The vague correlations between bladder cancer and

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cytokines, and growth factors). The vague correlations between bladder cancer and allergy incidence can now be explained by the fact that some toxins were identified as inhibitors of inflammation (lowering natural cancer defenses), while other compounds can be inflammation (and allergy) inducers, which if left unchecked could actually increase the risk of cancer in the continually inflamed region (Balkwill, 2005). 5
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The Inflammation hypothesis and its predictions turn out to align with Sherman’s results better than any of the previous hypotheses. Chronic inflammation leading to cancer development could account for Sherman’s observations of a positive correlation in some instances (An Antigenic Stimulation-based approach). On the other hand, successful elimination of carcinogenic toxins by causing allergy symptoms, or inflammation, would contribute to the study proportion witnessed to have negative correlations by Sherman et al (A Prophylaxis-based approach). Another trend that the Inflammation hypothesis helps to explain, is the higher number of significant positive correlations in cases with single allergies, and the apparent reversal in cases with multiple allergies showing more significant inverse correlations. This can be explained by the fact that multiple allergies may be a stronger indicator of a hyper-active inflammation response, that is behind the added protection from bladder cancer (An Immunosurveilance-like explanation). The over-arching nature of the Inflammation hypothesis allows it to borrow from each of the other three hypotheses, and makes it a better fit as an explanation for Sherman’s results. Inflammation is part of an ancient and diverse set of pathways designed to combat infection or any other foreign substance (Borello et al, 2005). Part of the reason for the system’s survival is its ability to regulate DNA-repair enzymes and their production. A down- regulation of these enzymes would create an environment where totally destroyed-DNA- containing cells are allowed to die off, while simultaneously allowing slightly damaged DNA containing cells to proliferate without correction, a double-edged sword. Conversely, an increase in the repairing enzymes will assure correction or elimination of the potential carcinogen, though it may end up eliminating native cells in the process. 6
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Finally, the limitations of the Inflammation hypothesis and its statistical significance were explored. The largest challenge was most likely the mirage of potential confounding variables in the correlations between allergies and bladder cancer, bringing the significance of the observed correlations into question. From environmental circumstances, to genetic predisposition, the possible factors that contribute in determining overall bladder cancer risk are numerous, and their combinations almost always unique. Another gripe with the hypothesis could be its relatively vague nature, when compared with the exact reasoning of the Prophylaxis hypothesis. Until a definite pathway is revealed, the correlations will likely remain simple correlations, instead of the more powerful conclusions of causation.
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  • Fall '10
  • PAULW.SHERMAN
  • bladder cancer

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