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Basic fibroblast growth factor levels in cancer cells and in sera of patients suffering from proliferative disorders of the prostate
Author(s) -
Cronauer Marcus V.,
Hittmair Anton,
Eder Iris E.,
Hobisch Alfred,
Culig Zoran,
Ramoner Reinhold,
Zhang Ju,
Bartsch Georg,
Reissigl Andreas,
Radmayr Christian,
Thurnher Martin,
Klocker Helmut
Publication year - 1997
Publication title -
the prostate
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 123
eISSN - 1097-0045
pISSN - 0270-4137
DOI - 10.1002/(sici)1097-0045(19970601)31:4<223::aid-pros3>3.0.co;2-l
Subject(s) - basic fibroblast growth factor , immunohistochemistry , prostate cancer , prostate , pathology , medicine , cancer , reverse transcription polymerase chain reaction , growth factor , endocrinology , biology , messenger rna , receptor , biochemistry , gene
BACKGROUND Both benign and malignant growth of the prostate depend on the induction of a microvasculature. Basic fibroblast growth factor (bFGF), a potent angiogenic factor, is thought to play an important role in this process. METHODS bFGF expression in prostatic carcinoma was assessed by ELISA, reverse transcription polymerase chain reaction, and immunohistochemistry. RESULTS DU‐145 and PC‐3 tumor cells produced bFGF. Almost 80–90% of it was localized in the cytoplasm, and 10–20% was associated with extracellular matrix components. Immunohistochemical analysis of prostatic tissue sections showed that cancer cells stained more intensively as compared to putatively healthy epithelium. In prostate cancer patients, mean bFGF serum levels were significantly elevated when compared to a healthy control group (6.64 pg/ml vs. 1.28 pg/ml). Serum bFGF levels did not correlate with any other clinical marker such as PSA, tumor stage, or grade. Four out of five patients who progressed to a more advanced stage showed an increase in serum bFGF levels. CONCLUSIONS These results suggest that increased bFGF release may be associated with a more aggressive tumor phenotype. Prostate 31:223–233, 1997. © 1997 Wiley‐Liss, Inc.