Loss of the intrinsic FGF7/FGF10-type 2 FGF receptor (FGFR2) pathway and gain of the ectopic type 1 FGF receptor (FGFR1) pathway are associated with the progression to malignancy in prostate cancer (PCa) and many other epithelial originating lesions.
Specifically, KGF is currently being evaluated in clinical trials sponsored by Amgen (Thousand Oaks, CA) to test its ability to ameliorate severe oral mucositis (OM) that results from cancer chemoradiotherapy.
There was widespread expression of FGFs, including FGF7, in all tissues but, FGF3 and FGF19 were expressed by malignant cell lines and cancer tissue but were not present in normal tissue.
These findings suggest that administration of rhKGF and over-expression of endogenous KGF genes in colorectal cancer cells increase VEGF-A production and may relate to angiogenesis in cancer.
KGF is currently being evaluated in clinical trials to test its ability to ameliorate severe oral mucositis (OM) that results from cancer chemoradiotherapy.
Normal human breast stromal cells which do not response to estradiol-17 have lower KGF mRNA level than the cancer cells which KGF expression is stimulated by estradiol-17.
The present study was designed to investigate the messenger ribonucleic acid (mRNA) expression of transforming growth factor (TGF)-alpha, TGF-beta 1, TGF-beta 2, TGF- beta 3, keratinocyte growth factor (KGF), epidermal growth factor (EGF), EGF receptor (EGF-R), and KGF receptor (KGF-R) in human fetal and adult prostatic tissues and cancer cell lines by reverse-transcriptase-polymerase chain reaction-(RT-PCR) using specific oligonucleotide primers.