Anti-hyperalgesic activity of the cox-2 inhibitor lumiracoxib in a model of bone cancer pain in the rat

Fox, Alyson; Medhurst, Stephen J.; Courade, Jean-Philippe; Glatt, Markus; Dawson, Janet; Urbán, László; Bevan, Stuart; González, Isabel Martín

doi:10.1016/j.pain.2003.09.003

Cited by 45 publications

(22 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results have suggested that chronic administration of a COX-2 inhibitor can block prostaglandin synthesis at multiple sites, and may have significant clinical utility in the management of bone cancer and bone cancer pain. A similar reduction in bone cancer pain was observed in mice treated with another COX-2 inhibitor, lumiracoxib (Fox et al, 2004). The same was true for pain control in patients with osteoid osteoma treated with rofecoxib, a selective COX-2 inhibitor (Bottner et al, 2001).…”

Section: Discussionsupporting

confidence: 56%

Microsomal prostaglandin E synthase-1 enhances bone cancer growth and bone cancer-related pain behaviors in mice

et al. 2011

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 56%

Microsomal prostaglandin E synthase-1 enhances bone cancer growth and bone cancer-related pain behaviors in mice

et al. 2011

View full text Add to dashboard Cite

“…In many of these conditions, there are good animal models that have been used to test potential treatments of central sensitization and allodynia. COX inhibitors [52][53][54], N-methyl-D-aspartate antagonists [55][56][57], antiepileptics [58][59][60], antidepressants [61][62][63], drugs that block nitric oxide production [64], and cannabinoids [65][66][67] show potential in these animal models, but fall short in the clinic. Many of these same classes of drugs are commonly used as preventives in the treatment of migraine.…”

Section: Discussionmentioning

confidence: 99%

Insights from experimental studies into allodynia and its treatment

Oshinsky

2006

Current Science Inc

View full text Add to dashboard Cite

Migraine is a common disorder that often is accompanied by cutaneous allodynia. Cutaneous allodynia on the head has been linked to sensitization of neurons in the trigeminal nucleus caudalis in animal models of migraine. In addition, migraine with allodynia is refractory to acute treatment with triptans. Understanding the mechanisms of allodynia, preventing its development, and finding effective treatments have become a priority in headache research. This paper reviews recent research on the pathogenesis of headache and the generation of allodynia. We discuss the regions of the nervous system that are involved in generating and maintaining headache pain and allodynia. We also discuss recent advances in the treatment of migraine based on translation research.

show abstract

“…Previous experimental models studying painful breast cancer tumors have been limited to rat mammary cancer (MRMT-1; refs. 29,30). Development of a murine breast cancer model of bone pain is significant as unique reagents and investigative opportunities using genetically engineered mice are now feasible.…”

Section: Discussionmentioning

confidence: 99%

Novel Cytosine Deaminase Fusion Gene Enhances the Effect of Radiation on Breast Cancer in Bone by Reducing Tumor Burden, Osteolysis, and Skeletal Fracture

Goblirsch

Zwolak

Ramnaraine

et al. 2006

Clinical Cancer Research

View full text Add to dashboard Cite

Background: Painful breast carcinoma metastases in bone are a common manifestation of malignant disease. Eradication of these tumors can be evasive, and as a result, skeletal morbidity increases with disease progression. Experimental Design: The treatment potential of cytosine deaminase (CD) gene therapy combined with radiation treatment was evaluated in vitro and in vivo using a 4T1 murine breast carcinoma model. 4T1 carcinoma cells were transduced with a fusion gene encoding the extracellular and transmembrane domains of the human nerve growth factor receptor and the cytoplasmic portion of the yeast CD gene (NGFR-CD y ). Results and Conclusions: CD-expressing tumor cells (4TCD y ) were highly sensitive to treatment by 5-fluorocytosine prodrug (P < 0.0001). 5-Fluorocytosine treatment of 4TCD y , but not 4T1 cells, enhanced the effects of radiation in vitro (P < 0.0001). 5-Fluorocytosine prodrug treatment also increased the therapeutic potential of radiation in vivo. Mice with 4TCD y intrafemoral tumors showed increased effectiveness of radiation based on improved reductions in tumor size, reductions in tumorigenic osteolysis, and a decrease in skeletal fractures (P < 0.01).Enzyme/prodrug gene therapy involves expression of a nonmammalian enzyme that converts a nontoxic prodrug to a cytotoxic agent at sites of tumor. The cytosine deaminase (CD)/5-fluorocytosine (5-FC) enzyme/prodrug system converts 5-FC to the highly cytotoxic compound 5-fluorouracil (5-FU) and is a promising therapeutic approach for the treatment of tumors because of its potential for sensitizing tumor cells to radiation treatment. Deamination of 5-FC by CD-expressing tumor cells produces 5-FU. Intracellular 5-FU is then converted to the active metabolites 5-fluoro-2-dUMP (FdUMP) or 5-fluoro-2-dUTP. 5-FU can passively diffuse across the cell membrane and enter adjacent cells where intracellular conversion of 5-FU to FdUMP is done by thymidine kinase. FdUMP inhibits cellular DNA synthesis by binding to and inhibiting thymidylate synthase (1, 2). Although 5-FU has both DNA-directed and RNA-directed effects, its radiationenhancing effects result from DNA-directed mechanisms (3). These include lethal influences on radioresistant S-phase cells and reduction in DNA repair after radiation-induced DNA injury (1).Because 5-FU has been shown to enhance the effect of radiation on tumor cells, the CD/5-FC enzyme/prodrug system is attractive as an adjuvant for treating tumors that will receive radiation treatment (4). The CD/5-FC enzyme/prodrug system has been used in conjunction with radiation treatment in experimental animal models and clinical trials for treating softtissue cancers. Soft-tissue cancers studied with this concomitant therapy include colon, nasopharyngeal, prostate, esophageal, and breast cancers, malignant gliomas and sarcomas, and epidermoid carcinoma (4 -10). Treatment of soft-tissue cancers in experimental models has involved delivery of the CD gene via tumor cell transduction or delivery of adenovirus containing the CD gene fo...

show abstract

Anti-hyperalgesic activity of the cox-2 inhibitor lumiracoxib in a model of bone cancer pain in the rat

Cited by 45 publications

References 37 publications

Microsomal prostaglandin E synthase-1 enhances bone cancer growth and bone cancer-related pain behaviors in mice

Microsomal prostaglandin E synthase-1 enhances bone cancer growth and bone cancer-related pain behaviors in mice

Insights from experimental studies into allodynia and its treatment

Novel Cytosine Deaminase Fusion Gene Enhances the Effect of Radiation on Breast Cancer in Bone by Reducing Tumor Burden, Osteolysis, and Skeletal Fracture

Contact Info

Product

Resources

About