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NIDA News Release Contact: Beverly Jackson
Michelle Muth
FOR RELEASE, June 20, 2000



A team of researchers at UCLA's Jonsson Comprehensive Cancer Center found in experiments in mice that THC limits immune response by increasing the availability of two forms (IL-10 and TGF-ß) of cytokine, a potent, tumor-specific, immunity suppresser.

The authors also suggest that smoking marijuana may be more of a cancer risk than smoking tobacco. The tar portion of marijuana smoke, compared to that of tobacco, contains higher concentrations of carcinogenic hydrocarbons, including benzapyrene, a key factor in promoting human lung cancer. And marijuana smoke deposits four times as much tar in the respiratory tract as does a comparable amount of tobacco, thus increasing exposure to carcinogens.

Dr. Steven M. Dubinett, head of the research team that conducted the study, says, "What we already know about marijuana smoke, coupled with our new finding that THC may encourage tumor growth, suggests that regular use of marijuana may increase the risk of respiratory tract cancer and further studies will be needed to evaluate this possibility."

The UCLA researchers examined the effects of THC on the immune response to lung cancer in mice. Over a two-week period, the animals were injected four times per week with either THC or a saline solution. Fourteen days after the injections were started, murine Lewis lung cancer and line 1 alveolar cell cancer cells were implanted in the mice. The mice continued to receive THC or saline injections after the tumor cells were implanted, and tumor growth was assessed three times each week. To test the hypothesis that THC impairs tumor-specific immune system response, a group of mice with compromised immune systems was also studied.

The researchers found that in the mice with normal immune systems there was significant enhancement of tumor growth, but THC had no effect on tumor growth in the immunodeficient mice. The study also showed that when lymphocytes from the THC-treated mice were injected into untreated mice, the immune deficit was transferred and tumor growth was accelerated in the normal controls.

Additionally, the UCLA research team demonstrated that when anti-IL-10 and anti-TGF-ß were administered, there was no acceleration of tumor growth in THC-treated mice. These results suggest that enhanced tumor growth is prompted by THC's ability to stimulate production of IL-10 and TGF-ß, which inhibits anti-tumor immune response.


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