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1

Assessment of prognostic significance of cytoplasmic survivin expression in advanced oesophageal cancer

100%
Dabrowski A., Filip A., Zgodzinski W., Dabrowska M., Polanska D., Wojcik M., Zinkiewicz K., Wallner G.
Folia Histochemica et Cytobiologica
|
2004
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tom 42
|
nr 3
2
Content available remote

Molecular imaging of epidermal growth factor-receptor and survivin in vivo in porcine esophageal and gastric mucosae using probe-based confocal laser-induced endomicroscopy: proof of concept

72%
Nakai Y., Shinoura S., Ahluwalia A., Tarnawski A. S., Chang K. J.
Journal of Physiology and Pharmacology
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2012
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tom 63
|
nr 3
3

Immunohistochemical study on survivin in sinonasal tumors and its relationship with the immunoexpression of Ki67 and Bcl-2

72%
Stasikowska-Kanicka O., Wagrowska-Danilewicz M., Danilewicz M.
Folia Histochemica et Cytobiologica
|
2013
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tom 51
|
nr 3
4

Reversal of drug resistance by silencing Survivin gene expression in acute myeloid leukemia cells

72%
Wu Y. H., You Y., Chen Z.-C., Zou P.
Acta Biochimica Polonica
|
2008
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tom 55
|
nr 4
673-680
The role of Survivin in the pathogenesis of leukemia was explored in order to discover the effective avenues for gene therapy. Most primary leukemia cells isolated from patients as well as three leukemia cell lines (HL-60, K562, and U937) all expressed Survivin gene. To investigate the relationship between Survivin and chemotherapeutic resistance, HL-60 cells were treated with daunorubicin (DNR), mitoxantrone (MIT) or arsenious oxide (As2O3), and it was found that after 24h the level of Survivin mRNA was decreased by 9.7%, 41.0% and 27.5%, respectively. At 72 h, the level of Survivin mRNA was increased by 21.2% and 65.2% in HL-60 cells treated with DNR or MIT, but decreased by 33.2% in those treated with As2O3 as compared with that in the cells treated for 24 h. These results showed that DNR and MIT could initally decrease the expression of Survivin and then increase it, but As2O3 could decrease the Survivin expression continually. Furthermore, shRNA plasmids targeting the Survivin gene (pEGFP-Survivin), which can silence the expression of Survivin with a high specificity, were constructed. pEGFP-Survivin and pEGFP-H1 were transfected into HL-60 cells via electroporation and selected by G418, and HL-60/Survivin and HL-60/EGFP cells were obtained. After treatment with DNR, the cell survival rate and IC50 of DNR in HL-60/Survivin cells were decreased substantially as compared with those of HL-60/EGFP and HL-60 cells (IC50of DNR:18.3±2.45 vs40.8±6.37 and 39.2±5.91 ng/ml, respectively), and the apoptosis rate was elevated ((84.3±19.7)% vs(45.8±13.8)% and (50.9±12.4)%, respectively). These results suggest that shRNA can down-regulate the expression of Survivin in HL-60 cells substantially and improve their sensitivity to DNR. They also further explain the pathogenesis of leukemia drug resistance and provide new theory in the design of clinical therapies.
5

Biomarkers of epithelial-mesenchymal transition in localized, surgically treated clear-cell renal cell carcinoma

72%
Gasinska A., Jaszczynski J., Adamczyk A., Janecka-Widla A., Wilk W., Cichocka A., Stelmach A.
Folia Histochemica et Cytobiologica
|
2018
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tom 56
|
nr 4
6

Endogenne bialka przeciwdzialajace apoptozie.

72%
Rozynkowa D., Filip A.
Postępy Biologii Komórki
|
1999
|
tom 26
|
nr 3
561-578
7

Survivin antiapoptotic gene expression as a prognostic factor in non-small cell lung cancer: in situ hybridization study

72%
Karczmarek-Borowska B., Filip A., Wojcierowski J., Smolen A., Pilecka I., Jablonka A.
Folia Histochemica et Cytobiologica
|
2005
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tom 43
|
nr 4
8

The significance of Survivin and Nectin-4 expression in the prognosis of breast carcinoma

58%
Athanassiadou A. M., Patsouris E., Tsipis A., Gonidi M., Athanassiadou P.
Folia Histochemica et Cytobiologica
|
2011
|
tom 49
|
nr 1
9
Content available remote

