Cancer can teach us about our own evolution


Medical science treats cancer as a disease in which rogue cells proliferate uncontrollably, running amok around the body. Therapy focuses on killing the cancer before it kills the host. Unfortunately, the emphasis on cancer cells as defective loose cannons is at odds with the stubborn way they outwit both the body’s defences and the physician’s armoury.

Cancer is such a ruthless adversary because it behaves as if it has its own fiendishly cunning agenda. Cancer cells come pre-programmed to execute a well-defined cascade of changes, seemingly designed to facilitate both their enhanced survival and their dissemination through the bloodstream. There is even an air of conspiracy in the way that tumours use chemical signals to create cancer-friendly niches in remote organs.

In the frantic search for an elusive “cure”, few researchers stand back and ask a very basic question: why does cancer exist? What is its place in the grand story of life? Astonishingly, in spite of decades of research, there is no agreed theory of cancer, no explanation for why, inside almost all healthy cells, there lurks a highly efficient cancer subroutine that can be activated by a variety of agents – radiation, chemicals, inflammation and infection.

Cancer, it seems, is embedded in the basic machinery of life, a type of default state that can be triggered by some kind of insult. That suggests it is not a modern aberration but has deep evolutionary roots, a suspicion confirmed by the fact that it is not confined to humans but is widespread among mammals, fish, reptiles and even plants. Scientists have identified genes implicated in cancer that are thought to be hundreds of millions of years old. Clearly, we will fully understand cancer only in the context of biological history.

Two relevant evolutionary transitions stand out. The first occurred over 2 billion years ago, when large, complex cells emerged containing mitochondria – tiny factories that supply energy to the cell. Biologists think mitochondria are the remnants of ancient bacteria. Tellingly, they undergo systematic changes as cancer develops, profoundly altering their chemical and physical properties.

For most of Earth’s history, life was confined to single-celled organisms. Over time, however, a new possibility arose. Earth’s atmosphere became polluted by a highly toxic and reactive chemical – oxygen – created as a waste product of photosynthesis. Cells evolved ingenious strategies to either avoid the accumulating oxygen or to combat oxidative damage in their innards. But some organisms turned a vice into a virtue and found a way to exploit oxygen as a potent new source of energy. In modern organisms, it is mitochondria that harness this dangerous substance to power the cell.

Written By: Paul Davies
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  1. @OP:disqus 
    With the appearance of energised oxygen-guzzling cells, the way lay open for the second major transition relevant to cancer – the emergence of multicellular organisms. This required a drastic change in the basic logic of life.

    Single cells have one imperative – to go on replicating.
    In that sense, they are immortal. But in multicelled organisms, ordinary cells have outsourced their immortality to specialised germ cells – sperm and eggs – whose job is to carry genes into future generations.

    The price that the ordinary cells pay for this contract is death; most replicate for a while, but all are programmed to commit suicide when their use-by date is up, a process known as apoptosis.
    And apoptosis is also managed by mitochondria.
    Cancer involves a breakdown of the covenant between germ cells and the rest.
    Malignant cells disable apoptosis and make a bid for their own immortality, forming tumours as they start to overpopulate their niches.
    In this sense, cancer has long been recognised as a throwback to a “selfish cell” era.

    A throwback to ancient genes with broken “off switches”!

  2. Maybe cancers are a consequence of viral genes blended with host genes, but which don’t exist as independent viral organisms.

    There’s some similarities of cancers with viruses that lie relatively dormant indefinitely but are triggered to proliferate when the host organism weakens and is more likely to die. Presumably a mechanism to enable the virus genes to increase the probability of their transferring to a new replacement host.

    Something similar has been observed with some cancers. When the organism is starved the tumour cells become more profligate with their host’s energy resources, by increasing their rate of activity attempting to grow and multiply. While the host organism’s normal cells respond to starvation by conserving energy and reducing their activity. So the tumour cells might be triggered into responding like a virus when their host is threatened, implying they may soon need to find new territory to exploit. But the more active tumour cells then become more prone to failure because there is less energy available from the host once the host’s cells have switched into hoarding their reduced energy remains during starvation. The weakened tumour cells deplete their internal energy, which is not as easily replaced, and so might become more susceptible to other stresses like chemotherapy.

    So what needs to be avoided is triggering the tumour cells into some kind of end of life cycle frenzied proliferation, but while still allowing the host cells to provide unlimited resources to the tumour cells.

    If this idea proves out one implication might be that the modern era impact of cancer epidemics could be a consequence of people suffering from inadequate malnourishment.

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