Publications by authors named "Camilla Appel"

Background: Calcitonin gene-related peptide monoclonal antibodies (CGRP mAbs) are recommended by the United Kingdom National Institute of Health and Care Excellence for the prevention of migraine as treatment beyond third line. We report migraine prevalence and preventive treatment patterns in the adult United Kingdom primary care population over a 7.5-year period, focusing on patients ceasing ≥ 3 oral preventive medication classes.

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The dissemination of cancer to bone can cause significant cancer-induced bone pain (CIBP), severely impairing the patient's quality of life. Several rodent models have been developed to explore the nociceptive mechanisms of CIBP, including intratibial inoculation of breast carcinoma cells in syngeneic Sprague Dawley rats. Using this model, we investigated whether resident spinal microglial cells are involved in the transmission and modulation of CIBP, a long-debated disease feature.

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Article Synopsis
  • - The study investigates how cancer-induced bone pain affects burrowing behavior in mice and rats, which is a natural behavior sensitive to chronic pain.
  • - After being inoculated with breast cancer cells, the rodents exhibited decreased bone density and reduced limb use, confirming the presence of the disease.
  • - The results show that burrowing performance diminished over time in both models, suggesting that burrowing tests are valuable for evaluating cancer-induced bone pain in research.
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Article Synopsis
  • The study investigates the effects of AFC5261, a selective P2X7 receptor antagonist, on cancer-induced bone pain in rats, given the conflicting results from previous research on P2X7R inhibition.
  • Acute treatment with a high dose of AFC5261 showed no beneficial effects on pain-related behaviors, while morphine was effective in improving limb use and weight-bearing.
  • Chronic administration of AFC5261 at a higher dose worsened pain-related behaviors without affecting bone degradation or tumor progression, suggesting long-term inhibition may increase cancer-induced bone pain.
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Bone cancer metastasis is extremely painful and decreases the quality of life of the affected patients. Available pharmacological treatments are not able to sufficiently ameliorate the pain, and as patients with cancer are living longer, new treatments for pain management are needed. Decitabine (5-aza-2'-deoxycytidine), a DNA methyltransferases inhibitor, has analgesic properties in preclinical models of postsurgical and soft-tissue oral cancer pain by inducing an upregulation of endogenous opioids.

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Pain remains a major concern in patients suffering from metastatic cancer to the bone and more knowledge of the condition, as well as novel treatment avenues, are called for. Neuropeptide Y (NPY) is a highly conserved peptide that appears to play a central role in nociceptive signaling in inflammatory and neuropathic pain. However, little is known about the peptide in cancer-induced bone pain.

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Pain is a severe and debilitating complication of metastatic bone cancer. Current analgesics do not provide sufficient pain relief for all patients, creating a great need for new treatment options. The Src kinase, a non-receptor protein tyrosine kinase, is implicated in processes involved in cancer-induced bone pain, including cancer growth, osteoclastic bone degradation and nociceptive signalling.

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Background: Pain caused by bone metastases has a severe impact on the quality of life for many patients with cancer. Good translational in vivo models are required to understand the molecular mechanism and develop better treatment. In the current study we evaluated the influence of sex differences on the progression of cancer-induced bone pain.

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