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Protein Markers for Identification of Brain Tumor

by Medindia Content Team on Oct 31 2005 7:21 PM

Professor Waldemar Debinski and his team from Wake Forest University Baptist Medical Center have found a new treatment for the brain tumor – glioblastoma multiforme. The scientists have found that the inactive form of EphA2 protein in the brain cells were responsible for spread of cancer cells and the work was published in the Journal Molecular Cancer Research. Glioblastoma multiforme is the most common form of brain tumor and the least curable of all human cancers.

The Protein – EphA2:

Debinski has found a protein EphA2 in large amount in brain tumor patients compared to normal people, but they found that the protein in large amount was in an inactive form. EphA2 protein, which is found in cell membranes, allows normal cells to communicate with their environment and each other. In its normal active state, the protein seems to inhibit abnormal cell growth and division. Debinski found that the inactive form of EphA2 aids in the survival and spread of cancer cells.

Professor tested the treatment hypothesis by treating glioblastoma cells with ephrinA1, a naturally occurring molecule that binds to EphA2 and activates it. They had already demonstrated that ephrinA1 is present at much lower levels in cells and tumors with increased levels of inactive EphA2. The researchers found that cells treated with ephrinA1 slowed down their growth and were less likely to exhibit invasive properties. By changing the levels of EphA2 and ephrinA1 offers new promise for successfully treating glioblastoma multiforme.

Professor Debinski said, “We’ve found that a particular protein may play a major role in the progression of these tumors, suggesting an attractive new treatment approach and the EphA2 represents a novel target for the development of molecular therapeutics for the imaging and treatment of patients with glioblastoma,” Professor added that , “New therapies are clearly needed because, despite the standard treatment of surgically removing the tumor and treating the patient with chemotherapy and radiation, survival has increased only slightly over the past 30 years.”

Earlier Work of Debinski: Interleukin 13 –

Debinski had earlier found that cancer cells had a specific receptor for Interleukin 13 (IL-13), which is a naturally occurring protein that regulates the immune system in the body. Normal cells do not have these same receptors. Debinski developed a drug that combines a form of IL-13 with a toxin that kills cancer cells. By targeting the therapy to these receptors, the drug finds and kills the cancer cells. Debinski has been focusing on identification of new novel molecular markers, which helps in diagnosis of cancer in an early stage.

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Source: Newswise.


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