Wyniki wyszukiwania - Biblioteka Nauki

1

The expression of HSP 27, HSP 70 and HSP 90 in U937 sublines exhibiting different patterns of sensitivity to TNF

100%

Pierzchalski A. , Sychowska D. , Bartczak M. , Bigda J.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

|

nr Suppl.

2

Application in tumor therapy of cells engineered to express new biologically active molecules

88%

Jakobisiak M.

Folia Histochemica et Cytobiologica. Supplement

|

1997

|

tom 35

|

nr 2

3

A novel apoptosis-like cell death, independent of caspase-3, induced by curcumin

88%

Sikora E.

Cellular and Molecular Biology Letters

|

2000

|

tom 05

|

nr 2

4

Application of photodynamic therapy in the sterilisation of tumour cells transplanted into laboratory animals

75%

Jurczyszyn K. , Ziolkowski P. , Klytta M. , Piasecki T.

Bulletin of the Veterinary Institute in Puławy

|

2009

|

tom 53

|

nr 1

123-128

EN

In this study, we tried to estimate the effectiveness of the antimicrobial activity of photodynamic therapy (PDT) without the destruction of tumour cells. Chlorin e6 in concentrations from 0.05 to 1.0 µg/mL and total dose of light 100 J/sq.cm were used. Samples from different tumours were tested for a presence of bacteria. Next, cells from the same tumours were treated with chlorin e6-PDT, chlorin e6, and light alone, or not treated. The survival rate was counted, and the cells were injected back into the animals. PDT caused the eradication of bacteria such as Proteus sp., Streptococcus α-haemolyticus, and others: the specimen became aseptic. After Ce6-PDT treatment and in control groups, tumour growth was observed in all rats 7-10 d after transplantation. The tumours were palpable and macroscopically visible. Our studies showed that PDT kills bacterial flora without the destruction of tumour cells. Thus, tumour cells free of bacteria could be used for other experiments.

5

Potential role of transforming growth factor beta 1 in drug resistance of tumor cells

75%

Stoika R. , Yakymovych M. , Souchelnytskyi S. , Yakymovych I.

Acta Biochimica Polonica

|

2003

|

tom 50

|

nr 2

EN

Acquired drug resistance of tumor cells is frequently observed in cancer patients undergoing chemotherapy. We studied murine leukemia L1210 cells sensitive and resistant to the cytotoxic action of cisplatin and showed that cisplatin-resistant leukemia cells were also refractory to TGF /β1-dependent growth inhibition and apoptosis. Addressing the question about the mechanisms responsible for the cross-resistance to cisplatin and TGF /β1, we found that cisplatin- and TGF /β1-resistant L1210 cells possessed a decreased expression of type I TGF /β1 receptor, while the expression of type II TGFβ1 receptor was not affected. Western blot analysis of Smad proteins 2, 3, 4, 6, and 7, which participate in signal transduction pathway down-stream of the TGF /β1 receptors, revealed an increased expression of Smad 6, inhibiting TGF β1 action, only in cisplatin- and TGFβ1-resistant L1210 cells. TGFβ1 and especially the cytotoxic mistletoe agglutinin increased Smad 6 expression in TGF β1-sensitive but not in TGF /β1-resistant L1210 cells. TGF /β1-resistant L1210 cells also differed from TGF /β1-sensitive cells by the lack of expression of the pro-apoptotic p53 protein and higher level of expression of the anti-apoptotic Bcl-2 protein. Thus, the described co-expression of tumor cell refractoriness to an anti-cancer drug and to the inhibitory cytokine TGF β1 is accompanied by multiple changes in the TGF β1 signal transduction pathway and in other regulatory systems of the target cells. Besides, we found that various anti-tumor drugs and cytotoxic plant lectins increased the level of TGF β1 expression in both TGF β1-sensitive and -resistant L1210 cells. A hypothesis is proposed that TGF β1 can at least partly mediate the effect of cell-stressing agents and, thus, the development of TGF β1 resistance may be responsible for the appearance of tumor cell refractoriness to the action of some anti-cancer drugs.

6

Apoptotic polykaryons, chromatin diminution and survival mechanism in polyploid giant cells derived from P53 mutant lymphoma cell lines after genotoxic damage

75%

Erenpreisa J. , Cragg M. S. , Alston R. , Page A. , Illidge T. M.

Cellular and Molecular Biology Letters

|

2000

|

tom 05

|

nr 2

7

The shape of cells adhering to sulfonated copolymer surfaces

75%

Kowalczynska H. M. , Nowak-Wyrzykowska M. , Inkielman M. , Stolowska L. , Marciniak E.

Cellular and Molecular Biology Letters

|

2005

|

tom 10

|

nr 1

8

Echinococcus multilocularis: the effect of alveolar hydatid cyst extract on the viability and blastogenic response of murine splenocytes and the K562 tumor cell in vitro

75%

Alkarmi T. , Dar F. K. , Abdo S. , Lazarus A. , Ali-Khan Z.

