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'Reprogrammed' treatment-resistant lymphomas respond to cancer drugs
Date:8/16/2013

rogramed to a more benign disease," said Cerchietti. "We think this work has the potential to change the standard of care for patients with aggressive lymphomas."

The researchers conducted the clinical trial based on the results of their extensive preclinical experiments to determine the mechanisms by which lymphomas evade chemotherapy drugs. They found that compared with normal cells, all DLBCLs possess a high degree of aberrant DNA methylation, a process which "silences" certain genes, causing resistance to treatment.

Using DLBCL cells and mice bearing human lymphoma xenografts, the researchers showed that DNA methyltransferase inhibitors are most effective if administered prior to chemotherapy, but not concurrently. They also found the gene SMAD1 to be silenced in the unresponsive tumors.

When the researchers looked for SMAD1 status in the biopsy specimens collected from patients enrolled in the phase I trial, they found that after treatment with azacitidine, there was a decrease in SMAD1 methylation and increase in SMAD1 protein, providing proof of principle.

Cerchietti and colleagues are currently conducting clinical trials with patients with lymphomas whose tumors failed to respond to standard therapies. They are in the process of conducting larger, multicenter trials to extend this treatment to other cancers as well.


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Contact: Jeremy Moore
jeremy.moore@aacr.org
215-446-7109
American Association for Cancer Research
Source:Eurekalert

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