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1
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Partition coefficient of organophosphorus insecticides evaluated by fluorescence quenching

100%
Błasiak J., University of Łódź D. o. M. G.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1996
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vol. 11
PL
Badając tłumienie fluorescenęji przez malation i metyloparation stwierdzono, że pierwszy związek nie tłumi iluorescencji żadnego ze stosowanych w badaniach znaczników (perylen i ANS). Opisując tłumienie za pomocą równania Stema-Volmera stwierdzono, że metyloparation wiązał się z liposomami utworzonymi z fasfatydylocholiny. Wiązanie to wykazywało silną zależność od stężenia insektycydu. Wiązanie insektycydu było znacznie słabsze, gdy liposomy tworzone były z różnych ilośd molowych fosfatydylocholiny i cholesterolu. Tłumienie iluorescencji było wyraźniejsze, gdy stosowano znacznik wiążący się z rdzeniem dwuwarstwy lipidowej (perylen), niż wówczas, gdy stosowano znacznik wiążący się z bardziej zewnętrznym obszarem dwuwarstwy (ANS). Uzyskane wyniki wskazują, że wiązanie niektórych insektycydów fosforoorganicznych może być zmieniane przez cholesterol.
2
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Kinetic properties of the (Ca²+ + Mg²+)-ATPase bound to and extracted from the pig erythrocyte membrane

100%
Błasiak J., University of Łódź D. o. M. G.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1996
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vol. 11
3
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Non-homologous DNA end joining.

64%
Pastwa E., Błasiak J.
|
2003
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vol. 50
|
issue 4
891-908
EN
DNA double-strand breaks (DSBs) are a serious threat for the cell and when not repaired or misrepaired can result in mutations or chromosome rearrangements and eventually in cell death. Therefore, cells have evolved a number of pathways to deal with DSB including homologous recombination (HR), single-strand annealing (SSA) and non-homologous end joining (NHEJ). In mammals DSBs are primarily repaired by NHEJ and HR, while HR repair dominates in yeast, but this depends also on the phase of the cell cycle. NHEJ functions in all kinds of cells, from bacteria to man, and depends on the structure of DSB termini. In this process two DNA ends are joined directly, usually with no sequence homology, although in the case of same polarity of the single stranded overhangs in DSBs, regions of microhomology are utilized. The usage of microhomology is common in DNA end-joining of physiological DSBs, such as at the coding ends in V(D)J (variable(diversity) joining) recombination. The main components of the NHEJ system in eukaryotes are the catalytic subunit of DNA protein kinase (DNA-PKcs), which is recruited by DNA Ku protein, a heterodimer of Ku70 and Ku80, as well as XRCC4 protein and DNA ligase IV. A complex of Rad50/Mre11/Xrs2, a family of Sir proteins and probably other yet unidentified proteins can be also involved in this process. NHEJ and HR may play overlapping roles in the repair of DSBs produced in the S phase of the cell cycle or at replication forks. Aside from DNA repair, NHEJ may play a role in many different processes, including the maintenance of telomeres and integration of HIV-1 genome into a host genome, as well as the insertion of pseudogenes and repetitive sequences into the genome of mammalian cells. Inhibition of NHEJ can be exploited in cancer therapy in radio-sensitizing cancer cells. Identification of all key players and fundamental mechanisms underlying NHEJ still requires further research.
4
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Interaction between organophosphorus compounds and DNA assayed by the restriction endonuclease EcoRI

64%
Błasiak J., Kowalik J., University of Łódź D. o. M. G.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1998
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vol. 13
PL
Enzymy restrykcyjne ze względu na istotę swojego działania mogą być źródłem informacji na temat miejsca lub specyficzności sekwencyjnej wiązania substancji do DNA. Z drugiej strony, działanie enzymów może być zaburzone przez związki mające zdolność do metylacji zasad DNA. Cecha ta może być wykorzystywana do pierwotnej selekcji związków potencjalnie genotoksycznych. W pracy badano działanie enzymu restrykcyjnego £coRI na DNA, które było uprzednio inkubowane ze związkami fosforoorganicznymi. DNA plazmidu pUC19 0 stężeniu 78 μg/ml był inkubowany przez 72 h z insektycydami fosforoorganicznymi parationem i metyloparationem oraz z ich głównymi metabolitami, odpowiednio paraoksonem 1 metyloparaoksonem o stężeniu 300 μM. Po inkubacji nie związane insektycydy były usuwane przez ultrafiltrację, a DNA poddawano 1 h inkubacji z endonukleazą restrykcyjną EcoRI i analizowano przez elektroforezę w 0.8% żelu agarozowym. Związek fosforoorganiczny metyloparaokson powodowa! rozwinięcie superskręconego DNA plazmidu pUC19, a działanie EcoRI na ten DNA było zaburzone, co znalazło swe odbicie w zmienionym obrazie elektroforetycznym.
5
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Recognition and repair of DNA-cisplatin adducts.

