( Researchers from University of North Ca...)Gene responsible for developing prostate cancer identified,Health

Researchers from University of North Carolina have identified a molecule Ack1, which is responsible for suppressing the activity of Tumor// suppressor protein. Tumor suppressor protein is responsible for maintaining the integrity of cell and prevents the cell from developing tumor by maintaining a control growth of cell. Ack1 is found to be a growth promoting tyrosine kinase gene family. The results of the study has been published in the Journal Cancer research.

Tests of Ack1 demonstrate a profound effect on tumor growth in experimental systems, Earp said. 'It's a remarkable effect. Tumors grew more rapidly and invaded as if they were converted to advanced prostate cancer.'

Another major finding of the study involved an experimental drug developed by the National Cancer Institute, called geldanamycin. In laboratory tests, the UNC Lineberger group found Ack1 activity could be inhibited through interference with its molecular interactions, thus offering a target for treatment. First, the group discovered that Ack1 bound to a protein called Hsp90 (heat shock protein 90), which associated with many oncogenic, or cancer-causing, signaling proteins.

'If you add geldanamycin to the prostate cancer cell, the drug knocks Hsp90 off oncogenic signaling molecules. This dramatically decreases Ack1 activity and slows tumor formation,' Earp said.

In addition, the team compared Ack1 activation in advanced prostate cancer tissue from patients with that found in benign prostatic hypertrophy, or non-cancerous prostate enlargement. The team showed the levels of the activated Ack1 to be much higher in the advanced tumors.

'We saw that Mer was expressed at reasonably high levels in prostate cancer cells. And so Dr. Nupam Mahajan, the study's first author, decided to look at whether Mer had an effect on prostate cancer growth signaling,' Earp said. In experiments, which used the university's Michael Hooker Proteomics Core Facility,
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