Cancer research issues. Two opposing positions

Here are what I would consider two opposing viewpoints on cancer research.

The optimistic we are really making headway point of view.

And what I thought at the time was a very insightful take down of cancer research hype by Tom Bethell, science writer for AMSPEC, who had a pessimistic view but emphasized the research that pointed to multiploidy, which is not mutations. No doubt multiploid cell lines dominate cancer, so why is multiploidy being ignored on and off:


4 responses to “Cancer research issues. Two opposing positions

  1. John, the article by Bethell is outstanding. The evidence for aneuploidy rather than gene mutation as a cause for most, if not all, cancers is compelling. It’s hard to dismiss the one common feature of all cancers as unimportant. Peter Duesberg is that extremely rare bird—a true scientist who is not afraid to buck the establishment and backs his theories with solid reasoning and research. For those who would like to explore this oncogene vs. aneuploidy debate in more depth there is a book titled “Oncogenes, Aneuploidy, and AIDS: A Scientific Life & Times of Peter H. Duesberg” by Harvey Bialy. Not an easy read but well worth the time and trouble.

  2. The “pessimistic view” sounds more like the beginning of a long-suppressed realization that cancer is just a normal and expected outcome of normal, unbounded development. Nobody can command his cells to stop developing, nor would it be desirable to have it stopped. Life is not possible without ongoing development. Having cancer is a mark of maturity, just like wrinkled skin, loss of bone tissue, and a lot of other age-related effects.

    Now it appears like surgeons are the only class of healthcare professionals who at least have some grip on the maintenance of unwanted growth and differentiation. They can’t prevent it or stop it, but they can deal with it.

    Not true, though, that aneuploidy has been overlooked. I don’t know of any company in cancer diagnostics business that wouldn’t be working on aneuploidy and copy number determination.

  3. The multiploidy aneuploidy is undeniable–malignant cell lines have nuclei with tremendous loads of genetic material.

    The theory is an age related malfunction of the telomeres during mitosis that cause the arms to double up instead of replicate and split.

    I think that makes sense. I would have to say you can’t posit that age related malfunctions of mitosis explain childhood cancers, so that has to be addressed.

    There is also the theory that killer mechanisms for new malignant cell lines decline with age, also makes sense.

    • Pediatric cancers are better explained by point mutations, rather than whole systems slowly growing out of whack. They are all different, but every time the mechanism is unravelled, it is down to a small change that either eliminates or enables a regulator, or simply affects the timing of events, as in the case of tyrosine kinase receptor in neuroblastoma. That is by no means the only possible cause of neuroblastoma, but it is a good illustration for how a small tweak can lead to a catastrophic change in development.

      Here’s a good overview of the mechanisms:

      So the difficulties in finding “cancer genes” simply mean that every gene that is somehow involved in development can be a cancer gene. A lot of them are. Many strong effects are post-genetic. The killer mechanisms, in particular, are very unstable, complex, and panicky (that is why such a small dose of cyanide can kill so easily — not that it really is so toxic; it is our response to it that is completely insane: there’s this apparently uncaused and unregulated hypoxia; we have no idea what it is, so let’s die, just in case it may be caused by cancer). Early development is full of surprises like that.

      If you’re lucky to make it through the outrageously haphazard early stages, it does not mean you’re done. Development never stops, and it never really is as orderly as we like to think. It just takes a bit longer to arrive at the next disaster. That might take a lifetime, for some of us that don’t get killed while having fun or fighting for a cause. But there is always terminal maturity of some kind waiting in the end, whether you’er a human, a worm, or a tree.

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