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1
Czynniki wzrostowe rodziny EGF i ich rola w karcinogenezie jelita grubego
100%
Malecka-Panas E.
Postępy Biologii Komórki
|
1996
|
tom 23
|
nr 1
107-125
2
Content available remote Role of adipokines in the assessment of severity and predicting the clinical course of acute pancreatitis
51%
Wos-Wroniewicz E. , Caban M. , Malecka-Panas E.
Journal of Physiology and Pharmacology
|
2020
|
tom 71
|
nr 5
3
Content available remote Experimental studies as an inspiration for clinical investigation
51%
Malecka-Panas E. , Talar-Wojnarowska R. , Kotynia J. , Majumdar A. P. N.
Journal of Physiology and Pharmacology. Supplement
|
2004
|
tom 55
|
nr 2
139-150
EN
This study represents an attempt of showing own author's example of using basic research data as an inspiration for the clinical studies. The project evaluates the role of gastrin in colorectal carcinogenesis as well as the differences of its action in proximal and distal colon. Colonocytes were isolated from Fischer-344 rats and incubated for 2 minutes with gastrin (10-8M). This treatment resulted with 60-70% rise in tyrosine kinase (Tyr-k) and 150-200% - in phospholipase C activity as regards to basal levels. In vivo infusion of gastrin for 5 days to Fischer-344 rats resulted with 90-150% increase in distal but not proximal colonic mucosal proliferative activity as well as tyrosine phosphorylation of several colonic mucosal proteins. In clinical study, the mean fasting gastrin level in the control group was significantly lower (p<0.01) than in patients with colorectal cancer before surgery. Mean plasma gastrin level in patients with distal tumor yielded 105,31 ± 12,5 µ U/l and was significantly higher than in patients with the proximal tumor site (42, 2 ± 3,1 µU/l) (p<0,001). We conclude, that Tyr-k is involved in the mechanism of the trophic action of gastrin, particularly in distal colon. The differences in gastrin concentration in patients with distal and proximal tumors may probably contribute to the distinct pathogenesis and biological properties of those cancers.
4
Etanol i aldehyd octowy: udzial w procesach mutagenezy i karcynogenezy
51%
Trzeciak A. , Malecka-Panas E. , Romanowicz-Makowska H. , Kulig A.
Postępy Biologii Komórki
|
2001
|
tom 28
|
nr 4
543-559
5
Gastrin activates tyrosine kinase and phospholipase C in isolated rat colonocytes
51%
Malecka-Panas E. , Tureaud J. , Majumdar A. P. N.
Acta Biochimica Polonica
|
1996
|
tom 43
|
nr 3
EN
Postreceptor regulation of the trophic action of gastrin is not fully elucidated. Tyrosine kinase (Tyr-kinase) has been associated with receptors of a number of growth factors and plays an important role in regulation of cellular growth within the gastrointestinal tract. The aim of this study was to determine, whether Tyr-kinase plays a role in mediating the growth promoting action of gastrin and whether phos­pholipase C (PLC) is involved in the signal transduction pathway. Colonocytes isolated from Fischer 344 rats were incubated for 2 min with gastrin (10-8 M) and assayed for Tyr-kinase and PLC activities. Incubations with gastrin resulted in 60%-70% rise in Tyr-kinase and 150%-200% rise in PLC activities over the corresponding basal levels. When processed separately, in proximal colon Tyr-kinase activation by gastrin was 15%-20%, while in distal colon 70%-80% as compared to the buffer control. Gastrin activation of both Tyr-kinase and PLC was abolished by Tyr-kinase inhibitor, tyrphostin-25 (3.2 nM) and was not affected by staurosporine (20 ng/ml). We conclude that Tyr-kinase is involved in the mechanism of trophic action of gastrin, and PLC activation appears to be the next step in the signal transduction pathway.
6
Content available remote Clinical significance of activin A and myostatin in patients with pancreatic adenocarcinoma and progressive weight loss
45%
Talar-Wojnarowska R. , Wozniak M. , Borkowska A. , Olakowski M. , Malecka-Panas E.
Journal of Physiology and Pharmacology
|
2020
|
tom 71
|
nr 1
7
Content available Ocena eozynofilii, stezenia immunoglobuliny E i eozynofilowego bialka kationowego podczas leczenia toksokarozy
45%
Niedworok M. , Sordyl B. , Borecka A. , Gawor J. , Malecka-Panas E.
Wiadomości Parazytologiczne
|
2008
|
tom 54
|
nr 3
225-230
8
Ocena stężeń wybranych adipohormonów u chorych z nowotworami jelita grubego
45%
Kumor A. , Daniel P. , Jasinska A. , Malecka-Panas E. , Pietruczuk M.
|
2007
|
tom 43
|
nr 3
9
Content available Prevalence of Helicobacter pylori in children dependently on age and living conditions
45%
Czkwianianc E. , Bak-Romaniszyn L. , Malecka-Panas E. , Suski S. , Woch G.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 1
10
Content available Giardiosis complicated with mycosis
45%
Materla S. , Malecka-Panas E. , Lipczyk J. , Planeta-Malecka I. , Kurnatowska A.
Wiadomości Parazytologiczne
|
1998
|
tom 44
|
nr 3
11
DNA damage in human colonic mucosa cells induced by bleomycin and the protective action of vitamin E
45%
Wozniak K. , Arabski M. , Malecka-Panas E. , Drzewoski J. , Blasiak J.
