Peer-reviewed veterinary case report
Meloxicam drug slows growth of dog bone cancer cells
By Wolfesberger, Birgitt et al.·Published in Research in veterinary science·2006·Clinic of Internal Medicine and Infectious Diseases·View original on PubMed →
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Original publication title: Antineoplastic effect of the cyclooxygenase inhibitor meloxicam on canine osteosarcoma cells.
- Species:
- dog
Plain-English summary
A study looked at how meloxicam, a common anti-inflammatory medication, affects osteosarcoma cells in dogs. Researchers found that meloxicam can slow down the growth of these cancer cells and even cause them to die off through a process called apoptosis (programmed cell death). While the results are promising, more research is needed to see how effective meloxicam could be as a treatment for dogs with osteosarcoma.
People also search for: dog osteosarcoma treatment · meloxicam for dog cancer · canine cancer medications
Abstract
A decisive role in cancer development has been attributed to cyclooxygenase-2 (COX-2) activity, but the significance of COX-2 inhibitors in cancer treatment still needs to be thoroughly investigated. We studied the influence of meloxicam, a non-steroidal antiinflammatory drug with preferential inhibitory effects on COX-2 compared to COX-1, on canine osteosarcoma (D-17) cells. We demonstrated that D-17 cells expressed mRNA and COX-2 protein. Treatment with meloxicam induced a time- and dose-dependent inhibition of cellular growth. To determine if apoptosis plays a role in meloxicam-induced cell death, we performed agarose gel electrophoresis and found a DNA-ladder pattern, typically seen in apoptosis, as well as early apoptotic changes by Annexin V tests. Furthermore, electron microscopy revealed ultrastructural alterations typical of apoptosis. Quantification of apoptotic cells by immunohistochemical staining of caspase 3 confirmed the results. However, further studies with meloxicam are necessary to assess its potential use for treatment of osteosarcomas in dogs.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/16182328/