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1
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Nowy paradygmat: Onkogeny a czynniki wzrostu

100%
Szala S., Śląska Akademia Medyczna I. O.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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1988
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vol. 6
EN
In this short review the ability of protooncogenes to make cancer cells autonomous in respect to growth factors requirements has been discussed.
2
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Antitumour activity of Salmonella typhimurium VNP20047 in B16(F10) murine melanoma model.

64%
Jazowiecka-Rakus J., Szala S.
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vol. 51
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issue 3
851-856
EN
A tumour therapy is proposed based on attenuated Salmonella typhimurium VNP20047 expressing the Escherichia coli cytosine deaminase gene. VNP20047 was administered intravenously to B16(F10) melanoma-bearing C57BL/6 mice. VNP20047 proliferated within tumours and livers regardless of the initial inoculum dose. After 10 days the number of bacteria increased in livers up to 4.2 × 106 cfu/g and decreased in tumours down to 5.9 × 106 cfu/g. VNP20047 at 1 × 105 cfu/mouse, when combined with 5-fluorocytosine, inhibited tumour growth by 85% without prolonging animal survival. Histology studies revealed severe lesions in tumours and livers. These data suggest that S. typhimurium VNP20047 induced inflammatory responses, even though the strain was attenuated.
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Recombinant angioarrestin secreted from mouse melanoma cells inhibits growth of primary tumours

52%
Smagur A., Szary J., Szala S.
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2005
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vol. 52
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issue 4
875-879
EN
Angioarrestin is a recently described anti-angiogenic protein whose expression is down-regulated in solid tumours of various origins. It has a sequence identical to angiopoietin related protein-1. In this study we investigated anti-tumour properties of angioarrestin in B16 (F10) melanoma tumour model. We constructed an expression vector encoding human angioarrestin under the control of EF-1α promoter. This vector was transferred to B16 (F10) cells and recombinant angioarrestin secreted from the transfected cells was tested for anti-angiogenic activity using endothelial cell proliferation assay. Finally, mice were injected subcutaneously with cells that had been transfected with either angioarrestin-encoding vector or empty vector and tumor growth was compared. The obtained recombinant angioarrestin inhibited proliferation of bovine aortic endothelial cells. Tumours derived from an angioarrestin-secreting B16 (F10) cell clone grew in vivo more slowly than tumours derived from a cell clone transfected with empty vector. These data show, to our knowledge for the first time, that angioarrestin can inhibit primary melanoma tumour growth.
4
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Combination of vasostatin gene therapy with cyclophosphamide inhibits growth of B16(F10) melanoma tumours

52%
Jazowiecka-Rakus J., Jarosz M., Szala S.
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2006
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vol. 53
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issue 1
199-202
EN
Angiogenesis, i.e. formation of new blood vessels out of pre-existing capillaries, is essential to the development of tumour vasculature. The discovery of specific antiangiogenic inhibitors has important therapeutic implications for the development of novel cancer treatments. Vasostatin, the N-terminal domain of calreticulin, is a potent endogenous inhibitor of angiogenesis and tumour growth. In our study, using B16(F10) murine melanoma model and electroporation we attempted intramuscular transfer of human vasostatin gene. The gene therapy was combined with antiangiogenic drug dosing schedule of a known chemotherapeutic (cyclophosphamide). The combination of vasostatin gene therapy and cyclophosphamide administration improved therapeutic effects in melanoma tumours. We observed both significant inhibition of tumour growth and extended survival of treated mice. To our knowledge, this is one of the first reports showing antitumour efficacy of electroporation-mediated vasostatin gene therapy combined with antiangiogenic chemotherapy.
5
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Antiangiogenic gene therapy in inhibition of metastasis.

52%
Szala S., Szary J., Cichoń T., Sochanik A.
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2002
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vol. 49
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issue 2
313-321
EN
This short review attempts to demonstrate the usefulness of antiangiogenic gene therapy in achieving inhibition of growth in experimentally-induced metastases. Certain normal tissues (for example skeletal muscle) may be used in vivo, after genetic modification, as a "bioreactor", able to produce and secrete into the bloodstream proteins known to exert antiangiogenic effects. By inhibiting neoangiogenesis these proteins would thus prevent the development of metastases. The review discusses also the perspectives of antimetastatic therapy based on certain types of allogenic cells (for example myoblasts and fibroblasts) that had been genetically modified and then microencapsulated. The strategy of encapsulation is aimed at protecting the modified cells secreting antiangiogenic factors from being eliminated by the immune system. Secretion of antiangiogenic proteins by these microencapsulated cells can be controlled with inducible promoters. Antiangiogenic genes remaining under the transcriptional control of such promoters may be switched on and off using antibiotics, such as tetracycline derivatives, or steroid hormones.
6
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Various cationic carriers for in vitro transfection of tumor and endothelial cell lines.