Survivin is a key factor in the differential susceptibility of gastric endothelial and epithelial cells to alcohol-induced injury

58%
Jones M. K., Padilla O. R., Zhu E.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 3
253-264
We previously demonstrated that the anti-apoptosis protein, survivin, plays a protective role against alcohol-induced gastric injury. Since the endothelium is a primary target of alcohol-induced gastric damage, we investigated whether survivin expression is a key factor in the greater susceptibility of gastric endothelial vs. epithelial cells to alcohol-induced injury. Here, we demonstrate that rat gastric epithelial cells (RGM1 cells, an epithelial cell line derived from normal rat gastric mucosa) expressed 7.5-fold greater survivin protein levels vs. rat gastric endothelial cells. Survivin expression correlated with resistance of gastric epithelial vs. endothelial cells to both alcohol-induced cell damage and alcohol-induced apoptosis. Suppression of survivin protein expression levels using siRNA rendered the gastric epithelial cells as susceptible to both alcohol-induced cell damage and apoptosis as the gastric endothelial cells. Conversely, forced overexpression of survivin by transient transfection rendered gastric endothelial cells as resistant to both alcohol-induced cell damage and apoptosis as mock-transfected gastric epithelial cells. Moreover, overexpression of a threonine-34 to glutamate phosphorylation mimic mutant survivin construct rendered gastric endothelial cells significantly more resistant to alcohol-induced damage and apoptosis vs. mock-transfected gastric epithelial cells. These findings indicate that disparate survivin expression levels can explain the discrepancy between gastric epithelial and endothelial cell susceptibility to alcohol-induced injury; and, that a negative charge at amino acid residue 34 on survivin, such as that which naturally occurs by phosphorylation of threonine-34, enhances its property in conferring gastric mucosal protection.
10
Content available remote

Gastric cancer and Helicobacter pylori infection

58%
Konturek P. C., Konturek S. J., Brzozowski T.
Journal of Physiology and Pharmacology. Supplement
|
2006
|
tom 57
|
nr 3
51-65
The Nobel prize in Physiology and Medicine in 2005 was presented to Barry Marshall and Robin Warren for their discovery of Helicobacter pylori (Hp), but only the involvement of this germ in gastritis and peptic ulcer has been mentioned in the award sentence, while numerous epidemiological, clinical and experimental studies and reports emphasized the crucial role of Hp in pathogenesis of gastric cancer (GC). This review is based on the old concept proposed by P. Correa much before the discovery of spiral bacteria in the stomach, postulating the cascade of mucosal changes from acute/chronic gastritis into the atrophic gastritis with intestinal metaplasia and finally to dysplasia and GC. It is now widely accepted view that Hp infection is the major initiator of the inflammatory and atrophic changes in gastric mucosa accompanied by an over-expression of certain growth factors such as gastrin as well as of cyclooxygenase-2 (COX-2) and anti-apoptotic proteins including survivin and B-cl2, leading to proliferation of mutated atrophic cells, excessive angiogenesis, inhibition of apoptosis and formation of gastric tumour. All the morphological and biochemical changes associated with the transformation of mucosal cells into the cancer cells can be traced in excellent experimental model of gastric cancerogenesis induced by infection of Hp in Mongolian gerbils. Since the eradication therapy was proved in several prospective clinical trials to greatly reduce the incidence of GC and this was confirmed on the gerbil model of Hp-induced GC, it has been postulated; a) that Hp is the major causal factor in pathogenesis of GC and b) that the only rational approach in attempt to reduce the occurrence of GC is the global eradication of Hp.
11

Serum levels of HMGB1, survivin, and VEGF in patients with advanced non-small cell lung cancer during chemotherapy

58%
Naumnik W., Niklinska W., Ossolinska M., Chyczewska E.
Folia Histochemica et Cytobiologica
|
2009
|
tom 47
|
nr 4
12

A multiple marker analysis of apoptosis-associated protein expression in non-small cell lung cancer in a Chinese population

58%
Fan C.-F., Xu H.-T., Lin X.-Y., Yu J.-H., Wang E.-H.
Folia Histochemica et Cytobiologica
|
2011
|
tom 49
|
nr 2
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