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Medicine Biotech

Why a Cure For Cancer Is So Elusive 366

Hugh Pickens DOT Com writes "George Johnson writes in the NYT that cancer is on the verge of overtaking heart disease as the No. 1 cause of death and although cancer mortality has actually been decreasing bit by bit in recent decades, the decline has been modest compared with other threats. The diseases that once killed earlier in life — bubonic plague, smallpox, influenza, tuberculosis — were easier obstacles. For each there was a single infectious agent, a precise cause that could be confronted. But there are reasons to believe that cancer will remain much more resistant because it is not so much a disease as a phenomenon, the result of a basic evolutionary compromise. As a body lives and grows, its cells are constantly dividing, copying their DNA — this vast genetic library — and bequeathing it to the daughter cells. They in turn pass it to their own progeny: copies of copies of copies. Along the way, errors inevitably occur. Some are caused by carcinogens but most are random misprints. Mutations are the engine of evolution. Without them we never would have evolved. The trade-off is that every so often a certain combination will give an individual cell too much power. It begins to evolve independently of the rest of the body and like a new species thriving in an ecosystem, it grows into a cancerous tumor. 'Given a long enough life, cancer will eventually kill you — unless you die first of something else (PDF). That would be true even in a world free from carcinogens and equipped with the most powerful medical technology,' concludes Johnson. 'Maybe someday some of us will live to be 200. But barring an elixir for immortality, a body will come to a point where it has outwitted every peril life has thrown at it. And for each added year, more mutations will have accumulated. If the heart holds out, then waiting at the end will be cancer.'"
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Why a Cure For Cancer Is So Elusive

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  • by Anonymous Coward on Sunday January 05, 2014 @06:56PM (#45873757)

    Yes, it is. Some are viral, some by metabolic imbalances in the cells, others by poisoning, some by transcription errors, and a few are bizarrely fungal. The only thing that "cancer" is, if it's anything at all, is a bunch of very different diseases that are characterized by the cells in the body multiplying faster than they should. Not all are even tumorous; think about leukemia.

  • Re:Money (Score:4, Informative)

    by RDW ( 41497 ) on Sunday January 05, 2014 @07:41PM (#45874051)

    So how do the conspiracy theories explain the dramatic improvement in survival rates in those cancers where research-guided improvements in treatment have been very successful?: [] []

    Clearly there's a great deal to be done, and finding 'cures' is a very complex and difficult task. But we finally have the tools to do this in a systematic and rational way, and targeted therapies are already emerging.

  • by OneAhead ( 1495535 ) on Monday January 06, 2014 @02:14AM (#45876089)

    Assuming that it doesn't lead to autoimmune problems down the road, I strongly suspect that immunotherapy (programming the immune system to identify the damaged cells and attack them) will become a much more commonplace treatment for cancer, precisely because it cuts off that metastasis process.

    The immune system already does that []; severely immunodeficient individuals are prone to getting cancer. Cancer is a complicated process - 5 to 7 distinct cell mechanisms (depending on how you count) need to be malfunctioning before one can speak of a life-threatening cancer (at first glance, wikipedia [] seems to have left a few out). One of them is that the cell must lose the ability to display outwards signs of being cancerous to the immune system, else it will be eliminated in short order. Now, if you're going to modulate the immune system to attack cells that don't display outwards signs of being cancerous, then your assumption that "it doesn't lead to autoimmune problems" will likely turn out false. (Mostly experimental) therapeutic approaches involving the immune system rely on the therapeutic agent recognizing tumor cells and making them recognizable to the immune system in turn. The challenge there is that cancers are diverse and have a high mutation rate - even if you're lucky enough to have an agent on the shelf that recognizes the specific cancer you're having, it may stop working in a few months. So you're again in a place where you can never truly cure each and every patient.

    BTW, I'm a cancer researcher. I'm not saying this as an appeal to authority, just to explain where I got this information and to confirm that the view in TFA is somewhat of a consensus in the field. This does not make it a depressing job: as the field progresses we can beat back more cancers for longer with fewer side effects, which is exciting. Some might say that maybe some day we will get so good that 99.9% of people die of other causes before they get the chance to develop a life-threatening cancer we can't cure. However, my (admittedly one-sided) view is that most other age-related causes I can think of are easier to cure than cancer, and that the latter is at #1 to stay (barring a collapse of civilization). And even if I'm proven false, 99.9% is not 100%. We can't cure cancer 100% just like we can't manufacture hard drives with a 0% failure rate. Nature seems to abhor systems that never fail.

  • by stoploss ( 2842505 ) on Monday January 06, 2014 @03:50AM (#45876375)

    I see you have brought the machine analogies into play.

    Are you conflating "cure" for cancer with "complete prevention" then? To go back to the machine analogy, I believe it is sufficient to define a machine as "not failing" if it can be repaired. I agree with you that machines inevitably fail; however, I don't automatically conflate that with permanent failure.

    Dropping the analogies, if your sole claim is that we will never be able to prevent each and every individual cell from accumulating mutations and failing to undergo apoptosis when critical failures have accumulated, then you may be correct (likely because that problem isn't worth solving). If you are claiming that we will never be able to prevent a single, uncontrolled mutant cell from eventually causing death from metastatic disease (or cerebral disruption) then I suggest you are being fatalistic.

    My comment about the rabbits was intended to point out the tautology of any type of claim that cancer will kill you if nothing else does. I believe Larry Niven once threw out a plausible stat that "immortality is ~200 years of life", mostly due to the accumulated odds of accidental death. To put it in terms of biological engineering, we may not be able to reduce the risk of metastatic disease to zero, but we may have a practical "cure" that reduces the risk to a practically infinitesimal level.

    The machine isn't permanently broken if it can be repaired.

  • by sandertje ( 1748324 ) on Monday January 06, 2014 @08:03AM (#45877087)
    Human cells already do some sort of checksumming on their genes. To start with, polymerases - the proteins that copy DNA - have proof-reading activity. That is to say, they check whether their copied DNA is equal to the parent DNA molecule. Then, if DNA damage occurs - which happens more frequently than you'd think - it gets repaired almost entirely flawlessly. Single strand breaks are easy to repair for the cellular machinery; they can use the opposite strand of the same DNA molecule as a scaffold for repair. Double strand breaks are indeed more difficult to repair, but luckily we have two sets of each chromosome (one from mommy, and one from daddy), so if one breaks, the other pair member is used as a reference. Sure, these pairs of chromosomes are not entirely identical, but for most cases, it suffices. As a result, the human mutation rate is on the order of about once every 100 million times. That's really low. Try to copy a 3GB file (roughly the size of human DNA) 100 million times on your computer, and I'm sure you'd have a lot more corrupted files than just 1. Unfortunately, the human body contains several trillions of cells, leaving enough room for incremental errors. One hallmark of cancer is that it relies on (partially) shutting down this "checksumming", and as such can attain a much higher rate of mutation - and as a result, a much higher rate of evolution - than normal cells. (see: [] for a very nice overview). Besides that, just guarding the genes is not enough. Our genetics is more than enough to induce heavy proliferating cells. How else would we be able to grow from a single-celled individual (the fertillized egg) to a fully-grown body of several trillion cells? Healthy humans NEED proliferation (of certain cells), and thus we have genes that code for just that. The key here is activating certain genes in certain environments, and inactivating other genes. Every cell type has a different transcriptional landscape. This is controlled by epigenetics. Just guarding your genes would not guard against any changes in epigenetics, and you would still be prone to cancer.

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