Cellular and Molecular Biology Letters
|
2004
|
tom 09
|
nr 1
EN
Using the alkaline comet assay, we showed that bleomycin at 0.1-5 μg/ml induced DNA strand breaks and/or alkali-labile sites, measurable as the comet tail moment, in human colonic mucosa cells. This DNA damage was completely repaired during a 120-minute post-treatment incubation of the cells. Post-treatment of the bleomycin-damaged DNA with 3-methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing alkylated bases, gave rise to a significant increase in the extent of DNA damage, indicating that the drug could induce alkylative bases in DNA. We did not observe any change in the comet tail moment in the presence of catalase. Vitamin E ((+)-α-tocopherol) decreased DNA damage induced by bleomycin. The results obtained suggest that hydrogen peroxide might not be involved in the formation of DNA lesions induced by bleomycin in the colonic mucosa cells, and that vitamin E may exert protective effects on these cells.
12
Immune response to Helicobacter pylori in gastritis and duodenal ulcer in children
45%
Bak-Romaniszyn L. , Zeman K. , Czkwianianc E. , Malecka-Panas E. , Fornalczyk E.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
13
Ocena stężenia wybranych adipohormonów w ostrym zapaleniu trzustki
38%
Jasinska A. , Kumor A. , Lesniowski B. , Daniel P. , Malecka-Panas E. , Pietruczuk M.
|
2007
|
tom 43
|
nr 3
14
Granulocyte-macrophage colony stimulating factor [GM-CSF] augments Helicobacter pylori-induced oxidative burst in human THP-1 monocytes
38%
Chmiela M. , Wadstrom T. , Folkesson H. , Lawnik M. , Malecka-Panas E. , Rechcinski T. , Rudnicka W.
Journal of Physiology and Pharmacology. Supplement
|
1997
|
tom 48
|
nr 1
15
Content available remote Adiponectin and leptin receptors expression in Barrett's esophagus and normal squamous epithelium in realtion to central obesity status
32%
Mokrowiecka A. , Sokolowska M. , Luczak E. , Dudojc M. , Wieczfinska J. , Kacprzak D. , Wierzchniewska-Lawska A. , Pawliczak R. , Malecka-Panas E.
Journal of Physiology and Pharmacology
|
2013
|
tom 64
|
nr 2
16
Content available remote Usufulness of p16 and K-ras mutation in pancreatic adenocarcinoma and chronic pancreatitis differential diagnosis
32%
Talar-Wojnarowska R. , Gasiorowska A. , Smolarz B. , Romanowicz-Makowska H. , Strzelczyk J. , Janiak A. , Kulig A. , Malecka-Panas E.
Journal of Physiology and Pharmacology. Supplement
|
2004
|
tom 55
|
nr 2
129-138
EN
The differentiation of chronic pancreatitis (CP) from pancreatic adenocarcinoma (PA) remains a great challenge. The purpose of the study was to compare the prevalence of p16 and K-ras mutation in PA and CP in order to evaluate their usefulness in differential diagnosis of those diseases. Methods: The study included 44 patients who underwent Whipple resection or distal pancreatectomy for PA (23 subjects) or CP (21 subjects). DNA from pancreatic tissue was analysed for K-ras mutation (codon 12) and p16 mutations with PCR amplifications. Results: The K-ras gene mutation has been shown in 17 (73,9%) cases with pancreatic adenocarcinoma which was significantly more often than in chronic pancreatitis - 9 (42,8%) (p<0,01). Prevalence of p16 mutations in patients with PA was 18 (78,3%) and with CP - 7 (33,3%) (p<0,01). K-ras and p16 mutations together have been observed in 16 (69,6%) cases in patients with PC and only in 3 (14,3%) - with CP (p<0,01). No statistically significant association between K-ras or p16 mutations and tumor size, sex or patient age has been observed. Conclusion: It is suggested that simultaneous measurement of K-ras and p16 mutations may provide an additional tool in differential diagnosis of chronic pancreatitis and pancreatic adenocarcinoma.
17
Content available remote Adipohormones as prognostic markers in patients with nonalcoholic steatohepatitis [NASH]
32%
Krawczyk K. , Szczesniak P. , Kumor A. , Jasinska A. , Omulecka A. , Pietruczuk M. , Orszulak-Michalak D. , Sporny S. , Malecka-Panas E.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 3
71-75
18
Content available remote Vascular endothelial growth factor (VEGF) genotype and serum concentration in patients with pancreatic adenocarcinoma and chronic pancreatitis
32%
Talar-Wojnarowska R. , Gasiorowska A. , Olakowski M. , Lekstan A. , Lampe P. , Smolarz B. , Romanowicz-Makowska H. , Kulig A. , Malecka-Panas E.
Journal of Physiology and Pharmacology
|
2010
|
tom 61
|
nr 6
19
Content available Helicobacter pylori infection in the etiopathogenesis of duodenal ulcer in children
32%
Bak-Romaniszyn L. , Malecka-Panas E. , Zeman K. , Czkwianianc E. , Kozlowski W. , Kulig A. , Kaluzynski A. , Suski S.
Journal of Physiology and Pharmacology
|
1996
|
tom 47
|
nr 1
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