From Our 2012 Archives

Researchers Spot Potential Bile Duct Cancer Drug Targets

THURSDAY, Jan. 26 (HealthDay News) -- Researchers who identified a new genetic signature associated with bile duct cancer say their discovery could lead to targeted treatment for the deadly cancer.

The team at the Massachusetts General Hospital Cancer Center screened samples from 287 patients with gastrointestinal tumors and found that growth-enhancing mutations in two genes (IDH1 and IDH2) may account for nearly one-fourth of bile duct tumors that develop in the liver.

Mutations in IDH1 were found in 13 percent of all bile duct tumors and in 23 percent of those within the liver itself. Mutations in IDH2 were less common.

It may be possible to develop drugs that target this mutation in order to control tumor growth, they said.

The findings were published online in The Oncologist.

Bile duct cancer occurs in a duct that carries bile from the liver to the small intestine.

"Patients with bile duct cancer have a generally poor prognosis. Most of them are diagnosed with advanced or metastatic disease, so surgical resection [removal] is not feasible," study co-senior author Dr. Andrew Zhu, director of Liver Cancer Research at the MGH Cancer Center, said in a hospital news release.

"Identifying this new and relatively common mutation in intrahepatic [within the liver] bile duct cancer may have significant implications for the diagnosis, prognosis and therapy of patients whose tumors harbor this mutation," Zhu added.

Currently, there are no drugs that target IDH mutations, but extensive efforts are underway to develop such drugs, the researchers say.

Each year in the United States, 12,000 people are diagnosed with cancers of the gallbladder and bile duct, but only 10 percent of those cancers are discovered early enough for successful surgical treatment. Average survival, even with chemotherapy, is less than a year.

-- Robert Preidt

MedicalNewsCopyright © 2012 HealthDay. All rights reserved.

SOURCE: Massachusetts General Hospital, news release, Jan. 18, 2012





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