Multiple myeloma is a cancer of plasma cells in the blood that causes tumor growths in bone marrow. More than 30,000 people are diagnosed with the cancer each year, and only about half of them will survive longer than five years, according to the National Cancer Institute.
African-Americans are three times as likely to be diagnosed and two times more likely than White Americans to die from multiple myeloma. Yet, most scientific research on the disease has been based on people of European descent, according to a study led by researchers at the Keck School of Medicine at the University of Southern California in Los Angeles.
The research found that multiple myeloma patients of European descent were six times more likely than their African peers to have mutations in the TP53 gene, a tumor suppressor that helps prevent cancer. African-Americans, on the other hand, experienced heightened mutations in a different tumor suppressor gene.
“There are clearly molecular differences between African-American and Caucasian multiple myeloma cases, and it will be critical to pursue these observations to better improve clinical management of the disease for all patients,” said John D. Carpten, senior author of the study and chair of the Department of Translational Genomics at the Keck School of Medicine.
Dr. Carpten added that “in the past decade, new treatments for the disease have spurred a remarkable improvement in survival for myeloma patients, but those benefits have disproportionately increased survival rates for Caucasian patients. We in the cancer genomics community have a responsibility to ensure that our studies represent true population diversity. The myeloma genes we identified in the African-American population may have been overlooked because of the lack of diversity in previous genomic efforts.”
The full study, “Comprehensive Molecular Profiling of 718 Multiple Myelomas Reveals Significant Differences in Mutation Frequencies Between African and European Descent Cases,” was published on the website of PLOS Genetics. It may be accessed here.