52%
Zemlińska B., Sochanik A., Missol-Kolka E., Szala S.
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2002
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vol. 49
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issue 1
285-290
EN
We compared the efficiency of in vitro DNA transfer into selected tumor and endothelial cell lines using complexes of plasmid DNA and cationic carriers: DDAB/DOPE, DC-Chol/DOPE, Arg-Chol/DOPE, Gly-Chol/DOPE, Arg-Gly-Chol/DOPE, BGTC/DOPE, and PEI. The best carriers for transfecting the majority of tested cells lines at optimized carrier-to-DNA weight ratios were PEI and BGTC/DOPE.
7
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Combination of combretastatin A4 phosphate and doxorubicin-containing liposomes affects growth of B16-F10 tumors

52%
Mitrus I., Sochanik A., Cichoń T., Szala S.
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issue 1
161-165
EN
The study aimed to check the effectiveness of anticancer therapy combining a vascular-disruptive drug (combretastatin phosphate, CA4P) and a liposomal formulation of a chemotherapeutic (doxorubicin). CA4P was synthesized in our laboratory according to a previously described procedure. The antivascular drug and long-circulating doxorubicin-loaded liposomes were used to treat B16-F10 murine melanoma experimental tumors. Seventy-four hours after drug administration, a decrease in the number of tumor blood vessels was apparent and necrotic areas within tumors were visible. Combination therapy consisting of alternate administrations of CA4P and liposomal doxorubicin yielded greater inhibition of tumor growth than monotherapies alone. The best therapeutic results were obtained with the antivascular drug administered intratumorally every second day at 50 mg/kg body mass. In the case of combined therapy, the best results were obtained when the vascular-disruptive agent (CA4P) and the antineoplastic agent (liposomal doxorubicin) were administered in alternation.
8
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Inhibition of tumor growth by interleukin 10 gene transfer in B16(F10) melanoma cells

52%
Walos S., Szary J., Szala S.
Acta Biochimica Polonica
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1999
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vol. 46
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issue 4
967-970
EN
Interleukin 10 (IL-10) is a potent immunosuppressive cytokine with an antitumor activity. The effect of IL-10 on tumor growth was tested in murine melanoma cells manipulated by gene transfer to secrete IL-10. In mice bearing B16(F10) tumors expressing IL-10  tumor growth was decreased depending on the amount of secreted IL-10.
9
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Direct transfer of IL-12 gene into growing Renca tumors.

52%
Budryk M., Wilczyńska U., Szary J., Szala S.
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2000
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vol. 47
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issue 2
385-391
EN
We investigated the feasibility of transferring naked plasmid DNA containing a therapeutic gene (IL-12) into mice harboring growing Renca tumors. We found that naked DNA transferred into growing Renca and B16(F10) tumors gives higher expression level of reporter gene than complexes of DNA with DDAB/ DOPE or DC-Chol/DOPE. Transfer of naked DNA carrying the IL-12 gene into growing Renca tumors causes a distinct therapeutic effect that depends on the time span between inoculation of mice with cancer cells and the beginning of the therapy. Therapy started on day 3 resulted in total cure (100%) of mice.
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Direct in vivo transfer of plasmid DNA into murine tumors: Effects of endotoxin presence and transgene localization.

52%
Budryk M., Cichoń T., Szala S.
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EN
The purpose of this study was to investigate the effect of endotoxin presence in plasmid DNA preparations on the efficiency of transfection achieved in vivo with B16(F10) and Renca tumors and to determine transgene localization. Our data show that endotoxin markedly decreases the efficiency of transfection. Furthermore, the transgene transferred in vivo can be found in both neoplastic and normal (most likely myofibroblast) cells lying in proximity of the administration site.
11
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Combined delivery of an antiangiogenic protein (angiostatin) and an immunomodulatory gene (interleukin-12) in the treatment of murine cancer.

