Antibody identified to boost cancer therapy

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A new monoclonal antibody that can target proteins inside cancer cells has been developed by researchers and tested in the laboratory and in mice.

Monoclonal antibodies are naturally occurring human antibodies that are genetically altered in a laboratory, cloned in large numbers and introduced into the patient to target disease sites.

In the new study, a monoclonal antibody, called ESK1, targets a protein associated with many types of cancer.

The targeted protein, called WT1, is over-produced in a range of leukemias and other cancers, including myeloma and breast, ovarian and colorectal cancers. WT1 is an oncogenic protein, which means it supports the formation of cancer.

Because WT1 is found in few healthy cells, patients are less likely to suffer side effects from drugs that would potentially target the protein, the researchers said.

How the study was done

"This is a new approach for attacking WT1, an important cancer target, with an antibody therapy," Dr David Scheinberg, an inventor of the antibody, said in a news release from the Memorial Sloan-Kettering Cancer Center in New York City. "This is something that was previously not possible."

"There has not been a way to make small molecule drugs that can inhibit WT1 function," said Scheinberg, who is chairman of the molecular pharmacology and chemistry program at the center. "Our research shows that you can use a monoclonal antibody to recognize a cancer-associated protein inside a cell, and it will destroy the cell."

Although studies involving animals can be useful, they frequently fail to produce similar results in humans.

In laboratory research, the antibody showed promise as a treatment for leukemia, the researchers said. Their findings appear in the March 13 issue of the journal Science Translational Medicine.

The Sloan-Kettering researchers created the new antibody in collaboration with Eureka Therapeutics.

More information

The American Academy of Family Physicians outlines current cancer treatments.

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