Wyniki wyszukiwania

1

Expression of Toll-like receptors on human rectal adenocarcinoma cells

100%

Tchorzewski M., Lewkowicz P., Dziki A., Tchorzewski H.

Archivum Immunologiae et Therapiae Experimentalis

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2014

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tom 62

|

nr 3

2

Transcriptional upregulation of gastrin in response to peroxisome proliferator-activated receptor gamma agonist triggers cell survival pathways

100%

Ptak-Belowska A., Pawlik M. W., Krzysiek-Maczka G., Brzozowski T., Pawlik W. W.

Journal of Physiology and Pharmacology

|

2007

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tom 58

|

nr 4

Peroxisome proliferator-activated receptor (PPAR ) are members of the largest nuclear hormone receptor family of transcription factors (1). PPAR gamma (PPAR) plays an important role in adipogenesis, control of sensitivity to insulin, inflammation and atherosclerosis but recent studies also suggest that PPAR is involved in cell cycle withdrawal. PPAR can promote cell differentiation, exert an antiproliferative action and inhibit angiogenesis (2, 3). However, there are studies showing that activation of PPAR promotes the development of colon cancer (4). These data are in sharp contrast with studies that attribute anticancer effects to PPAR in gastrointestinal malignancies. Probably, the action of PPAR on cell cycle and proliferation depends on the cell type and presence of other stimuli that predispose cells to cancer development. Amidated and non-amidated gastrins may play an important role in the proliferation and carcinogenesis of GI cancers. It is known that gastrin peptides activate phosphorylation of Protein Kinase B (PKB/Akt) and anti-apoptotic signalling but there is little known about the link between gastrins and PPAR receptors in relation to apoptosis.

3

Cytological picture of the oral mucosa in patients with gastric and colon cancer

84%

Kedra B., Chomczyk M., Zlotkowski M., Stokowska W., Borsuk A., Bicz M., Pietruska M., Tokajuk G., Charkiewicz R., Czajka P., Chyczewski L., Zimnoch L., Kedra B.

Folia Histochemica et Cytobiologica

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2012

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tom 50

|

nr 3

4

Opioids, neutral endopeptidase, its inhibitors and cancer: Is there a relationship among them?

84%

Mizerska-Dudka M., Kandefer-Szerszen M.

Archivum Immunologiae et Therapiae Experimentalis

|

2015

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tom 63

|

nr 3

5

Metabolic transformations of antitumor imidazoacridinone, C-1311, with microsomal fractions of rat and human liver

84%

Wisniewska A., Chrapkowska A., Kot-Wasik A., Konopa J., Mazerska Z.

Acta Biochimica Polonica

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2007

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tom 54

|

nr 4

831-838

The imidazoacridinone derivative C-1311 is an antitumor agent in Phase II clinical trials. The molecular mechanism of enzymatic oxidation of this compound in a peroxidase model system was reported earlier. The present studies were performed to elucidate the role of rat and human liver enzymes in metabolic transformations of this drug. C-1311 was incubated with different fractions of liver cells and the reaction mixtures were analyzed by RP-HPLC. We showed that the drug was more sensitive to metabolism with microsomes than with cytosol or S9 fraction of rat liver cells. Incubation of C-1311 with microsomes revealed the presence of four metabolites. Their structures were identified as dealkylation product, M0, as well as a dimer-like molecule, M1. Furthermore, we speculate that the hydroxyl group was most likely substituted in metabolite M3. It is of note that a higher rate of transformation was observed for rat than for human microsomes. However, the differences in metabolite amounts were specific for each metabolite. The reactivity of C-1311 with rat microsomes overexpressing P450 isoenzymes, of CYP3A and CYP4A families was higher than that with CYP1A and CYP2B. Moreover, the M1 metabolite was selectively formed with CYP3A, whereas M3 with CYP4A. In conclusion, this study revealed that C-1311 varied in susceptibility to metabolic transformation in rat and human cells and showed selectivity in the metabolism with P450 isoenzymes. The obtained results could be useful for preparing the schedule of individual directed therapy with C-1311 in future patients.

6

Development of a new, simple and cost-effective diagnostic tool for genetic screening of hereditary colorectal cancer - the DNA microarray assay

84%

Stojcev Z., Banasiewicz T., Kaszuba M., Sikorski A., Szczepkowski M., Bobkiewicz A., Paszkowski J., Krokowicz L., Biczysko M., Szmeja J., Jurkowska M., Majewski P., Mackiewicz A., Lamperska K., Drews M., Wojciechowicz J.