52%
Wilczyńska U., Kucharska A., Szary J., Szala S.
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2001
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vol. 48
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issue 4
1077-1084
EN
We investigated the feasibility of a novel therapeutic approach to treat neoplastic diseases in mice. This novel strategy consists in delivering a protein (angiostatin) with strong antiangiogenic properties, followed by administration of the interleukin 12 gene that is strongly immunomodulatory and has also some antiangiogenic effects. When angiostatin-mediated antiangiogenic therapy was used in combination with intratumor delivery of the IL-12 gene (a strategy much safer than IL-12 protein administration), this produced a synergistic therapeutic effect.
12
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CEA-negative glioblastoma and melanoma cells are sensitive to cytosine deaminase/5-fluorocytosine therapy directed by the carcinoembryonic antigen promoter.

45%
Dąbrowska A., Szary J., Kowalczuk M., Szala S., Ugorski M.
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vol. 51
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issue 3
723-732
EN
Recent studies have suggested that carcinoembryonic antigen (CEA)-promoter sequences are active only in CEA-positive cells, filing in the criteria for tumor specific targeting of suicide genes. However, the present study on gene therapy of colon cancer and cell-specificity of CEA promoter, provide evidence that CEA-positive and CEA-negative cells transfected with E. coli cytosine deaminase (CD) gene under the control of CEA promotor sequence are sensitive to enzyme/pro-drug therapy with 5-fluorocytosine (5-FC). Individual clones derived from the CEA-negative cell lines: melanoma Hs294T and glioblastoma T98G after transfection with CD differed profoundly in their sensitivity to 5-FC. The IC50 values for several clones of the CEA-negative cells were almost the same as for CEA-positive colon cancer cells. Such 5-FC-sensitive clones derived from the population of CEA-negative cells, present even in small number, because of the very effective bystender effect of this enzyme/pro-drug system can cause severe problems during therapy by efficiently killing surrounding normal cells. Safety is the major issue in gene therapy. Our data suggest that the safety of gene-directed enzyme pro-drug therapy (GDEPT) with CEA promoter driven expression of therapeutic genes is not so obvious as it has originally been claimed.
13
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Combination of IL-12 gene therapy and CTX chemotherapy inhibits growth of primary B16(F10) melanoma tumors in mice

45%
Mitrus I., Delić K., Wróbel N., Missol-Kolka E., Szala S.
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2006
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vol. 53
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issue 2
357-360
EN
We investigated suppression of murine B16(F10) melanoma tumor growth following a therapy which involved concomitant administration of cyclophosphamide and plasmid DNA bearing interleukin-12 gene. Since both therapeutic factors display antiangiogenic capabilities, we assumed that their use in blocking the formation of new blood vessels would result in augmented inhibition of tumor growth. This combined therapy regimen indeed resulted in a considerable suppression of tumor growth. We observed a statistically significant extension of treated animals' lifespan. Interestingly, the therapeutic effect was also obtained using a plasmid without an interleukin gene insert. This observation suggests that plasmid DNA, which has been widely applied for treating neoplastic tumors, contains element(s) that elicit immune response in mice.
14
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Combination of vasostatin and cyclophosphamide in the therapy of murine melanoma tumors

45%
Jazowiecka-Rakus J., Jarosz M., Kozłowska D., Sochanik A., Szala S.
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2007
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vol. 54
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issue 1
125-133
EN
Growth of tumors is strongly dependent upon supply of nutrients and oxygen by de novo formed blood vessels. Inhibiting angiogenesis suppresses growth of primary tumors as well and affects development of metastases. We demonstrate that recombinant MBP/vasostatin fusion protein inhibits proliferation of endothelial cells in vitro. The therapeutic usefulness of such intratumorally delivered recombinant protein was then assessed by investigating its ability to inhibit growth of experimental murine melanomas. In the model of B16-F10 melanoma the MBP/vasostatin construct significantly delayed tumor growth and prolonged survival of treated mice. A combination therapy involving MBP/vasostatin construct and cyclophosphamide was even more effective and led to further inhibition of the tumor growth and extended survival. We show that such combination might be useful in the clinical setting, especially to treat tumors which have already formed microvessel networks.
15
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Chimeric protein ABRaA-VEGF121 is cytotoxic towards VEGFR-2-expressing PAE cells and inhibits B16-F10 melanoma growth

