Perhaps the key to fighting some cancers is to reactivate a process that normally prevents cell proliferation. Now in the case of large B-cell lymphoma, scientists have found such a mechanism.
They reactivated a gene that controls the normal aging program in tumor cells so they can no longer divide. The researchers believe the discovery may lead to new drug targets for treating the cancer.
In a report about their work published online this week in Nature Communications, the researchers describe how they found a new tumor-suppressive role for a protein called Smurf2 that is known to enforce cell aging (senescence) in a subset of diffuse large B-cell lymphoma (DLBCL).
Senior author Hong Zhang, assistant professor of cell and developmental biology at University of Massachusetts (UMass) Medical School, says:
"It's possible that restoration of Smurf2 expression may provide therapeutic benefits for patients and help encourage remission in difficult to treat cases."
He explains that normally this pathway regulates cell aging and stops B cells dividing and multiplying.
But humans with DLBCL show low expression of Smurf2, and such low activity of the protein affects a pathway that promotes unchecked cell division and tumor growth.
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