scholarly journals Serum levels of hepatocyte growth factor and epiregulin are associated with the prognosis on anti-EGFR antibody treatment in KRAS wild-type metastatic colorectal cancer

2014 ◽  
Vol 110 (11) ◽  
pp. 2716-2727 ◽  
Author(s):  
N Takahashi ◽  
Y Yamada ◽  
K Furuta ◽  
Y Honma ◽  
S Iwasa ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Metastatic Colorectal Cancer ◽  
Serum Levels ◽  
Wild Type ◽  
Antibody Treatment ◽  
Hepatocyte Growth ◽  
Egfr Antibody

scholarly journals Decreased Serum Hepatocyte Growth Factor (HGF) in Autistic Children with severe Gastrointestinal Disease

2009 ◽  
Vol 4 ◽  
pp. BMI.S3656 ◽  
Author(s):  
A.J. Russo ◽  
A. Krigsman ◽  
B. Jepson ◽  
Andrew Wakefield
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Gastrointestinal Disease ◽  
Serum Levels ◽  
Autistic Children ◽  
Functional Connection ◽  
Disease Symptoms ◽  
Lymphoid Nodular Hyperplasia ◽  
Lymphoid Nodules ◽  
Hepatocyte Growth

Aim To assess serum Hepatocyte Growth Factor (HGF) levels in autistic children with severe gastrointestinal (GI) disease and to test the hypothesis that there is a relationship between GI pathology and HGF concentration. Subjects and Methods Serum from 29 autistic children with chronic digestive disease (symptoms for a minimum of 6–12 months), most with ileo-colonic lymphoid nodular hyperplasia (LNH—markedly enlarged lymphoid nodules) and inflammation of the colorectum, small bowel and/or stomach), and 31 controls (11 age matched autistic children with no GI disease, 11 age matched non autistic children without GI disease and 9 age matched non autistic children with GI disease) were tested for HGF using ELISAs. HGF concentration of autistic children with GI disease was compared to GI disease severity. Results Autistic children with GI disease had significantly lower serum levels of HGF compared to controls (autistic without GI disease; p = 0.0005, non autistic with no GI disease; p = 0.0001, and non autistic with GI disease; p = 0.001). Collectively, all autistic children had significantly lower HGF levels when compared to non autistic children (p < 0.0001). We did not find any relationship between severity of GI disease and HGF concentration in autistic children with GI disease. Discussion These results suggest an association between HGF serum levels and the presence of GI disease in autistic children and explain a potential functional connection between the Met gene and autism. The concentration of serum HGF may be a useful biomarker for autistic children, especially those with severe GI disease.

Induction of liver growth in normal mice by infusion of hepatocyte growth factor/scatter factor

1995 ◽  
Vol 268 (2) ◽  
pp. G380-G386 ◽  
Author(s):  
F. Roos ◽  
A. M. Ryan ◽  
S. M. Chamow ◽  
G. L. Bennett ◽  
R. H. Schwall
Keyword(s):  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Dextran Sulfate ◽  
Plasma Concentrations ◽  
Elevated Serum ◽  
Serum Levels ◽  
Serum Biochemistry ◽  
Scatter Factor ◽  
Liver Growth ◽  
Hepatocyte Growth

Hepatocyte growth factor/scatter factor (HGF/SF) is a potent stimulator of DNA synthesis in a variety of epithelial cells, including hepatocytes, and has been implicated in liver regeneration. We show here that combining dextran sulfate with HGF/SF markedly increases the plasma concentrations of HGF/SF that are achieved during intraperitoneal infusion. Three days of administration of HGF/SF by this mechanism caused a dose-dependent increase in liver wet weight. Mitotic figures were rarely observed in control livers but were abundant in livers exposed to HGF/SF, and liver DNA content was elevated. Serum levels of triglycerides, cholesterol, total protein, and albumin were also dose dependently increased, whereas alkaline phosphatase was reduced. From these data we conclude 1) that combining HGF/SF with dextran sulfate provides a novel method for delivering HGF/SF in a continuous manner, 2) that HGF/SF can induce liver growth in an intact animal, and 3) that HGF/SF-induced liver enlargement is associated with changes in serum biochemistry.

Serum Levels of Hepatocyte Growth Factor/Scatter Factor in Patients with Liver Metastases from Breast Cancer

Tumor Biology ◽  
2007 ◽  
Vol 28 (1) ◽  
pp. 36-44 ◽  
Author(s):  
Michael H.R. Eichbaum ◽  
Thomas M. de Rossi ◽  
Sepp Kaul ◽  
Thomas Bruckner ◽  
Andreas Schneeweiss ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Liver Metastases ◽  
Serum Levels ◽  
Scatter Factor ◽  
Hepatocyte Growth

scholarly journals Urokinase-type plasminogen activator increases hepatocyte growth factor activity required for skeletal muscle regeneration

Blood ◽  
2009 ◽  
Vol 114 (24) ◽  
pp. 5052-5061 ◽  
Author(s):  
Thomas H. Sisson ◽  
Mai-Huong Nguyen ◽  
Bi Yu ◽  
Margaret L. Novak ◽  
Richard H. Simon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Growth Factor ◽  
Hepatocyte Growth Factor ◽  
Muscle Regeneration ◽  
Wild Type ◽  
Blocking Antibody ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Hepatocyte Growth ◽  
Pai 1

Abstract The plasminogen system plays a crucial role in the repair of a variety of tissues, including skeletal muscle. We hypothesized that urokinase-type plasminogen activator (uPA) promotes muscle regeneration by activating hepatocyte growth factor (HGF), which, in turn, stimulates proliferation of myoblasts required for regeneration. In our studies, levels of active HGF and phosphorylation of the HGF receptor c-met were increased after muscle injury in wild-type mice. Compared with wild-type animals, mice deficient in uPA (uPA−/−) had markedly reduced HGF levels and c-met activation after muscle damage. This reduced HGF activity in uPA−/− animals was associated with decreased cell proliferation, myoblast accumulation, and new muscle fiber formation. On the other hand, HGF activity was enhanced at early time points in PAI-1−/− mice compared with wild-type mice and the PAI-1−/− animals exhibited accelerated muscle fiber regeneration. Furthermore, administration of exogenous uPA rescued HGF levels and muscle regeneration in uPA−/− mice, and an HGF-blocking antibody reduced HGF activity and muscle regeneration in wild-type mice. We also found that uPA promotes myoblast proliferation in vitro through its proteolytic activity, and this process was inhibited by an HGF-blocking antibody. Together, our findings demonstrate that uPA promotes muscle regeneration through HGF activation and subsequent myoblast proliferation.

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