Wyniki wyszukiwania

1

Uncertainty in biological modelling

100%

Wosniok W.

Folia Histochemica et Cytobiologica. Supplement

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2001

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tom 39

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nr 1

2

Carcinogenesis, an overview with special reference to endocrine disrupting mechanisms

100%

Pluygers E., Sadowska A.

Folia Histochemica et Cytobiologica. Supplement

|

2001

|

tom 39

|

nr 1

3

Genotoxicity testing using higher plants

100%

Sadowska A., Pluygers E.

Folia Histochemica et Cytobiologica. Supplement

|

2001

|

tom 39

|

nr 1

4

Biologically based models of carcinogenesis biological, mathematical and statistical considerations

100%

Luebeck E. G.

Folia Histochemica et Cytobiologica. Supplement

|

2001

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tom 39

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nr 1

5

Preneoplastic changes in lungs

100%

Chyczewski L., Niklinski J., Chyczewska E.

Folia Histochemica et Cytobiologica. Supplement

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2001

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tom 39

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nr 1

6

Complex mechanistic carcinogenicity modelling

100%

Kopp-Schneider A., Edler L.

Folia Histochemica et Cytobiologica. Supplement

|

2001

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tom 39

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nr 1

7

Paraneoplastic autoimmunity

88%

Zouali M.

Polish Journal of Veterinary Sciences

|

2007

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tom 10

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nr 1

Loss of homeostasis is a hallmark of malignant tumorigenesis and autoimmune diseases. Recent studies have implicated apoptotic cell death pathways in initiating and propagating autoimmune diseases in susceptible individuals. During malignancy, however, there is an accumulation of cells resistant to apoptosis. Intriguingly, some patients with malignant tumors develop symptoms that cannot be explained solely on the basis of the effects produced by either the primary tumor or its metastases. The mechanisms responsible for these complex symptoms, known as paraneoplastic autoimmunity, remain the focus of investigation.

8

Promoting phorbol-ester-TPA enhances migration of C3H 10T1-2 cells. The role of protein kinase C and its relation to carcinogenesis

88%

Janik P., Szaniawska B., Kowalczyk D., Maternicka K.

Folia Biologica

|

1995

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tom 43

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nr 3-4

9

Antioxidant status and proteolytic-antiproteolytic balance in colorectal cancer

88%

Skrzydlewska E., Stankiewicz A., Michalak K., Sulkowska M., Zalewski B.

Folia Histochemica et Cytobiologica. Supplement

|

2001

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tom 39

|

nr 1

10

Advances in studies on invasive tumor growth and metastasis

88%

Radzikowski C.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

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nr Suppl.

11

Mechanism of inhibition of the protein kinase C by nonstructure protein 3 of hepatitis C virus

88%

Hartjen P., Reinholz M., Baier A., Borowski P.

Cellular and Molecular Biology Letters

|

2005

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tom 10

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nr Suppl.2

12

The role of cathelicidin LL-37 in cancer development

75%

Piktel E., Niemirowicz K., Wnorowska U., Watek M., Wollny T., Gluszek K., Gozdz S., Levental I., Bucki R.

Archivum Immunologiae et Therapiae Experimentalis

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2016

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tom 64

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nr 1

13

Role of mitochondria in carcinogenesis

75%

Tokarz P., Blasiak J.

Acta Biochimica Polonica

|

2014

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tom 61

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nr 4

14

Differential effects of heterocyclic amines on poly[ADP-ribose] polymerase-1 and mono-ADP-ribosyltransferase A

75%

Banasik M., Stedeford T., Strosznajder R. P., Hsu C.-H., Tanaka S., Ueda K.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

15-22

Heterocyclic amines (HCAs) have been shown to be carcinogenic in a variety of experimental systems. The purpose of the present study was to determine the in vitro effect of HCAs on the activity of the DNA repair enzyme poly(ADP-ribose) polymerase-1 (PARP-1). HCAs were also tested on the arginine-specific mono-ADP-ribosyltransferase A (MART-A), an enzyme involved in signal transduction and cytoskeletal realignment. 3-Amino-1-methyl-5H-pyrido[4,3-b]indole (Trp-P-2) at 1 mM caused a 134% increase in PARP-1 activity and a 93% decrease in activity at 5 mM (IC50 = 2.2 mM). This dual effect is unique among inhibitors of this enzyme. On the other hand, Trp-P-2 activated MART-A at all concentrations tested, the peak being at 3 mM (>171% increase). In contrast, 3-amino-1,4-dimethyl-5H-pyrido[4,3-b]indole (Trp-P-1) inhibited concentration-dependently both enzymes, PARP-1 (IC50 = 0.22 mM) and MART-A (IC50 = 2.8 mM). With nine other HCAs tested, predominantly inhibitory effects were observed. These results may assist our understanding of the carcinogenic mechanism of action and the dose-dependency of HCAs in animal bioassays.