Acta Biochimica Polonica

|

2013

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tom 60

|

nr 2

Detection of mutations in families with a hereditary predisposition to colon cancer gives an opportunity to precisely define the high-risk group. 36 patients operated on for colon cancer, with familiar prevalence of this malignancy, were investigated using the DNA microarrays method with the potential detection of 170 mutations in MLH1, MSH2, MSH6, CHEK2, and NOD2 genes. In microarrays analysis of DNA in 9 patients (25% of the investigated group), 6 different mutations were found. The effectiveness of genetic screening using the microarray method is comparable to the effectiveness of other, much more expensive and time-consuming methods.

7

Foodomics: new omics for new foods

84%

Ibanez E., Herrero M., Garcia-Canas V., Simo C., Cifuentes A.

Polish Journal of Food and Nutrition Sciences

|

2011

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tom 61

|

nr Suppl.1

8

The knockdown of c-myc expression by RNAi inhibits cell proliferation in human colon cancer HT-29 cells in vitro and in vivo

84%

Zhang X., Ge Y.-L., Tian R.-H.

Cellular and Molecular Biology Letters

|

2009

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tom 14

|

nr 2

305-318

We investigated the effects of RNA interference-mediated silencing of the c-myc gene on celluar proliferation and apoptosis in human colon cancer HT-29 cells in vitro and in vivo. A small interfering RNA (siRNA) targeting c-myc was designed, the DNA template was synthesized, and the siRNA was obtained by in vitro transcription. After siRNA transfection into HT-29 and human neuroblastoma IMR-32 cells with Lipofectamine 2000™, the proliferation of the HT-29 and IMR-32 cells was assessed via 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) colorimetry, and Hoechst 33258 staining was used to observe cell apoptosis. Following gene transfer to HT-29 cells, the expression of c-myc mRNA was examined via reverse transcription polymerase chain reaction, and the level of the protein via Western blot assay. Growth curves were constructed and in vivo experiments were performed on nude mice to assess the effects of c-myc silencing on tumor growth. The c-myc expression in the tumor tissue was measured by reverse transcription polymerase chain reaction and subsequently by immunohistochemistry. Our paper demonstrates that the delivery of siRNA directed against c-myc not only efficiently down-regulated the expression of c-myc, inhibited the proliferation of HT-29 cells and induced apoptosis in vitro, but also suppressed the growth of colon cancer cells in vivo.

9

Capsaicin induces apoptosis by generating reactive oxygen species and disrupting mitochondrial transmembrane potential in human colon cancer cell lines

84%

Yang K. M., Pyo J. O., Kim G.-Y., Yu R., Han I. S., Ju S. A., Kim W. H., Kim B.-S.

Cellular and Molecular Biology Letters

|

2009

|

tom 14

|

nr 3

497-510

Although genetic factors are a well-known cause of colorectal cancer, environmental factors contribute more to its development. Despite advances in the fields of surgery, radiotherapy and chemotherapy, the cure rates for colon cancer have not substantially improved over the past few decades. Capsaicin (trans-8-methyl-N-vanillyl-6-nonenamide), the principal pungent ingredient of hot chili pepper, has exhibited an anti-tumor effect in many cell types. However, the mechanisms responsible for the anti-tumor effect of capsaicin are not yet completely understood. In this study, we investigated whether capsaicin induces apoptosis in colon cancer cell lines. Capsaicin decreased cell viability in a dose-dependent manner in Colo320DM and LoVo cells. In addition, capsaicin produced cell morphology changes and DNA fragmentation, decreased the DNA contents, and induced phosphatidylserine translocation, which is a hallmark of apoptotic cell death. We showed that capsaicin-induced apoptosis is associated with an increase in ROS generation and a disruption of the mitochondrial transmenbrane potential. A possible mechanism of capsaicin-induced apoptosis is the activation of caspase 3, a major apoptosis-executing enzyme. Treatment with capsaicin induced a dramatic increase in caspase 3 activity, as assessed by the cleavage of Ac-DEVD-AMC, a fluorogenic substrate. In conclusion, our results clearly showed that capsaicin induced apoptosis in colon cancer cells. Although the actual mechanisms of capsaicin-induced apoptosis remain uncertain, it may be a beneficial agent for colon cancer treatment and chemoprevention.

