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Contact: Angela Colmone, Ph.D.
acolmone@asip.org
301-634-7953
American Journal of Pathology

Morphine blocks tumor growth

Minneapolis, MN Current research suggests that taking morphine can block new blood vessel and tumor growth. The related report by Koodie et al, "Morphine suppresses tumor angiogenesis through a HIF1α/p38MAPK pathway," appears in the August 2010 issue of the American Journal of Pathology.

Morphine is currently the gold standard of analgesics used to relieve severe pain and suffering. Angiogenesis, or new blood vessel growth, is critical for tumor progression from dormant to malignant. Morphine is commonly used to treat cancer pain, but the effects of morphine use on new blood vessel and tumor growth remain controversial.

Using a clinically relevant morphine dose in a mouse model of Lewis lung carcinoma, researchers led by Dr. Sabita Roy of the University of Minnesota Medical School in Minneapolis, MN examined the effect of morphine use on new blood vessel growth in tumors. They found that chronic morphine use decreased levels of tumor angiogenesis in a manner dependent on the opioid receptor. This effect was mediated by suppression of signaling induced by low oxygen concentrations, leading to a reduction in the levels of pro-angiogenic factors. Therefore, morphine may not only serve as an analgesic for cancer patients, but may also inhibit tumor angiogenesis and growth.

Koodie et al conclude that "morphine is a potential inhibitor of tumor growth, through the suppression of tumor cell-induced angiogenesis and hypoxia-induced p38 MAPK activation of HIF-1. In addition to its analgesic potential, morphine can be exploited for its anti-angiogenic potential in cancer pain management; these findings support the use of morphine for cancer pain management."

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This work was supported by the National Institutes of Health (NIDA/NIH, F31-DA021005-01 to LK; CA114340 to SR; and NIDA/NIH grants RO1 DA 12104; RO1 DA 022935; KO2 DA 015349; P50 DA 011806 to SR).

Koodie L, Ramakrishnan S, Roy S: Morphine suppresses tumor angiogenesis through a HIF1α/p38MAPK pathway. Am J Pathol 2010, 177: 984-997

For more information on Dr Sabita Roy, please contact her at the University of Minnesota Medical School, Department of Surgery, MMC 195, 420 Delaware Street, SE, Minneapolis, MN 55455. E-mail: royxx002@umn.edu.

For press copies of the articles, please contact Dr. Angela Colmone at 301-634-7953 or acolmone@asip.org.

The American Journal of Pathology, official journal of the American Society for Investigative Pathology, seeks to publish high-quality, original papers on the cellular and molecular biology of disease. The editors accept manuscripts that advance basic and translational knowledge of the pathogenesis, classification, diagnosis, and mechanisms of disease, without preference for a specific analytic method. High priority is given to studies on human disease and relevant experimental models using cellular, molecular, animal, biological, chemical, and immunological approaches in conjunction with morphology.



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