Mechanisms and Management of Cancer Pain

Anand, Uma

doi:10.1002/9780470025079.chap310

Cited by 4 publications

(4 citation statements)

References 107 publications

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“…Though advances in cancer detection and therapy have significantly advanced life expectancy in cancer patients, quality of life may be severely compromised due to the development of painful neuropathy [1][2][3][4]. Chemotherapyinduced peripheral neuropathy is a common, rapidly induced effect observed soon after administration of anticancer agents [5][6][7] resulting in numbness, tingling and pain distributed in a distal stocking-and-glove pattern [8,9].…”

Section: Introductionmentioning

confidence: 99%

Sensitization of Capsaicin and Icilin Responses in Oxaliplatin Treated Adult Rat DRG Neurons

2010

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BackgroundOxaliplatin chemotherapy induced neuropathy is a dose related cumulative toxicity that manifests as tingling, numbness, and chronic pain, compromising the quality of life and leading to discontinued chemotherapy. Patients report marked hypersensitivity to cold stimuli at early stages of treatment, when sensory testing reveals cold and heat hyperalgesia. This study examined the morphological and functional effects of oxaliplatin treatment in cultured adult rat DRG neurons.Results48 hour exposure to oxaliplatin resulted in dose related reduction in neurite length, density, and number of neurons compared to vehicle treated controls, using Gap43 immunostaining. Neurons treated acutely with 20 μg/ml oxaliplatin showed significantly higher signal intensity for cyclic AMP immunofluorescence (160.5 ± 13 a.u., n = 3, P < 0.05), compared to controls (120.3 ± 4 a.u.). Calcium imaging showed significantly enhanced capsaicin (TRPV1 agonist), responses after acute 20 μg/ml oxaliplatin treatment where the second of paired capsaicin responses increased from 80.7 ± 0.6% without oxaliplatin, to 171.26 ± 29% with oxaliplatin, (n = 6 paired t test, P < 0.05); this was reduced to 81.42 ± 8.1% (P < 0.05), by pretretreatment with the cannabinoid CB2 receptor agonist GW 833972. Chronic oxaliplatin treatment also resulted in dose related increases in capsaicin responses. Similarly, second responses to icilin (TRPA1/TRPM8 agonist), were enhanced after acute (143.85 ± 7%, P = 0.004, unpaired t test, n = 3), and chronic (119.7 ± 11.8%, P < 0.05, n = 3) oxaliplatin treatment, compared to control (85.3 ± 1.7%). Responses to the selective TRPM8 agonist WS-12 were not affected.ConclusionsOxaliplatin treatment induces TRP sensitization mediated by increased intracellular cAMP, which may cause neuronal damage. These effects may be mitigated by co-treatment with adenylyl cyclase inhibitors, like CB2 agonists, to alleviate the neurotoxic effects of oxaliplatin.

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Section: Introductionmentioning

confidence: 99%

Sensitization of Capsaicin and Icilin Responses in Oxaliplatin Treated Adult Rat DRG Neurons

2010

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“…These are the mainstay of the World Health Organization three-step analgesic “ladder,” first proposed in 1986, which provides some 71%–100% of patients with adequate analgesia when used appropriately. 9 Various other guidelines are in place. 20 However, up to 30% of patients do not respond to morphine, or experience excessive side effects, or both.…”

Section: Orthodox Analgesics Given To Cancer Patients: An Overviewmentioning

confidence: 99%

“…Cancer pain can result from the growing primary tumor putting pressure on nerves and bones and/or as nearby tissues are destroyed. Secondary tumors may also cause pain, as in the case of bone metastases, which occur in 90% of patients with advanced cancers of breast, prostate, or lung 9. In particular, cytokines produced by the tumor cells and/or the cells in the bone micro-environment activate osteoclasts and thus contribute to the signaling of cancer-associated pain in bones 10.…”

Section: Introductionmentioning

confidence: 99%

“…Secondary tumors may also cause pain, as in the case of bone metastases, which occur in 90% of patients with advanced cancers of breast, prostate, or lung. 9 In particular, cytokines produced by the tumor cells and/or the cells in the bone micro-environment activate osteoclasts and thus contribute to the signaling of cancer-associated pain in bones. 10 Compression of the spinal cord occurs when a tumor grows on the spine.…”

Section: Introductionmentioning

confidence: 99%

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Management of cancer pain: 1. Wider implications of orthodox analgesics

Lee

Dawson²,

Lee

et al. 2014

IJGM

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In this review, the first of two parts, we first provide an overview of the orthodox analgesics used commonly against cancer pain. Then, we examine in more detail the emerging evidence for the potential impact of analgesic use on cancer risk and disease progression. Increasing findings suggest that long-term use of nonsteroidal anti-inflammatory drugs, particularly aspirin, may reduce cancer occurrence. However, acetaminophen may raise the risk of some hematological malignancies. Drugs acting upon receptors of gamma-aminobutyric acid (GABA) and GABA “mimetics” (eg, gabapentin) appear generally safe for cancer patients, but there is some evidence of potential carcinogenicity. Some barbiturates appear to slightly raise cancer risks and can affect cancer cell behavior in vitro. For cannabis, studies suggest an increased risk of squamous cell carcinoma of the tongue, larynx, and possibly lung. Morphine may stimulate human microvascular endothelial cell proliferation and angiogenesis; it is not clear whether this might cause harm or produce benefit. The opioid, fentanyl, may promote growth in some tumor cell lines. Opium itself is an emerging risk factor for gastric adenocarcinoma and possibly cancers of the esophagus, bladder, larynx, and lung. It is concluded that analgesics currently prescribed for cancer pain can significantly affect the cancer process itself. More futuristically, several ion channels are being targeted with novel analgesics, but many of these are also involved in primary and/or secondary tumorigenesis. Further studies are needed to elucidate possible cellular and molecular effects of orthodox analgesics and their possible long-term impact, both positive and negative, and thus enable the best possible clinical gain for cancer patients.

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Pain Management in Cancer

Pino

2019

Cancer

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Mechanisms and Management of Cancer Pain

Cited by 4 publications

References 107 publications

Sensitization of Capsaicin and Icilin Responses in Oxaliplatin Treated Adult Rat DRG Neurons

Sensitization of Capsaicin and Icilin Responses in Oxaliplatin Treated Adult Rat DRG Neurons

Management of cancer pain: 1. Wider implications of orthodox analgesics

Pain Management in Cancer

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