45%
Smagur A., Boyko M. M., Biront N. V., Cichoń T., Szala S.
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issue 1
115-124
EN
It has been known that VEGF121 isoform can serve as a carrier of therapeutic agents targeting tumor endothelial cells. We designed and constructed synthetic cDNA that encodes a chimeric protein comprising abrin-a (ABRaA) toxin A-chain and human VEGF121. Expression of the ABRaA-VEGF121 chimeric protein was carried out in E. coli strain BL21(DE3). ABRaA-VEGF121 preparations were isolated from inclusion bodies, solubilized and purified by affinity and ion-exchanged chromatography (Ni-agarose and Q-Sepharose). Finaly, bacterial endotoxin was removed from the recombinant protein. Under non-reducing conditions, the recombinant protein migrates in polyacrylamide gel as two bands (about 84 kDa homodimer and about 42 kDa monomer). ABRaA-VEGF121 is strongly cytotoxic towards PAE cells expressing VEGFR-2, as opposed to VEGFR-1 expressing or parental PAE cells. The latter are about 400 times less sensitive to the action of this fusion protein. The biological activity of the ABRaA domain forming part of the chimeric protein was assessed in vitro: ABRaA-VEGF121 inhibited protein biosynthesis in a cell-free translation system. Preincubation of ABRaA-VEGF121 with antibody neutralizing the biological activity of human VEGF abolished the cytotoxic effect of the chimeric protein in PAE/KDR cells. Experiments in vivo demonstrated that ABRaA-VEGF121 inhibits growth of B16-F10 murine melanoma tumors.
16
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Transcription of rat DNA fractions reassociated to various C_0t values

45%
Grabowska M., Szala S., Chorąży M.
Acta Biochimica Polonica
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1977
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vol. 24
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issue 2
143-151
17
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Antitumor effect of RGD-4C-GG-D(KLAKLAK)2 peptide in mouse B16(F10) melanoma model

39%
Smolarczyk R., Cichoń T., Graja K., Hucz J., Sochanik A., Szala S.
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2006
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vol. 53
|
issue 4
801-805
EN
Vasculature targeting agents have been tested as cancer therapeutics for the past few years. Such therapy could be accomplished using, for example, bifunctional (two-domain) peptides. RGD-4C-GG-D(KLAKLAK)2, a peptide designed by Ellerby and coworkers (1999) (full sequence: ACDCRGDCFCGGKLAKLAKKLAKLAK), binds selectively to αVβ3 integrin receptors expressed in tumor neovasculature and, after internalization, effectively induces apoptosis of endothelial cells. The aim of this study was to examine if RGD-4C-GG-D(KLAKLAK)2 would efficiently target cells, among them B16(F10), that overexpress αVβ3 receptors, and whether it would be suitable for therapeutic treatment of primary B16(F10) murine melanoma tumors. Thus, the peptide would target two distinct tumor compartments: that formed by endothelium of blood vessels and that made up of neoplastic cells. The therapeutic peptide was recognized and did induce apoptosis in B16(F10) cell line. Tumor growth inhibition was observed following direct intratumoral administration. However, cessation of peptide administration led to rapid tumor growth and death of the animals.
18
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In vivo gene transfer using cetylated polyethylenimine.

39%
Sochanik A., Cichoń T., Makselon M., Stróżyk M., Smolarczyk R., Jazowiecka-Rakus J., Szala S.
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vol. 51
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issue 3
693-702
EN
This report describes gene transfer in vitro as well as in vivo using cetylated low-molecular mass (600 Da) polyethylenimine (28% of amine groups substituted with cetyl moieties), termed CT-PEI. This compound is hydrophobic and has to be incorporated into liposomes in order to be suitable for gene transfer studies. Serum-induced plasmid DNA degradation assay demonstrated that CT-PEI-containing liposomal carriers could protect complexed DNA (probably via condensation). In vitro luciferase gene expression achieved using medium supplemented with 10% serum was comparable to that achieved in serum-reduced medium and was highest for CT-PEI/cholesterol liposomes, followed by CT-PEI/dioleoylphosphatidylcholine liposomes and PEI 600 Da (uncetylated) carrier. In vivo systemic transfer into mice was most efficient when liposome formulations contained CT-PEI and cholesterol. Higher luciferase expression was then observed in lungs than in liver. In conclusion: liposomes containing cetylated polyethylenimine and cholesterol are a suitable vehicle for investigating systemic plasmid DNA transfer into lungs.
19
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Complexity of liver mRNA from normal and thioacetamide-treated rats

39%
Wągiel B., Szala S., Chorąży M.
Acta Biochimica Polonica
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1982
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vol. 29
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issue 1-2
111-119
20
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On the strategy of using nonviral carriers in cancer gene therapy

38%
Sochanik A., Szala S.
Acta Biochimica Polonica
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1996
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vol. 43
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issue 2
293-300
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