Opioid Painkillers Could Be Replaced by Cancer Drugs

저자：   업로드：2017-08-10  조회수：

    The discovery of a new biological pathway involved in pain processing offers hope of using existing cancer drugs to replace the use of opioids in chronic pain treatment, according to scientists at McGill University.

    A newly discovered pain-processing pathway could lead to alternative treatments for chronic pain. The new treatments could even make use of existing cancer drugs that block the epidermal growth factor receptor (EGFR). This receptor, long a target in cancer therapies, has only recently received attention for its therapeutic potential against pain.

    A recent study implicating EGFR in pain processing found that this receptor and its natural ligand, epiregulin (EREG), interact to heighten pain perception. This finding, derived from experiments with mouse models, suggests that both EGFR and EREG could be suitable therapeutic targets for chronic pain in humans. Even if existing drugs that interfere with EGFR/EREG interactions were to fail to manage pain effectively, they could serve as a starting point for engineering more useful variants.

    There is likely sufficient incentive to develop alterative pain killers that could replace opioids, given that opioids carry the risk of addition and undesirable side effects.

    Details from the new study appeared in the Journal of Clinical Investigation, in an article entitled “Epiregulin and EGFR Interactions Are Involved in Pain Processing.” The article reported that EGFR blockers, routinely given to lung cancer patients to inhibit tumor growth, were as potent analgesics as morphine in mouse models of inflammatory and chronic pain. The article also attributed the analgesic effect to a mechanism thought to regulate pain, but never before evaluated with behavioral or cellular models specifically relevant to pain processing.

    “EREG-mediated activation of EGFR enhanced nociception through a mechanism involving the PI3K/AKT/mTOR pathway and matrix metalloproteinase-9,” wrote the article’s authors. “Moreover, EREG application potentiated capsaicin-induced calcium influx in a subset of sensory neurons. Both the EGFR and EREG genes displayed a genetic association with the development of chronic pain in several clinical cohorts of temporomandibular disorder.”

    The study, which was led by McGill’s Luda Diatchenko, Ph.D., arrived at this last finding, the association with temporomandibular disorder, a human chronic pain syndrome, after they searched for evidence that EGFR contributes to pain in a clinical population. Th

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