Peripheral endothelin A receptor antagonism attenuates carcinoma‐induced pain

Schmidt, Brian L.; Pickering, Victoria; Liu, Stanley Yung‐Chuan; Quang, Phuong N.; Dolan, John C.; Connelly, Stephen; Jordan, Richard C.

doi:10.1016/j.ejpain.2006.05.007

Cited by 61 publications

(67 citation statements)

References 41 publications

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“…However, these cells do not infiltrate the carcinoma in the mouse model. [42] Therefore, CBr2 mediated antinociception in the athymic mouse model is likely mediated via release of opioids by keratinocytes.…”

Section: Discussionmentioning

confidence: 99%

“…[42] Mice were housed in a temperaturecontrolled room on a 12:12 h light cycle (0600-1800 h light), with unrestricted access to food and water; estrous cycles were not monitored. All procedures were approved by UCSF Committee on Animal Research.…”

Section: Scc Paw Modelmentioning

confidence: 99%

“…[42] Mice were placed in a plastic cage with a wire mesh floor which allowed access to the paws. Fifteen minutes were allowed for cage exploration prior to testing.…”

Section: Behavioral Testing For the Scc Paw Modelmentioning

confidence: 99%

“…To study soft tissue carcinoma pain, we produce a mouse model by injecting human oral squamous cell carcinoma (SCC) into the hindpaws which leads to mechanical hyperalgesia. [42] Oral SCC reproducibly produces mechanical hyperalgesia in mice and humans. The mouse model can be used to test for analgesics.…”

Section: Introductionmentioning

confidence: 99%

“…The mouse model can be used to test for analgesics. [6,42] We sought to determine whether peripheral cannabinoid agonists attenuate mechanical hyperalgesia in a carcinoma mouse model.…”

Section: Introductionmentioning

confidence: 99%

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Peripheral cannabinoids attenuate carcinoma-induced nociception in mice

Guerrero

Quang

Dekker³

et al. 2008

Neuroscience Letters

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We investigated the cannabinoid receptor (CBr) agonists Win55,212-2 (non-selective) and AM1241 (CBr2 selective) and the peripheral receptor (CBr1) in carcinoma-induced pain using a mouse model. Tumors were induced in the hind paw of female mice by local injection of a human oral squamous cell carcinoma (SCC). Significant pain, as indicated by reduction in withdrawal thresholds in response to mechanical stimulation, began at four days after SCC inoculation and lasted to 18 days. Local administration of Win55,212-2 (10 mg/kg) and AM1241 (10 mg/kg) significantly elevated withdrawal thresholds, indicating an antinociceptive effect. Ipsilateral expression of CBr1 protein in L5 DRG was significantly upregulated compared to ipsilateral L4 DRG and in normal tissue. These findings support the suggestion that cannabinoids are capable of producing antinociception in carcinoma-induced pain.

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Section: Discussionmentioning

confidence: 99%

Section: Scc Paw Modelmentioning

confidence: 99%

“…[42] Mice were placed in a plastic cage with a wire mesh floor which allowed access to the paws. Fifteen minutes were allowed for cage exploration prior to testing.…”

Section: Behavioral Testing For the Scc Paw Modelmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…The mouse model can be used to test for analgesics. [6,42] We sought to determine whether peripheral cannabinoid agonists attenuate mechanical hyperalgesia in a carcinoma mouse model.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Peripheral cannabinoids attenuate carcinoma-induced nociception in mice

Guerrero

Quang

Dekker³

et al. 2008

Neuroscience Letters

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Mechanisms of Cancer Pain

Pacharinsak¹,

Beitz²

2013

Pain Management in Veterinary Practice

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Oral Cancer Cells Release Vesicles that Cause Pain

Dubeykovskaya

Garcia

et al. 2022

Advanced Biology

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support the current understanding that oral cancer pain is attributed to release of mediators from the cancer and micro environment. On the one hand, the media tors sensitize or activate primary afferent sensory neurons that respond to nociceptive stimuli (nociceptors) and induce sprouting of sensory and sympathetic neurons into the microenvironment. [7][8][9][10] On the other hand, neuropeptides released from sensory neurons promote cancer. [10,11] Neuropeptides induce epidermal proliferation, angiogen esis, perineural invasion, and transforma tion of stromal cells. [12][13][14][15][16] The mechanisms of reciprocal interaction between oral cancer cells and neurons, and how the interactions promote cancer and pain, are not known. There is a need to define the mechanisms by which oral cancers and neurons interact with each other and the efficacy of dis rupting this interaction to treat oral cancer and associated pain. Patients with regional/nodal metastasis (N+) oral cancer experience greater pain than patients without metastasis (N0). [5,17] Patient reported pain on the University of California San Francisco Oral Cancer Pain Questionnaire [5] has potential to identify the presence of metas tasis prior to surgery to remove the cancer. [17] Proteins encoded by genes differentially expressed in N+ cancers from patients with high levels of pain, "pain and metastasis genes," are enriched for functions in extracellular matrix organization and angiogenesis. These genes have oncogenic and neuronal func tions. This set of genes overlaps with the metasignature of the partial epithelialtomesenchymal transition (pEMT) program, also recently described as an independent predictor of lymph node metastasis in HNSCC. [18,19] Pain and metastasis genes have been identified as cargo of extracellular vesicles (EVs) in publicly available databases such as ExoCarta. [20] Depletion of EVs from cancer cell line conditioned media (CM) reversed CMinduced thermal and mechanical allodynia in a mouse model, implicating EVs in the transport of pain mediators. [17] Extracellular vesicles carry proteins, nucleic acids, and lipids and provide a means of communication between cells. [21] Cancers release elevated levels of EVs and the protein cargo of EVs is cancer type specific. [21,22] EVs released into the circulation and their cargo are potential biomarkers for cancer detection and diagnosis of cancer type. [22] Recent studies highlight EV heterogeneity. [23][24][25] Subpopulations of EVs and nano particles, collectively referred to as EVPs, differ in size and cargoes. Small EVs (sEVs) or exosomes (40-150 nm in diameter) are formed within the endosomal system as intralumenal vesicles of multi vesicular bodies (MVBs) and are released into the extracellular Oral cancer pain is attributed to the release from cancers of mediators that sensitize and activate sensory neurons. Intraplantar injection of conditioned media (CM) from human tongue cancer cell line HSC-3 or OSC-20 evokes nociceptive behavior. By contrast, CM from noncancer cell lines, DOK, ...

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Peripheral endothelin A receptor antagonism attenuates carcinoma‐induced pain

Cited by 61 publications

References 41 publications

Peripheral cannabinoids attenuate carcinoma-induced nociception in mice

Peripheral cannabinoids attenuate carcinoma-induced nociception in mice

Mechanisms of Cancer Pain

Oral Cancer Cells Release Vesicles that Cause Pain

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