Mechanisms that Drive Cancer Pain
During the past 25 y, many references in the clinical literature have indicated that cancer pain is generated and maintained by 1 (or a combination) of the following anatomic mechanisms: compression of bone, soft tissue, or peripheral nerve; vascular occlusion; and tumor infiltration. In addition, cancer pain can arise as a result of diagnostic or therapeutic surgical procedures (such as biopsies and resection) or, particularly in people, as a side effect of toxicity relating to therapies used to treat cancer (for example, chemotherapy and radiation therapy). Although anatomic factors including compression, vascular occlusion, and tumor infiltration provide a mechanistic rationale that explains the basis of tumor-induced pain in gross pathologic terms, they fail to address the basic biochemical, molecular, and neurobiologic mechanisms that underlie the production of pain in patients with cancer. In this regard, tumor pain, particularly that from bone cancer, represents 1 of the most severe types of chronic pain in both humans and animals. Unfortunately because the mechanisms that generate cancer pain were until poorly understood until recently, the management of cancer pain has been largely empirical and based on scientific studies of noncancerous conditions such as inflammatory pain, where knowledge of the nociceptive mechanisms is quite extensive.