So far the clearest evidence of a link between cancer and inflammation is the data demonstrating that inflammation encourages the conversion of precancerous tissue to full malignancy for many cancers. But the biological response may also be involved in initiating the disease and in advancing metastasis. Infections with Helicobacter pylori bacteria induce inflammation that greatly increases the risk of gastric cancer, and the hepatitis C virus can bring on liver cancer, to name just two cancers. Pathogens may also generate free radicals, which can damage DNA. But although inflammation may be involved from the outset, few studies have shown yet that an inflammatory condition actually alters DNA to provide the initiating spark.
The case for a role in metastasis is stronger—and recent studies lend credence to this hypothesis. Karin’s group reported in the April 5 Nature that inflammation, not genetic changes in cancer cells, spurs metastasis in mice engineered to acquire prostate cancer. The research suggests that a cytokine produced by inflammatory cells near a prostate tumor induces tumor cells to decrease production of a protein that blocks metastasis. This result, Karin notes, may explain the puzzling observation that cutting into tumors, such as for a prostate biopsy, sometimes seems to encourage metastasis. If he is correct, the inflammation generated by the intervention could be at fault. Around the same time, Pollard’s group reported in Cancer Research on a study in mice that observed that macrophages accompany breast tumor cells in their migration toward blood vessels that will transport them to remote sites, all the while sending chemical messages to their partners.
The innate immune system has received the most attention in explorations of how inflammation might cause cancer. As with innate immunity, the adaptive immune system—the T cells and antibodies produced by B cells that target specific molecules on invading cells—contributes to pathology or may also fight against it. For decades, immunotherapies designed to enhance T cell responses against cancer have been explored, though often with disappointing results.
Furthermore, an emerging picture has begun to reveal an intricate cross talk between innate and adaptive immune cells that may participate in the promoting of malignant disease. Researchers working on cancer vaccines may need to take account of these interactions in designing their treatments if they are ever to prove effective. One study showed that ovarian tumors produce a signaling molecule that serves to attract regulatory T cells, a subclass of adaptive immune cells responsible for quieting other T cells [see “Subduing Suppressors,” by Lisa Melton; Scientific American, December 2002].
Meanwhile Coussens and her colleagues at U.C.S.F. found in a 2005 study published in Cancer Cell that the removal of antibody-making B cells from mice engineered to be prone to skin cancer prevented the tissue changes and angiogenesis that are prerequisites for disease progression. In their normal role as pathogen fighters, B cell–produced antibodies circulate through the bloodstream and mark viruses and bacteria for destruction by innate immune cells. In response to a signal from precancerous tissue, however, the antibodies induce the innate system to collaborate in cancer development. An open research question is how this process starts. One possibility suggests that a cancer cell may send a message to innate immune cells, perhaps dendritic cells, that then activate B cells. Signaling may involve toll-like receptors, which have emerged as prominent intermediaries in innate immune messaging [see “Immunity’s Early Warning System,” by Luke A. J. O’Neill; Scientific American, January 2005].
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Add CommentThis actually is not new news.. the theoretical model in Traditional Chinese Medicine ascribes the precursor to cancers as being "heat toxins" which can be loosely described as free radicals causing an inflammatory response in the body. A survey of herbal treatments for this condition may provide indicators for new pharmacologically active compounds that could prevent/protect the body from carcinogenic cellular growth
Reply | Report Abuse | Link to thisMany of the parasites which can colonise the human body influence our immune systems and dampen our inflammatory response to make us more hospitable hosts. I wonder are there any such organisms already producing their own ready-made pharmaceuticals which we could benefit from in this way to make us less susceptible to cancers and other inflammation-mediated disorders?
Reply | Report Abuse | Link to thisMany physicians believe that cellular inflammation is the basis for many of the common degenerative diseases that are impacting our population. With a host of information on anti-inflammatory supplements and diet guides, it just makes sense to pursue an anti-inflammatory lifestyle.
Reply | Report Abuse | Link to thisThere are indeed therapies based on helminths (hookworms) that offer promise. Sadly, however, this has not received much funding or media attention, likely because of the aversion of some to the idea of having living parasites in their body. The University of Iowa and Nottingham University in the UK have been two centers of study for helminth therapy.
Reply | Report Abuse | Link to thisHopefully soon helminth therapy will become more widely studied and available.
Thank you for such a great summary of Chronic Inflammation in Cancer study. It is very use to take information from cross-disciplines and apply it to your research such as Tissue Engineering/Regenerating tissues. Interestingly macrophage polarization determines positive regeneration or chronic inflammation and some of the information obtained in cancer studies can be borrowed to regenerate tissues & organs.
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