Oct. 10, 2007 | It often takes years for scientific findings to advance from the lab to the patient’s bedside, often because of the need for independent verification of those findings.
Now the simultaneous work of two groups of myeloma researchers, including some from the University of Arkansas for Medical Sciences (UAMS), may speed up the process for a promising new path for potential treatments.
Studies by two independent research groups – one led by National Cancer Institute (NCI) researcher Louis Staudt, M.D., Ph.D., and John D. Shaughnessy, Jr., Ph.D., and one led by Rafeal Fonseca and Leif Bergsagel, M.D., of the Mayo Clinic in Scottsdale, Ariz. – were published in the Sept. 19 issue of the journal Cancer Cell . Those studies both pointed to changes, or mutations, in multiple myeloma cells that may offer a new path for neutralizing malignant cells.
Shaughnessy and colleagues in UAMS’ Myeloma Institute for Research and Therapy, working with the Staudt group, identified an 11-gene expression signature for activating the so-called NF-kappaB pathway. They concluded that 82 percent of patients have the activated pathway. The Bergsagel group suggested the pathway can be used to select patients for certain types of drug treatments, said the article “Gene Mutation Revelation Points to New Target for Myeloma Treatment, Studies Say.”
What Shaughnessy also sees in the two groups pursuing the secrets of the pathway is the potential to get new treatments to patients more quickly.
“Scientific findings require independent validation and in this case two research teams made identical findings on separate patient groups. These coincident findings could ultimately benefit myeloma patients by speeding development of new therapies that target this particular pathway,” Shaughnessy said.
In the Cancer Cell article, Shaughnessy noted some of the diverging techniques of the two groups but said the independent groups working the same biological pathway offer a method for validation. The Cancer Cell article also said the implications of the NF-kappaB pathway go beyond myeloma to other tumor types.
Shaughnessy said testing in mouse models of myeloma is planned for new drugs that inhibit activation of the NF-kappaB pathway.
Shaughnessy’s recent work also includes development of a genetic analysis model for identifying patients with aggressive multiple myeloma. MIRT researchers identified 17 genes whose altered expression could distinguish patients with a high-risk or low-risk form of the disease