Jumping Genes a Cause of Cancer?


Within the human genome, small DNA elements called retrotransposons have the potential to wreak mutational havoc by copying themselves and reinserting into the genome at multiple locations. Normal adult cells have suppressive mechanisms to stop these elements from jumping about, but according to a report published today (June 28) in Science, those mechanisms can break down in certain cancers. The findings suggest that, in some cases, jumping genes might even cause cancer or contribute to its progression

 “The paper is very important,” said Keith Slotkin a molecular geneticist at Ohio State University in Columbus, who did not participate in the study. “There has long been a weak association between cancer and transposable element activity, but this paper now categorically shows that transposable element activation is a source of new mutations in cancer cells.”

Retrotransposons are common in eukaryotic genomes and, thanks to repeated rounds of copying and inserting themselves over the course of evolution, they generally comprise a significant fraction of a species’ DNA. Indeed, they make up a whopping 45 percent of the human genome.

“Most are molecular fossils—dead pieces of DNA,” explained John Moran a human geneticist at the University of Michigan Medical School in Ann Arbor, who did not participate in the research. That is, they have accumulated so many mutations over the course of evolution that they are now merely inactive remnants. “But,” he said, “Some are actively mobilizing.

Written By: Ruth Williams
continue to source article at the-scientist.com


  1. Selfish generic elements with only their own replication in mind. Mutational havoc versus replication and havoc is only an unconsidered side issue here to transponsons.

     Work on enhancing the suppressors?

  2. I agree. Suppression is everything.

    Am I missing something?They’ve identified something going wrong in gene processing and duplication. Which seems pretty much normal, as there’s scope for virtually anything to go wrong in any extremely complex information processing system. And they would also presumably know that error prevention is next to impossible and therefore system maintenance is most likely to be based on error detection and elimination, or possibly correction, of the affected erroneous data.

    But they are working on understanding the specific details of the kind of damage that’s being caused, instead of the obviously more useful situation of whatever is impairing the normally operating mechanisms of error detection, elimination, correction etc. Who cares about the predicting the effects of particular kinds of gene damage when the issue is avoiding the consequences of any kind of gene damage?

    Damaged genes might produce a rate of variation in outcomes, with the seriously damaging mostly eliminated by natural selection in the long run. But damage to the mechanisms the normally control this damage (reasonably efficiently, but never perfectly) would seem to be more interesting as this would be the real cause of cancer. Whatever might be the trigger of various cancer cells is necessary but not sufficient to lead to cancer becoming a significant threat to an organism.

  3. I think all avenues must be explored with regard to each and every type of cancer; is the search on for a common denominator?

  4. Exploring the mechanisms of each kind of genetic malfunction could be infite. Like identifying all the possible misprints and 
    barely noticeable defects that result from dropping spanners into the printing works. Better to avoid dropping spanners.
    I only know of one potential common cause for cancer, which is protein glycation. But that’s a possible cause of virtually everything that might result from chronic disruption to cellular function – a single cause concept isn’t fashionable and isn’t easily established because it’s hard to measure (Also linked to alzheimers, blood pressure, atherosclerosis, diabetes, immune dysfunction).
    But it might explain peculiar things like why overall community health can sometimes improve during moderate chronic starvation. As in wartime rationing, ghettos under nazi occupation, and for survivors of nuclear weapons. I know that starvation therapy is being researched as a potential new treatment for various cancers. Though there’s no obvious pharmaceutical payoff, which might mean that research is relatively minimal. For a treatment to be commercial effective it needs to cost money, so profit margin can be added. There’s no profit margin from getting someone to stop eating for several months.

  5. Cancer research, I think, really does expose the limitations of science. There comes a time when the permutations that seemingly need to be examined are so vast even the most powerful computers imaginable would not be able to assist within the lifespan of the universe. There is simply no way to be sure what the cause(s) are for a particular type of cancer and to avoid or remove them completely so as to guarantee one will never developer the disease.

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