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Pinpointing Proteins May Lead to New Mesothelioma Therapies

Mesothelioma Survivor

An international team including researchers in New York, Hawaii and Italy have pinpointed a protein known as HMGB1 as a key player in the development of malignant mesothelioma, a cancer associated with asbestos exposure.

The new study in the journal Cancer Research describes the role that HMGB1 plays in the growth of malignant mesothelioma. It also suggests the possibility of a novel therapeutic approach for mesothelioma patients.

Malignant mesothelioma is an aggressive and highly lethal cancer. Approximately 2,500 to 3,000 people in the U.S. are diagnosed with mesothelioma each year, and a similar number die of the disease. Most people diagnosed with mesothelioma are older workers, retirees and veterans who inhaled asbestos fibers in a workplace for an extended period of months or years. The microscopic fibers lodge deep in the lungs causing tissue inflammation. The disease develops slowly over decades.

In a previous 2010 study, a research team composed of many of the same medical scientists found that patients exposed to asbestos have higher levels of HMGB1 in their blood. HMBG1 protein is released when cells are damaged or when tissue is injured. The protein causes an inflammatory reaction.

In the latest study, the researchers said the presence of the protein influences the growth and survival of mesothelioma cells. When the researchers inhibited the HMGB1 using anti-bodies in laboratory mice, it reduced the growth of mesothelioma cells in the mice and extended their survival. Inhibiting HMGB1 interferes with the inflammation process.

The team of investigators including Haining Yang and Michele Carbone of the University of Hawaii Cancer Center and Harvey Pass of the New York University School of Medicine said their findings show that mesothelioma cancer cells rely on HMGB1. The research suggests that suppression of the protein HMGB1 using antibodies offers therapeutic promise as a new treatment for mesothelioma.

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Last Modified: March 4, 2019

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