work, Duesberg points out that when he was a young scientist, people were sure that viruses were the source of most cancers. What is accepted as fact now could be proven wrong in the future, he argues convincingly, and the deranged rearrangements and multiplications of chromosomes are key to understanding how the disease works. Other biologists agree, but most say Duesberg takes it too far when he claims that chromosome rearrangements alone are the cause, and that mutations in genes are a red herring.
With all this in mind, by all means, read the new paper. The fact that Duesberg is dead wrong about HIV/AIDS doesn't mean that he's necessarily wrong about chromosomes' involvement in cancer, to be sure. But his new idea is probably better seen as a philosophical exploration of "species" than a new understanding of an avenue for fighting such diseases.
