TUMORS DEVELOP IN CHRONIC inflammatory ENVIRONMENTS Virchow saw a correlation between inflammation and tumor back in 1863. Ever since, research has been changing in such a way that can barely be compared to those times. And yet, this postulate gained more relevance than ever. In <strong>the</strong> meantime we know from some chronic viral infections that <strong>the</strong>y can make <strong>the</strong> way for tumors to develop. And <strong>the</strong> same applies to chronic inflammations like rheumatism or chronic inflammatory gastro-intestinal diseases. Inflammations are usually self-limiting processes. With a fine-tuned immune response, <strong>the</strong> immune system makes sure that inflammatory and anti-inflammatory processes ultimately lead to healing. Characteristic of <strong>the</strong> immune situation of tumor patients is <strong>the</strong> fact that <strong>the</strong> immunity is weakened (suppressed). When a tumor start to grow or metastasize, <strong>the</strong>n it has usually already infiltrated <strong>the</strong> immune system with its monitoring strategies. An intact immune system patrols <strong>the</strong> body and removes <strong>the</strong> cells that are no longer behaving properly. Dvorak recognized <strong>the</strong> similarities between wound healing and tumors back in 1986. In contrast to a tumor, a wound heals itself. In a tumor, <strong>the</strong> process continues by factors being released unremittingly, which maintain <strong>the</strong> inflammation. As is <strong>the</strong> case with wound healing, <strong>the</strong> formation of vessels in <strong>the</strong> scope of a tumor emerging plays an important role for a tumor that measures more than one to two millimeters, blood vessels are vital. TO PUT IT A NUTSHELL: In order for a malignant tumor to start growing, an external or internal trigger, an inflamed environment and damage to <strong>the</strong> DNA must concur. An improbable event for an individual? Many malignant tumors are triggered off by infections. A history of infection can be assigned to more than 15% of all tumors worldwide; that is more than 1.2 million cases a year. Thus, tumors develop as <strong>the</strong> result of a multi-leveled process, which leads from an initial benign change to <strong>the</strong> cells to an invasive and <strong>the</strong>n metastasizing disease. This process takes many years until it has fully developed. The long period this process requires strongly implies that it has to assert itself against a background of strict and diversified control mechanisms that are supposed to prevent anarchical cell behavior. It is thus probable that a certain environment tied to a genetic disposition changes <strong>the</strong> cells to such an extent that <strong>the</strong>y become more receptive for endogenous and exogenous carcinogen influences. It may depend on whe<strong>the</strong>r <strong>the</strong> carcinogens can actually trigger off tumor growth and how long it takes until <strong>the</strong> process is clinically proven. IF YOU WANT TO KNOW MORE THEN YOU MAY BE interested IN WHAT HYPOTHESES SCIENTISTS ARE CURRENTLY WORKING WITH. One hypo<strong>the</strong>sis reads as follows: The cell reveals a gene defect that can no longer be repaired. For this reason, <strong>the</strong> external appearance of <strong>the</strong> cell deviates from that of <strong>the</strong> normal cell. Such a cell no longer divides itself up asymmetrically into a cell with a function (effector cell), which depends upon which organ or apparatus it is allocated to and into a stem cell but symmetrically into two cells with functions. Yet, it is not a tumor cell. As long as <strong>the</strong> environment surrounding <strong>the</strong> cell suppresses cell proliferation, a tumor does not yet develop. If, however, a carcinogen or a chronically inflammatory changed environment affects <strong>the</strong> cell to <strong>the</strong> extent that <strong>the</strong> brake preventing cell proliferation is released, <strong>the</strong>n <strong>the</strong> cell begins to proliferate in an uncontrolled manner. The result is a mass of cells such as polyps in <strong>the</strong> colon or papilloma in <strong>the</strong> skin. For a so-called malignant tumor to develop, a number of additional genetic or cellular changes must occur. It‘s not until now that <strong>the</strong> step towards <strong>the</strong> tumor becoming malignant follows. Ano<strong>the</strong>r hypo<strong>the</strong>sis - worded by Potter back in 1978 - explains <strong>the</strong> emergence of a tumor as being a blockage of cell development on <strong>the</strong>ir way from <strong>the</strong> stem cell, where it still carries a large number of possibilities, to <strong>the</strong> cell that is equipped with <strong>the</strong> function determined for that cell. An interruption to this development can happen at any stage of this process. Influences from <strong>the</strong> cell‘s environment can speed up cell division and prevent <strong>the</strong> normal death of <strong>the</strong> cell. You have probably often come across <strong>the</strong> term oncogene. More than 100 oncogenes have already been identified. Oncogenes are DNA parts that serve as <strong>the</strong> template for <strong>the</strong> syn<strong>the</strong>sis of protein substances with differing tasks like growth factors, receptors, signal-transferring molecules. The tumor suppressor genes have a quasi contrary task to <strong>the</strong> oncogenes. They form <strong>the</strong> template for <strong>the</strong> growth of inhibitive factors such as bridging molecules. These are structural proteins in cell membranes that form channels for <strong>the</strong> direct transfer of small molecules and ions between <strong>the</strong> cells. The bridging molecules between <strong>the</strong> cells are central structures of monitoring growth and differentiating normal cells. If a gene-defect cell still has bridging connections, it is still able to develop in its target cell to a certain extent. Its direct contact to <strong>the</strong> o<strong>the</strong>r cells in <strong>the</strong> network inhibits uncontrolled proliferation. 6 BIESTMILCH <strong>Tumor</strong> <strong>–</strong> <strong>see</strong> <strong>the</strong> <strong>opportunity</strong>
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