New Protein Linked to the Spread of PCa to the Bones.

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New Protein Linked to the Spread of Prostate Cancer to the Bones.

GEN News Highlights
Jul 11 2008

A protein called FGF9 plays an important role in the metastasis of prostate cancer to the bones, according to researchers at The University of Texas M. D. Anderson Cancer Center.

The team used two prostate cancer cell lines derived from the bones of an individual with osteoblastic bone metastases. Both cell lines lacked expression of androgen receptors to mimic tumors that have developed the ability to grow in the absence of this hormone.

These androgen receptor-negative prostate cancer cell lines grew when transplanted into immuno-compromised mice and generated osteoblastic bone metastases, the scientists report. FGF9 was expressed at higher levels in these cells lines than in other bone-derived prostate cancer cells and induced bone formation in an in vitro organ culture assay. Additionally, blocking FGF9 reduced osteoblastic bone metastases in mice transplanted with the cell lines.

The M.D. Anderson group also found that FGF9 was expressed in 24 of 56 primary tumors derived from human organ-confined prostate cancer and in 25 of 25 bone metastasis cases.

These results appear online on July 10 in The Journal of Clinical Investigation.

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Additional information:

Protein that underpins prostate cancer cells to cause disease in bones unveiled.

Washington, July 11 : Researchers at the University of Texas MD Anderson Cancer Center, Houston, have gained fresh insights into the mechanisms by which prostate cancer cells spread to the bones.

Researchers at the University of Texas MD Anderson Cancer Center, Houston, have gained fresh insights into the mechanisms by which prostate cancer cells spread to the bones.

The researchers point out that death mainly occurs as a result of the tumour spreading to the bones, where it is known as an osteoblastic bone metastasis.

According to them, treatments that deprive the tumor of male sex hormones (androgens) are usually effective, but only briefly as the tumors typically develop the ability to grow in the absence of androgens and the diseases progresses.

Now, Nora Navone and colleagues from the university have generated new data using two prostate cancer cell lines that lack expression of androgen receptors, and that were derived from the bones of an individual with osteoblastic bone metastases.

The data sheds light into the mechanisms by which prostate cancer osteoblastic bone metastases progress.

The androgen receptor, negative prostate cancer cell lines generated by the researchers grew when transplanted into immuno-compromised mice and generated osteoblastic bone metastases.

The researchers found a protein known as FGF9 that expressed at higher levels in these cells lines than in other bone-derived prostate cancer cells, and induced bone formation in an in vitro organ culture assay.

They also observed that blocking FGF9 reduced the osteoblastic bone metastases in mice transplanted with the cell lines.

Given that FGF9 was found to be expressed in all human prostate cancer osteoblastic bone metastases analysed during the study, the researchers believe that FGF9 plays a significant role in prostate cancer progression to osteoblastic bone metastases.

The cells lines generated are also likely to be an important preclinical model for researchers developing therapeutics for osteoblastic bone metastases in individuals with prostate cancer.

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Up-to-date information released.
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