Fibroblast growth factor-5 stimulates mitogenic signaling and is overexpressed in human pancreatic cancer: evidence for autocrine and paracrine actions

  title={Fibroblast growth factor-5 stimulates mitogenic signaling and is overexpressed in human pancreatic cancer: evidence for autocrine and paracrine actions},
  author={Marko Kornmann and Toshiyuki Ishiwata and Hans G. Beger and Murray Korc},
Fibroblast growth factor (FGF)-1 and -2 are overexpressed in human pancreatic cancer. In this study the role of FGF-5 in human pancreatic cancer was investigated, as FGF-5 has a classical signal sequence for secretion not found in FGF-1 or -2. Northern blot analysis with a 306 bp FGF-5 cDNA revealed the presence of 4.0 kb and 1.6 kb FGF-5 mRNA transcripts in both normal and cancerous pancreatic tissues. Densitometric analysis indicated that 4.0 kb and 1.6 kb FGF-5 mRNA transcripts levels were… 

IIIc isoform of fibroblast growth factor receptor 1 is overexpressed in human pancreatic cancer and enhances tumorigenicity of hamster ductal cells.

The data indicate that FGFR-1 IIIc is expressed in human pancreatic cancer cells, promotes mitogenic signaling via the FRS2-MAPK pathway, and has the potential to enhance pancreatic ductal cell transformation.

Enhanced fibroblast growth factor 5 expression in stromal and exocrine elements of the pancreas in chronic pancreatitis

Exocrine and stromal derived FGF-5 has the potential to participate in autocrine and paracrine pathways that may contribute to the pathobiology of chronic pancreatitis.

Human Fibroblast Growth Factor Receptor 1-IIIb Is a Functional Fibroblast Growth Factor Receptor Expressed in the Pancreas and Involved in Proliferation and Movement of Pancreatic Ductal Cells

The results demonstrate that the human FGFR-1 IIIb variant is a functional FGFR expressed in the pancreas that can alter pancreatic functions that regulate proliferation, adhesion, and movement.

Expression of the IIIc variant of FGF receptor-1 confers mitogenic responsiveness to heparin and FGF-5 in TAKA-1 pancreatic ductal cells

The data demonstrate that FGFR-1 IIIc can mediate FGF-5-induced mitogenesis via the MAPK pathway in pancreatic ductal cells, and suggest that expression ofFGFR- 1 IIIc in conjunction with F GF-5 may contribute to the pathobiology of human pancreatic cancer.

Expression of fibroblast growth factors in human non-papillary renal cell carcinoma: Correlation with tumor progression

FGF-5 expression in RCC tissues may be a useful prognostic marker for this cancer, and a close relationship between the expression of FGF- 5 and the development of RCC is demonstrated.

FGF-18, a Novel Member of the Fibroblast Growth Factor Family, Stimulates Hepatic and Intestinal Proliferation

Cloning a novel member of the FGF family that is expressed primarily in the lungs and kidneys and at lower levels in the heart, testes, spleen, skeletal muscle, and brain suggests that FGF-18 is a pleiotropic growth factor that stimulates proliferation in a number of tissues.

Increased expression of fibroblast growth factor 6 in human prostatic intraepithelial neoplasia and prostate cancer.

FGF6 is increased in PIN and prostate cancer and can promote the proliferation of the transformed prostatic epithelial cells via paracrine and autocrine mechanisms.

Characterization of keratinocyte growth factor and receptor expression in human pancreatic cancer.

Role of Fibroblast Growth Factors and Their Receptors in Pancreatic Cancer and Chronic Pancreatitis

This review summarizes the current information on the involvement of the FGF family and their receptors in human pancreatic cancer and chronic pancreatitis.

FGF5 as an oncogenic factor in human glioblastoma multiforme: autocrine and paracrine activities

It is demonstrated for the first time that FGF5 contributes to the malignant progression of human astrocytic brain tumours by both autocrine and paracrine effects.



Cell proliferation in cancer : regulatory mechanisms of neoplastic cell growth

This work focuses on cell proliferation and its role in carcinogenesis and therapy, and the potential and limitations of cytokine/growth factor manipulation in cancer therapy.


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