FGF17 is an autocrine prostatic epithelial growth factor and is upregulated in benign prostatic hyperplasia.

Background: Fibroblast growth factors (FGFs) are known to play an important role in the growth of prostatic epithelial cells. Benign prostatic hyperplasia (BPH) is characterized by increased epithelial and stromal proliferation within the transition zone of the prostate. FGF2, FGF7, and FGF9 are expressed in BPH tissue but expression of FGF17 has not been previously characterized in human prostate tissue.

Fibroblast growth factor 2 promotes tumor progression in an autochthonous mouse model of prostate cancer.

Fibroblast growth factor (FGF) 2 (or basic FGF) is expressed at increased levels in human prostate cancer. FGF2 can promote cell motility and proliferation, increase tumor angiogenesis, and inhibit apoptosis, all of which play an important role in tumor progression. To determine whether FGF2 plays a critical role in prostate cancer progression, we have used the transgenic adenocarcinoma of the mouse prostate (TRAMP) model system.

FGF-10 is expressed at low levels in the human prostate.

Background: Fibroblast growth factors (FGFs) are known to play an important role in the growth of normal prostatic epithelial cells. FGF-10 is a secreted growth factor that binds to FGF receptor-2 IIIb, which is expressed in prostatic epithelial cells and thus can potentially act as a growth factor for these cells. Prior work has indicated that FGF10 may play an important role in the development of the rat prostate, but its role in the adult human prostate is unclear.

Absence of PTEN/MMAC1 pseudogene in mice.

The PTEN gene encodes a phosphatase that acts as a tumor-suppressor gene and is mutated in a variety of human cancers. Alterations of the PTEN gene in these tumor samples were identified using exon-by-exon analysis of the gene using single-stranded conformational polymorphism or direct sequencing of PTEN cDNA. However, in humans, mutational analysis of a PTEN cDNA template can produce false results because of a highly conserved PTEN processed pseudogene that shares more than 98% homology with the coding region of functional PTEN.

FGF7 and FGF2 are increased in benign prostatic hyperplasia and are associated with increased proliferation.

Purpose: To determine if overexpression of FGF7 and FGF2 occurs in benign prostatic hyperplasia (BPH) and if so, whether such overexpression is correlated with increased proliferation of epithelial and/or stromal cells.

Materials And Methods: The FGF7 and FGF2 content of protein extracts of normal peripheral zone, normal transition zone and hyperplastic prostatic tissues were determined by enzyme-linked immunoabsorption assay. Proliferation of epithelial and stromal cells was assessed by immunohistochemistry with anti-Ki67 antibodies on frozen sections of the same tissues used for protein extraction.

FGF9 is an autocrine and paracrine prostatic growth factor expressed by prostatic stromal cells.

Polypeptide growth factors, including members of the fibroblast growth factor (FGF) family, play an important role in the growth and maintenance of the normal prostate. We have found that FGF9 is expressed at high levels in the normal peripheral and transition zone of the human prostate. Analysis of FGF9 production by primary cultures of prostatic epithelial and stromal cells has shown that FGF9 is produced and secreted by the prostatic stromal cells.

Alterations in expression of basic fibroblast growth factor (FGF) 2 and its receptor FGFR-1 in human prostate cancer.

Fibroblast growth factors (FGFs) play an important role in the growth and maintenance of the normal prostate. There is increasing evidence from both animal models and analysis of human prostate cancer cell lines that alterations of FGFs and/or FGF receptors (FGFRs) may play an important role in prostate cancer progression. To better define the role of FGF2 and FGF7 in human prostate cancer in vivo, we have quantified these two growth factors in clinically localized human prostate cancers and uninvolved prostate by ELISA and Western blotting and determined their localization by immunohistochemistry.