10

Rat colonic lipid peroxidation and antioxidant status: the effects of dietary luteolin on 1,2-dimethylhydrazine challenge

84%

Manju V., Balasubramaniyan V., Nalini N.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr 3

11

Antiapoptotic proteins as targets for bioactive compounds

84%

Pajak B.

Polish Journal of Veterinary Sciences

|

2007

|

tom 10

|

nr 2

One of the most promising strategies in colon cancer therapy is the sensitization of cancer cells to natural proapoptotic cytokines, such as death ligands and interferons, which are able to eliminate abnormal cells. The investigation of mechanisms determining the immune escape of cancer cells revealed the presence of antiapoptotic proteins, such as cFLIP, which inhibit cell death signal transduction. Numerous studies showed that the use of different metabolic inhibitors, such as cycloheximide (CHX), reduces the cFLIP protein level, thus restoring the susceptibility to TNF-a-induced apoptosis. However, high non-specific toxicity of CHX excludes the clinical use of this substance. The current efforts are focused on identification of bioactive compounds which could safely support immunotherapy. The review presents in vitro and in vivo evidence that butyrate (Bt), fatty acid produced in colon during fermentation process and parthenolide (PN), sesquiterpene lactone isolated from Tanacetum parthenium specifically affect different cancer cells. Among described various molecular mechanisms of Bt and PN action, one reduces the level of antiapoptotic proteins. This paper clearly demonstrates that bioactive compounds, especially combined with immune cytokines could be seriously considered as an alternative for routine colon anti-cancer therapy.

12

Novel Ru[III], Rh[III], Pd[II] and Pt[II] complexes with ligands incorporating azole and pyrimidine rings. I. Antiproliferative activity in vitro

84%

Wisniewski M. Z., Wietrzyk J., Opolski A.

Archivum Immunologiae et Therapiae Experimentalis

|

2000

|

tom 48

|

nr 1

13

Dietetic and prophylactic significance of calcium in milk

84%

Renner E.

Acta Academiae Agriculturae ac Technicae Olstenensis. Technologia Alimentorum

|

1995

|

tom 27

14

Increased expression of HSP70 by colon cancer cells is not always associated with access to the dendritic cell cross-presentation pathway

84%

Matera L., Forno S., Galetto A., Moro F., Garetto S., Mussa A.

Cellular and Molecular Biology Letters

|

2007

|

tom 12

|

nr 2

Dendritic cells (DCs) are highly specialized antigen-presenting cells endowed with the unique ability to not only present exogenous antigens upon exposure to MHC II, but also to cross-present these upon exposure to MHC I. This property was exploited to generate the tumor-specific CD8 cytotoxic lymphocyte (CTL) response in DCs-based cancer vaccine protocols. In this context, the source of tumor antigens remains a critical challenge. A crude tumor in the context of danger signals is believed to represent an efficient source of tumor antigens (TAs) for DCs loading. In our previous work, increased DCs cross-presentation of antigens from necrotic gastric carcinoma cells paralleled up-regulation of the heat shock protein hsp70. We studied the expression of hsp70 on primary colon carcinoma cells and its relevance in the cross-priming of anti-tumor CTL by tumor-loaded DCs. Hsp70 was expressed on all three of the tumors studied, but was never detected in the peritumoral normal mucosa (NM). The uptake of the tumor induced a trend towards down-modulation of the monocyte-specific marker CD14, but had no effect on the chemokine receptors CCR4 and CCR7. The IFN-γ enzyme-linked immunospot assay (ELIspot) showed cross-priming of CTL by tumor-loaded but not NM-loaded DCs in four of the six cases studied. The CTL response generated in DC+tumor cultures was directed towards the tumor, but not towards NM, and it was characterized by refractoriness to polyclonal (Ca ionophores, PKC activators) stimuli. Of the three CTL-generating tumors, only one expressed hsp70. This data indicates a tumor-specific expression of hsp70, but does not support its relevance in the DC cross-presentation of TAs.

15

Food-based strategies to modulate the composition of the intestinal microbiota and their associated health effects

67%

Bosscher D., Breynaert A., Pieters L., Hermans N.

Journal of Physiology and Pharmacology. Supplement

|

2009

|

tom 60

|

nr 6

16

Association between single-nucleotide polymorphisms of selected genes involved in the response to DNA damage and risk of colon, head and neck, and breast cancers in a Polish population

67%

Jelonek K., Gdowicz-Klosok A., Pietrowska M., Borkowska M., Korfanty J., Rzeszowska-Wolny J., Widlak P.

