Daily Cannabis Use Can Drive HPV-Related Tumor Growth, Study Finds
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Marijuana use may be a driving factor in the rise of head and neck cancer cases, according to a new study.
Published in Clinical Cancer Research, the research found that tetrahydrocannabinol (THC) can activate a molecular mechanism in the body that accelerates tumor growth in patients with human papillomavirus (HPV)-positive skin cancers.
The big (TH)C
To find their results, the research group from the University of California San Diego School of Medicine investigated how THC in the bloodstream affected the p38 MAPK pathway, a molecular mechanism that controls programmed cell death.
After injecting cannabinoids into animal cells, human cells, and mice, the researchers found that THC does activate p38 MAPK, which then inhibits cell death and allows any tumors to progress.
The team then checked the blood plasma levels of 32 people with head and neck squamous cell carcinoma (HNSCC). And like the cell lines, the blood samples showed p38 MAPK activation and loss of cell death in tumors from patients with THC in their blood.
“We now have convincing scientific evidence that daily marijuana use can drive tumor growth in HPV-related head and neck cancer,” Joseph A Califano III, the paper’s senior author, said in a statement.
HNSCC is the sixth most common cancer in the world, and approximately 30 percent of those living with the condition display an HPV infection. Coupled with lagging HPV vaccination rates, Califano and his colleagues are concerned that rising rates of cannabis use could boost the disease’s prevalence.
“HPV-related head and neck cancer is one of the fastest growing cancers in the United States,” he wrote in a press statement. “While at the same time, exposure to marijuana is accelerating. This is a huge public health problem.”
Cannabis and cancer
Previous studies have suggested that HPV status may be a modifier to any cannabis- HNSCC association. In a 2008 paper, researchers found an increased risk of head and neck cancer for cannabis-consuming HPV-16–positive patients, but found no association between the drug and the disease for HPV-16–negative patients.
Lung cancers, on the other hand, appear to have a null association with cannabis use, despite the presence of carcinogens in cannabis smoke. A popular explanation for this net inertia is that the tumor-suppressant effects of THC and other cannabinoids actually counteract any carcinogenic activity.
However, in the case of head and neck cancer in HPV-positive patients, these anti-tumor properties don’t appear to be having a benefit.
“Marijuana and other cannabis products are often considered benign,” Califano continued, “but it is important to note that all drugs that have benefits can also have drawbacks. This is a cautionary tale.”
Califano and his colleagues now suggest that THC’s cancer-fighting properties need additional critical evaluation.
“Past studies showing anticancer effects of THC and other cannabinoids often used levels of THC higher than those found with recreational use, but doses used recreationally clearly activate a cancer-causing pathway,” he added.
Speaking to Analytical Cannabis in September last year, cannabis-cancer researcher Dr David Meiri explained the importance of dosage when discussing cannabinoids’ anti-tumor properties. “When you have defect in [a] pathway, which sometimes happens in cancer, the cannabis can change things that will lead the cells to die,” he said.
“[But] the dosing is [also] very, very important,” he added. “You want to find the ratio that will kill the cancer, but not the normal cells. It's a matter of ratio and the amounts, and what caused the cancer, and why it's different from the normal.”
In their follow-up research, Califano and his team plan to test whether another famous cannabinoid, cannabidiol (CBD), affects cell growth in the same way as THC.