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Cellular molecule spurs growth of prostate cancer
November 29, 2005CHAPEL HILL - University of North Carolina at Chapel Hill scientists have identified a molecule that stimulates the aggressive growth of prostate cancer. The molecule, Ack1, a member of the growth-promoting tyrosine kinase gene family, stimulates tumor formation in part by signaling prostate cells to rid themselves of a tumor-suppressor protein. Normally, this suppressor protein would inhibit rapid cell growth by signaling the cell to destroy itself.
A report on the study, which appeared Nov. 15 in the journal Cancer Research, also points to Ack1 as a potential target for developing novel drugs against prostate cancer.
The study's senior author, Dr. Shelton Earp, directs the UNC Lineberger Comprehensive Cancer Center and is Lineberger professor of cancer research and a professor of pharmacology and medicine.
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.
In earlier work, Earp's UNC laboratory was the first to clone a cell surface tyrosine kinase, Mer.
"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, the team discovered that Mer activated Ack1. This finding led to the current study.
"Because we found Ack1 is more active in advanced prostate tumors, and its inhibition blocks experimental tumor growth, we believe Ack1 should be a target for novel drug development."
University of North Carolina School of Medicine
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.
In earlier work, Earp's UNC laboratory was the first to clone a cell surface tyrosine kinase, Mer.
"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, the team discovered that Mer activated Ack1. This finding led to the current study.
"Because we found Ack1 is more active in advanced prostate tumors, and its inhibition blocks experimental tumor growth, we believe Ack1 should be a target for novel drug development."
University of North Carolina School of Medicine
Prostate Cancer News and Current Prostate Cancer Events RSSToo much calcium in blood may increase risk of fatal prostate cancer
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Height linked to risk of prostate cancer development and progression
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Health risk behaviors associated with lower prostate specific antigen awareness
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Study shows PDE5 inhibitor more effective when used on demand in erectile dysfunction
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Satisfaction and regret after radical prostatectomy procedures studied
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State's first single incision robotic kidney removal
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Anti-tumor effects are enhanced by inhibiting 2 pathways rather than 1
Two independent research groups have found that simultaneous inhibition of two signaling pathways resulted in substantially enhanced antitumor effects in mouse models of prostate and breast cancer. In an accompany commentary, Steven Grant, at Virginia Commonwealth University Health Science Center, Richmond, discusses the clinical importance of these studies and highlights some of the questions that still need to be answered.
Why a common treatment for prostate cancer ultimately fails
Some of the drugs given to many men during their fight against prostate cancer can actually spur some cancer cells to grow, researchers have found. The findings were published online this week in a pair of papers in the Proceedings of the National Academy of Sciences.
PSA screening may be biased against obese men, leading to more aggressive cancers
Testing men for elevated levels of prostate-specific antigen (PSA) in the blood -- the gold standard screening test for prostate cancer -- may be biased against obese men, whose PSA levels tend to be deceptively low.
Study finds more PSA screening awareness needed among high-risk groups
In one of the first examinations of PSA screening in younger men, a study published by researchers at Duke Medicine's Prostate Center finds that one-fifth of men under age 50 reported undergoing a prostate specific antigen (PSA) test to detect prostate cancer in the previous year, yet only one in three young black men reported ever having a PSA test in the previous year.
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