Acta Parasitologica

|

1994

|

tom 39

|

nr 2

9

Different isoenzyme patterns of nonspecific esterases and the level of IL6 production as markers of macrophage functions

75%

Czajkowska B. , Ptak M. , Bobek M. , Bryniarski K. , Szczepanik M.

|

tom 33

|

nr 2

10

Intensive tumor suppression by anti-angiogenic photodynamic therapy with polycation-modified liposomal photosensitizer

75%

Takeuchi Y. , Kurohane K. , Nango N. , Oku N.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

|

nr 2

11

Induction of apoptosis in vitro using epigallocatechin-3-gallate [EGCG] in selected tumour cells

75%

Borska S. , Gebarowska E. , Wysocka T. , Drag-Zalesinska M. , Zabel M.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

|

nr Suppl.

12

Cancer immunogene therapy

75%

Yoshizawa H. , Kagamu H. , Gejyo F.

Archivum Immunologiae et Therapiae Experimentalis

|

2001

|

tom 49

|

nr 5

13

Strategies for the discovery of novel inhibitors of cyclin-dependent kinases

75%

Zaharevitz D. , Gussio R. , Meijer L. , Leost M. , Kunick C. , Schultz C. , Senderowicz A. , Lahusen T. , Sausville E.

Cellular and Molecular Biology Letters

|

1998

|

tom 03

|

nr 3

14

A single nucleotide polymorphism in the matrix metalloproteinase-1 promoter in breast cancer

75%

Przybylowska K. , Zielinska J. , Zadrozny M. , Rykala J. , Kolacinska A. , Morawiec Z. , Drzewoski J. , Blasiak J.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

|

nr Suppl.

15

Strategies for overcoming ABC-transporters-mediated multidrug resistance [MDR] of tumor cells

75%

Borowski E. , Bontemps-Gracz M. M. , Piwkowska A.

Acta Biochimica Polonica

|

2005

|

tom 52

|

nr 3

EN

The development of multidrug resistance (MDR) of tumors is a major cause of failure in antitumor chemotherapy. This type of crossresistance is due to the expression of ABC transporter glycoproteins actively effluxing the drug from the cells against the concentration gradient at the expense of metabolic energy, thus preventing the accumulation in cells of therapeutic concentration of active agents. In this review strategies for overcoming this adverse phenomenon are discussed. They comprise the control of expression of MDR glycoprotein transporters and control of the functioning of the expressed transporter proteins. The latter approach is discussed in more detail, comprising the following general strategies: (i) development of compounds that are not substrates of efflux pump(s), (ii) use of agents that inactivate (inhibit) MDR proteins, (iii) design of cytostatics characterized by fast cellular uptake, surpassing their mediated efflux, (iv) use of compounds competing with the drug for the MDR protein-mediated efflux. Positive and negative aspects of these strategies are analysed, with special attention put on strategy based on the use of MDR modulators in combination therapy, allowing the restoration of cytotoxic activity of clinical cytostatics towards resistant tumor cells.

16

In vitro cytotoxicity of the tricyclic analogues of acyclovir

75%

Wolun M. , Ciesielski M. , Goslinski T. , Warchol J. B. , Golankiewicz B.

Cellular and Molecular Biology Letters

|

1999

|

tom 04

|

nr 3

17

Tranformation of a human mixed GH-PRL adenoma cell population in response to long-term bromocriptine treatment

75%

Bacsy E. , Fazekas I. , Slowik F. , Pasztor E. , Czirjak S.

Folia Histochemica et Cytobiologica

|

1997

|

tom 35

|

nr 2

18

Adhesion and metastases

75%

Janik P. , Malecki M.

Cellular and Molecular Biology Letters

|

2002

|

tom 07

|

nr Suppl.

19

Purine nucleoside phosphorylases: properties, functions, and chemotherapeutic applications

75%

Shugar D.

Cellular and Molecular Biology Letters

|

1999

|

tom 04

|

nr 3

20

Accumulation of collagen in ovarian benign tumours

75%

Wolanska M. , Sobolewski K. , Bankowski E. , Drozdzewicz M.

|

nr 4

EN

Extracellular matrix components of benign ovarian tumours (cystadenoma, adenofibroma, cystadenofibroma) were analysed. The investigated tumours contained twice as much collagen than control ovarian tissues. Significant alterations in mutual quantitative relationships between collagens of various types were observed. The proportion of type I collagen decreased and that of type III collagen increased. The accumulation of collagen was accompanied by a reduction in sulphated glycosaminoglycan content whereas the amount of hyaluronic acid was not changed. Dermatan sulphate was the most abundant glycosaminoglycan component. It is suggested that the accumulation of collagen (natural barrier to the migration of tumour cells) and underexpression of glycosaminoglycans/proteoglycans (binding some growth factors and interleukins) may exert an inhibitory effect on tumour growth.