4 research outputs found
The combined effect of erythropoietin and granulocyte macrophage colony stimulating factor on liver regeneration after major hepatectomy in rats
<p>Abstract</p> <p>Background</p> <p>The liver presents a remarkable capacity for regeneration after hepatectomy but the exact mechanisms and mediators involved are not yet fully clarified. Erythropoietin (EPO) and Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) have been shown to promote liver regeneration after major hepatectomy.</p> <p>Aim of this experimental study is to compare the impact of exogenous administration of EPO, GM-CSF, as well as their combination on the promotion of liver regeneration after major hepatectomy.</p> <p>Methods</p> <p>Wistar rats were submitted to 70% major hepatectomy. The animals were assigned to 4 experimental groups: a control group (n = 21) that received normal saline, an EPO group (n = 21), that received EPO 500 IU/kg, a GM-CSF group (n = 21) that received 20 mcg/kg of GM-CSF and a EPO+GMCSF group (n = 21) which received a combination of the above. Seven animals of each group were killed on the 1st, 3rd and 7th postoperative day and their remnant liver was removed to evaluate liver regeneration by immunochemistry for PCNA and Ki 67.</p> <p>Results</p> <p>Our data suggest that EPO and GM-CSF increases liver regeneration following major hepatectomy when administered perioperatively. EPO has a more significant effect than GM-CSF (p < 0.01). When administering both, the effect of EPO seems to fade as EPO and GM-CSF treated rats have decreased regeneration compared to EPO administration alone (p < 0.01).</p> <p>Conclusion</p> <p>EPO, GM-CSF and their combination enhance liver regeneration after hepatectomy in rats when administered perioperatively. However their combination has a weaker effect on liver regeneration compared to EPO alone. Further investigation is needed to assess the exact mechanisms that mediate this finding.</p
Expression of c-kit in common benign and malignant breast lesions
Aims and background. c-kit (CD 117) is a transmembrane tyrosine kinase
that acts as a type III receptor for mast cell growth factor. In recent
years, the role of c-kit in the development of preinvasive and invasive
breast carcinomas has been investigated. The aim of our study was to
detect c-kit expression in the entire spectrum of common benign and
malignant breast lesions in correlation with a well-studied
myoepithelial or stem-cell like marker (p63).
Methods and study design. We evaluated 270 cases of benign and malignant
breast lesions including fibrocystic disease, fibroadenoma, sclerosing
adenosis, atypical ductal hyperplasia, ductal/lobular carcinoma in situ,
and ductal/lobular/mixed type carcinoma. C-kit staining was evaluated in
the cytoplasm/cell membrane in epithelial and myoepithelial cells and
p63 in the nuclei of myoepithelial cells.
Results. c-kit was highly expressed (85.3%) in benign lesions
(fibrocystic disease, sclerosing adenosis, fibroadenoma), and p63
expression was 95.5% in the aforementioned lesions. c-kit distribution
in preinvasive and invasive lesions was as follows: ductal/lobular
carcinoma in-situ, 43%/35%; ductal/lobular carcinoma, 36%/39%; and
mixed type carcinoma, 20%. c-kit was highly expressed in
myofibroblast/fibroblast cells only in grade III ductal/lobular
carcinomas, c-kit was totally absent in stromal cells in benign lesions
and in situ carcinomas whereas expression was weak in grade I and II
carcinomas.
Conclusions. Combined overexpression of c-kit and p63 is indicative of
benign breast lesions. In contrast, there is reduced expression of c-kit
in in situ and invasive breast carcinomas, with simultaneous
overexpression in the stromal cells. This suggests that c-kit may play a
role in breast cancer progression. Free full text available at
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