15

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Development of hammerhead ribozymes targeting miR-21

75%

Belter A., Naskret-Barciszewska M. Z.

BioTechnologia. Journal of Biotechnology Computational Biology and Bionanotechnology

|

2014

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tom 95

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nr 4

16

Non-specific inflammatory bowel diseases and the risk of tumour growth

75%

Dudzinska E., Gryzinska M., Ognik K., Krauze M., Listos P.

Medycyna Weterynaryjna

|

2018

|

tom 74

|

nr 04

Inflammatory bowel disease (IBD), which includes mainly ulcerative colitis (UC) and Crohn’s disease (Lesniowski-Crohn’s, ChL-C, CD), is a chronic and recurrent inflammatory condition of the gastrointestinal tract with multifactorial causes. Both types of IBD are characterized by chronic inflammation with periods of remission and exacerbation. An increasing number of studies have recently shown that chronic inflammation plays an important role in the carcinogenesis of colorectal cancer (CRC), generating suitable microenvironments for the formation and progression of the disease. The main factors are chronic inflammation as well as the scope and duration of the disease. The pro-inflammatory interleukins IL-13, IL-8 and TNF-α play an important role in tumorigenesis. It is further emphasized that reactive oxygen species (ROS) and reactive nitrogen species produced by inflammatory cells may interact with key genes involved in carcinogenic pathways, such as TP53. Carcinogenesis in IBD involves proteins determined by the genes DLG5, OCTN and NOD2. Immunosuppressive drugs, such as thiopurines and methotrexate, may play a role in extra-intestinal tumour development by impairing the immune system and surveillance of tumour cells or by inducing DNA damage. Recognition of neoplastic changes associated with IBD is difficult due to the heterogeneity of the endoscopic image and variation in the diagnosis depending on the observer. Therefore surveillance of IBD patients by a multidisciplinary team is essential for early detection of the neoplastic process.

17

Protein phosphatase 2A: Variety of forms and diversity of functions

75%

Lechward K., Awotunde O. S., Swiatek W., Muszynska G.

Acta Biochimica Polonica

|

2001

|

tom 48

|

nr 4

Protein phosphatase 2A (PP2A) comprises a diverse family of phosphoserine- and phosphothreonine-specific phosphatases present in all eukaryotic cells. All forms of PP2A contain a catalytic subunit (PP2Ac) which forms a stable complex with thestructural subunit PR65/A. The heterodimer PP2Ac-PR65/A associates with regulatory proteins, termed variable subunits, in order to form trimeric holoenzymes attributed with distinct substrate specificity and targeted to different subcellular compartments. PP2Ac activity can be modulated by reversible phosphorylation on Tyr307 and methylation on C-terminal Leu309. Studies on PP2A have shown that this enzyme may be implicated in the regulation of metabolism, transcription, RNA splicing, translation, differentiation, cell cycle, oncogenic transformation and signal transduction.

18

Telomerase as a therapeutic target

75%

Huminiecki L.

Acta Biochimica Polonica

|

1996

|

tom 43

|

nr 3

Ribonucleoprotein telomerase is an enzyme that elongates telomeric DNA. In cells without detectable telomerase activity telomeres shorten with every cell generation and reaching critical length is a signal for cell death. Normal human somatic cells express undetectable, or low (bone marrow and peripheral leukocytes), telomerase activity. Reactivation of telomerase (immortalization) is probably necessary during development of a fully malignant cancer. Consequently, telomerase was proposed to be a therapeutic target for the cancer therapy. Potential results (including side-effects) of telomerase inhibition are being considered. After all, telomerase inhibition can be useful not only in the therapy, but also in cancer biology research, elucidating ageing and immortalization phenomena.

19

The inhibition of protein kinase C by hepatitis C virus non-structural protein 3 depends on its conformational status

75%

Borowski P., Hartjen P.

Cellular and Molecular Biology Letters

|

2003

|

tom 08

|

nr 2A

20

Individual susceptibility to lung cancer in Polish population - polymorphism of NER genes

75%

Butkiewicz D., Rusin M., Chorazy M.

Folia Histochemica et Cytobiologica. Supplement

|

2001

|

tom 39

|

nr 1

Ograniczanie wyników

Uncertainty in biological modelling

Carcinogenesis, an overview with special reference to endocrine disrupting mechanisms