Journal of Applied Genetics

|

2010

|

tom 51

|

nr 3

Single-nucleotide polymorphisms in genes involved in DNA-damage-induced responses are reported frequently to be a risk factor in various cancer types. Here we analysed polymorphisms in 5 genes involved in DNA repair (XPD Asp312Asn and Lys751Gln, XRCC1 Arg399Gln, APE1 Aspl48Glu, NBS1 Glu185Gln, and XPA G-4A) and in a gene involved in regulation of the cell-cycle (CCND1 A870G). We compared their frequencies in groups of colon, head and neck, and breast cancer patients, and 2 healthy control groups: (1) matched healthy Polish individuals and (2) a NCBI database control group. Highly significant differences in the distribution of genotypes of the APE1, XRCC1 and CCND1 genes were found between colon cancer patients and healthy individuals. The 148Asp.APE1 allele and the 399Gln XRCC1 allele apparently increased the risk of colon cancer (OR = 1.9-2.3 and OR = 1.5-2.1, respectively). Additionally, frequencies of XPD genotypes differed between healthy controls and patients with colon or head and neck cancer. Importantly, no differences in the distribution of these polymorphisms were found between healthy controls and breast cancer patients. The data clearly indicate that the risk of colon cancer is associated with single-nucleotide polymorphism in genes involved in base-excision repair and DNA-damage-induced responses.

17

The dysfunction of NK cells in patients with type 2 diabetes and colon cancer

67%

Piatkiewicz P., Milek T., Bernat-Karpinska M., Ohams M., Czech A., Ciostek P.

Archivum Immunologiae et Therapiae Experimentalis

|

2013

|

tom 61

|

nr 3

18

Therapeutic endoscopy in gastroenterology

67%

Celinski K., Cichoz-Lach H.

Journal of Physiology and Pharmacology. Supplement

|

2007

|

tom 58

|

nr 3

33-41

19

Anticancer and antioxidant effects of fructooligosaccharide (FOS) on chemically-induced colon cancer in rats

67%

Moharib S. A.

Electronic Journal of Polish Agricultural Universities. Series Veterinary Medicine

|

2016

|

tom 19

|

nr 1

20

Sodium butyrate-dependent sensitization of human colon adenocarcinoma COLO 205 cells to TNF-alpha-induced apoptosis

67%

Pajak B., Orzechowski A.

Journal of Physiology and Pharmacology. Supplement

|

2007

|

tom 58

|

nr 3

163-176

Ograniczanie wyników

Expression of Toll-like receptors on human rectal adenocarcinoma cells

Transcriptional upregulation of gastrin in response to peroxisome proliferator-activated receptor gamma agonist triggers cell survival pathways

Cytological picture of the oral mucosa in patients with gastric and colon cancer

Opioids, neutral endopeptidase, its inhibitors and cancer: Is there a relationship among them?

Metabolic transformations of antitumor imidazoacridinone, C-1311, with microsomal fractions of rat and human liver

Development of a new, simple and cost-effective diagnostic tool for genetic screening of hereditary colorectal cancer - the DNA microarray assay

Foodomics: new omics for new foods

The knockdown of c-myc expression by RNAi inhibits cell proliferation in human colon cancer HT-29 cells in vitro and in vivo

Capsaicin induces apoptosis by generating reactive oxygen species and disrupting mitochondrial transmembrane potential in human colon cancer cell lines

Rat colonic lipid peroxidation and antioxidant status: the effects of dietary luteolin on 1,2-dimethylhydrazine challenge

Antiapoptotic proteins as targets for bioactive compounds

Novel Ru[III], Rh[III], Pd[II] and Pt[II] complexes with ligands incorporating azole and pyrimidine rings. I. Antiproliferative activity in vitro

Dietetic and prophylactic significance of calcium in milk

Increased expression of HSP70 by colon cancer cells is not always associated with access to the dendritic cell cross-presentation pathway

Food-based strategies to modulate the composition of the intestinal microbiota and their associated health effects

Association between single-nucleotide polymorphisms of selected genes involved in the response to DNA damage and risk of colon, head and neck, and breast cancers in a Polish population

The dysfunction of NK cells in patients with type 2 diabetes and colon cancer

Therapeutic endoscopy in gastroenterology

Anticancer and antioxidant effects of fructooligosaccharide (FOS) on chemically-induced colon cancer in rats

Sodium butyrate-dependent sensitization of human colon adenocarcinoma COLO 205 cells to TNF-alpha-induced apoptosis