Gene Expression

Interesting report out, Evolutionary biology research techniques predict cancer. Medicine has been around for thousands of years, from the “healings” of shamans to the “theoretical” paradigm of Galen. It seems possible that until the last 100 years or so medical techniques were just as likely (or more likely in many situations) to exacerbate illnesses as they were to help. The medical arts might be an outgrowth of our psychological biases, not materialist considerations (an analogy with financial “analysts” might be appropriate). Purely empirical sciences focused on proximate aspects of phenomena are often groping blindly in the dark, so the inclusion of microevolutionary theory can add in the elimination of alternative hypotheses. Modern medical science has progressed very far, but the integration of the temporal and spatial perspective of evolutionary science may help us in outwitting nature by cutting off the pathological dynamics at the pass.

Comments

  1. #1 Agnostic
    March 28, 2006

    In contrast to practices leading to iatrogenic disease, elimination of pathogens is the one area of medicine that was spot-on when originally developed and has had the best track record. For instance, at the bottom of the page you linked to, there’s this article about a virus suspected in prostate cancer. That’s in addition to infectious cervical cancer (and probably penile cancer from the same source), liver cancer, stomach cancer, etc.

    My guess as to this Barrett’s Esophagus progressing to cancer is also infectious. The background is set by stomach acid coming up to the esophagus & changing the cells there — kind of like slash & burn clearing out the flora & fauna of a forest, which sets the stage for an infestation of unchallenged weeds (germs in this case). The greater genetic diversity would be due to the presence of foreign genomes in the body (those of germs), plus the germs’ strategy of making the host’s cells create more diverse types of cells — this would allow for better camoflauge, like a criminal running to blend in w/ a heterogeneous crowd. That’s sort of what the HPV does in cervical cancer.

  2. #2 MIke McKeown
    March 28, 2006

    From the newspaper article it appears they type the particular growths in question for gene expression patterns in different cells within the growth. The stated conclusion is that those growths with more diversity of expression patterns are more likely to become cancerous.

    Aside from the trivial explanation – the more expression types present the greater probability that one of them is only a few additional changes away from immortality and/or loss of growth control – it is possible that greater diversity of expression patterns is a direct indication that the cells have already become genetically, or in terms of gene expression, unstable. This is already a characteristic of tumor cells. In other words, some cell back in the lineage of the growth was already prone to instabilty and the probability of one of its progeny cells becoming full blown cancer is much higher than for progeny of cells that are not unstable.

    There is some discussion among the aging and cancer research communities about the inverse relationship between aging and cancer. Specifically, it is speculated, with some data, that the more carefully the cells of an organism police themselves for genomic damage, the lower the cancer probability and the shorter the life span relative to members of the same species whose cells are less vigilant about genome damage. Part of the logic is that one of the key functions of the genome damage police is to kill cells in which genetic lessions occur. This protects against cancer by eliminating potentially dangerous mutations, but it also removes cells from the body and strains the ultimate replicative capacity of various cell populations and their precursors.

    Some data and speculation on this topic views p53, a protein originally identified as genetically changed in tumors and known to some as ‘the guardian of the genome,’ as the key target of a at least one ‘aging’ pathway. This pathway exists in multiple organisms, responds to resveratrol (the anti-aging component of red wine), and ends with Sir2 or its homologs (sirtuins). Sir2 can act as a chromatin modifying enzyme (it removes post translationally added actyl groups from histones), causing DNA to be less available for transcription. It also, apparently, deacetlyates p53, changing its activity as well. This is imporatant as at least some experiments indicate that moderately decreased p53 activity leads to extended life.

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