A Blog by Carl Zimmer

Cancer-Proof Rodents: My New “Matter” Column for the New York Times

Source: http://commons.wikimedia.org/wiki/File:Nacktmull.jpg
Source: http://commons.wikimedia.org/wiki/File:Nacktmull.jpg

At this weekend’s Cancer and Evolution meeting, one of the highlights was a talk from a husband-and-wife team of biologists at Rochester University about naked mole rats. As far as scientists can tell, naked mole rats don’t get cancer, despite living up to 30 years. That’s pretty remarkable when you consider that another rodent–the lab mouse–has a 47% cancer rate during its brief, two-year life.

So a number of researchers have been searching the biology of naked mole rats for their secret. The Rochester scientists may have found a crucial ingredient in their cancer defense. And, by happy coincidence, Nature is publishing their report today. That’s the subject of my “Matter” column this week. Check it out.

3 thoughts on “Cancer-Proof Rodents: My New “Matter” Column for the New York Times

  1. Well , let me give some input and ideas to those researchers obviously motivated with the –High Hyaluronan/Immunity to cancer- (wrongfully) presumed correlation in between ..It is NOT that simple …

    A- Very low metabolic rate and body temperature –so DNA molecule of mole rat subjected “less mutation/per generation” – The naked mole rat is well adapted for the limited availability of oxygen within the tunnels that are its habitat: its lungs are very small and its blood has a very strong affinity for oxygen, increasing the efficiency of oxygen uptake. It has a very low respiration and metabolic rate for an animal of its size, about 2/3 that of a similarly sized mouse, thus using oxygen minimally. In long periods of hunger, such as a drought, its metabolic rate can be reduced by up to 25 percent. The naked mole rat does not regulate its body temperature in typical mammalian fashion, homeostasis. They are thermo-conformers rather than thermo-regulators in that, unlike other mammals, body temperature tracks ambient temperatures. The relationship between oxygen consumption and ambient temperature, however, switches from a typical poikilothermic pattern to a homoeothermic mode at 28 °.http://en.wikipedia.org/wiki/Naked_mole_rat

    B- Mole rats lives dark underground and exposed “ less cosmic and ultraviolet radiation” so again –DNA molecule of mole rat subjected “less mutation/per generation”

    C- Mole rats ENTIRE Genome (DNA) evolved in order to ADAPT ITS ENVIRONMENT over millions of years ; as mentioned above section A and protected effectively –section B , so the Hyaluronan Gene and its transcription and regulation and high and specific content HAS NOTHING TO DO with the immunity against cancer .

    D- We are talking –Parenchymal /Visceral – organs , liver/intestine/kidney/genital organs/lungs etc of Mole Rats ALSO immune to cancer , NOT ONLY FLEXIBLE SKIN with high Hyaluronan .

    Bottom line , do not even waste time with the “Hyaluronan” molecule and its relationship with cancer ..It is simply ILLOGICAL PRESUMPTION that it is the only or one of the reasons of immunity against cancer . YOU HAVE TO LOOK AT THE “WHOLE PICTURE” of mole rat evolution and its ENTIRE GENOME + ENVIRONMENT IT LIVES in order to understand immunity against cancer ..

  2. Re: Metin – Correlation is not equal to causation, true. The press at large is oversimplifying and extrapolating too much from a nuanced biological situation, true. Much work must yet be done to understand the phenotypic discrepancies in cancer susceptibility, and you should never fear to question what cannot be proven. True. But your incensed response presents its own logical fallacies (and that you didn’t read the actual set of publications, most specifically http://www.nature.com/nature/journal/vaop/ncurrent/full/nature12234.html). To rebut your rebuttal points:

    A – This cancer resistance is also seen at the cellular level, in petri dishes, in controlled conditions identical to those of homologous mouse cells. Your assertion in (A) is reasonable, but refers to anatomy/physiology rather than the more directly relevant genetic/molecular components. This is a categorical mistake that weakens an otherwise promising argumentative direction (differing cellular metabolic rates/O2 concentrations affecting DNA degradation).

    B – Again, categorical mistake. Cell cultures in petri dishes almost certainly receive invariable UV radiation. In vivo, in nature, you have a point, but not in the humidity, CO2, and temperature-controlled incubator.

    C – to use an analogy from evolutionary biologist Ken Miller: a blind tinker can use a mousetrap for a tie clip and it works just fine. You are misrepresenting the results of evolution: it’s not exclusively directed and closed-ended, it is opportunistic and open-ended. Homologous components do not always have analogous functions. i.e. – a lower rate of HA degradation, and a uniquely high-molecular-mass HA might have more ramifications than simply flexy skin. Thus, your argument in this point is not applicable.

    D – A good point… if this was seen just in epidermal tissue. Just because HA allows for better epidermal flexibility, doesn’t mean it’s not expressed everywhere. In fact, if you had read just one scientific publication more (link above), you’d see that this HA content is high in fibroblasts, thus in all connective tissues. You miss the mark again.

    Bottom line, your repeated categorical mistakes betray a deeper lack of knowledge on the subject. You can learn more, though, and hone your argument. More factually-based reasoning and less unfocused outrage will hone your skepticism to an incisive and informing tool of knowledge.

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