64%
Woźniak K., Błasiak J.
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2002
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vol. 49
|
issue 3
583-596
EN
Anticancer activity of cisplatin (cis-diamminedichloroplatinum) is believed to result from its interaction with DNA. The drug reacts with nucleophilic sites in DNA forming monoadducts as well as intra- and interstrand crosslinks. DNA-cisplatin adducts are specifically recognized by several proteins. They can be divided into two classes. One constitutes proteins which recognize DNA damage as an initial step of the nucleotide excision and mismatch repair pathways. The other class contains proteins stabilizing cellular DNA-protein and protein-protein complexes, including non-histone proteins from the HMG (high-mobility-group) family. They specifically recognize 1,2-interstrand d(GpG) and d(ApG) crosslinks of DNA-cisplatin adducts and inhibit their repair. Many HMG-domain proteins can function as transcription factors, e.g. UBF, an RNA polymerase I transcription factor, the mammalian testis-determining factor SRY and the human mitochondrial transcription factor mtTFA. Moreover, it seems that some proteins, which probably recognize DNA-cisplatin adducts non-specifically, e.g. actin and other nuclear matrix proteins, can disturb the structural and functional organization of the nucleus and whole cell. The formation of complexes between DNA and proteins in the presence of cisplatin and the changes in the cell architecture may account for the drug cytotoxicity.
6
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Comparison of the DNA damaging activity of the organophosphorus insecticide m ethylparathion and its main metabolite

64%
Kowalik J., Błasiak J., University of Łódź D. o. M. G.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1998
|
vol. 13
PL
Badano zdolność indukowania uszkodzeń DNA plazmidu pUC19 przez powszechnie stosowany insektycyd fosforoorganiczny metyloparation i jego główny metabolit metyloparaokson po 72 h inkubacji z tymi związkami. Stosowano metodę elektroforezy w żelu agarozowym i analizowano zmianę intensywności pasm odpowiadających dwóm formom konformacyjnym plazmidu - kolistej superskręconej (CCC) i kolistej otwartej (OC). Metyloparation, w przeciwieństwie do swego metabolitu, nie wywoływał zmian konformacyjnych plazmidowego DNA. Działanie metyloparaoksonu powodowało przejście konformacyjne DNA z formy CCC do OC. Otrzymane rezultaty wskazują na potencjalną zdolność metyloparaoksonu do wywoływania uszkodzeń DNA in vivo.
7
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Protective action of vitamin C against DNA damage induced by selenium-cisplatin conjugate.

64%
Błasiak J., Kowalik J.
|
2001
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vol. 48
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issue 1
233-240
EN
Genotoxicity of anticancer drugs is of a special interest due to the risk of inducing secondary malignancies. Vitamin C (ascorbic acid) is a recognized antioxidant and, since human diet can be easily supplemented with vitamin C, it seems reasonable to check whether it can protect against DNA-damaging effects of antitumor drugs. In the present work the ability of vitamin C to modulate cytotoxic and genotoxic effects of a cisplatin analog, conjugate (NH3)2Pt(SeO3), in terms of cell viability, DNA damage and repair in human lymphocytes was examined using the trypan blue exclusion test and the alkaline comet assay, respectively. The conjugate evoked a concentration-dependent decrease in the cell viability, reaching nearly 50% at 250 μM. (NH3)2Pt(SeO3) at 1, 10 and 30 μM caused DNA strand breaks, measured as the increase in the comet tail moment of the lymphocytes. The treated cells were able to recover within a 30-min incubation in a drug-free medium at 37°C. Vitamin C at 10 and 50 μM diminished the extent of DNA damage evoked by (NH3)2Pt(SeO3) but had no effect on the kinetics of DNA repair. The vitamin did not directly inactivate the conjugate. Lymphocytes treated with endonuclease III, which recognises oxidised pyrimidines, displayed a greater tail moment than those untreated with the enzyme, suggesting that the damages induced by the drug have, at least in part, an oxidative origin. Vitamin C can be considered a potential protective agent against side effects of antitumor drugs, but further research with both normal and cancer cells are needed to clarify this point.
8
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Plasminogen activator inhibitor-1 (PAI-1) gene 4G/5G promoter polymorphism is not associated with breast cancer.

64%
Błasiak J., Smolarz B.
|
2000
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vol. 47
|
issue 1
191-199
EN
The antigen content of plasminogen activator inhibitor-1 (PAI-1) in primary breast cancer tissue extracts may be of strong prognostic value: high levels of PAI-1 in tumors predict poor prognosis for patients. The gene encoding PAI-1 is highly polymorphic and an insertion (5G)/deletion (4G) polymorphism in the PAI-1 gene promoter (the 4G/5G polymorphism), may have functional significance in PAI-1 expression. In the present work the distribution of genotypes and frequency of alleles of the 4G/5G polymorphism in subjects with breast cancer were investigated. Tumor tissues were obtained from 100 postmenopausal women with node-negative and node-positive ductal breast carcinoma with uniform tumor size. Blood samples from age matched healthy women served as control. The 4G/5G polymorphism was determined by PCR amplification using the allele specific primers. The distribution of the genotypes of the 4G/5G polymorphism in both control and patients did not differ significantly (P > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no differences in the genotype distributions and allele frequencies between node-positive and node-negative patients. The 4G/5G polymorphism may not be linked with elevated level of PAI-1 observed in breast cancer and therefore may not be associated with appearance and/or progression of breast cancer.
9
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Genotoxicity of the organophosphorus compound methylparaoxon evaluated by the comet assay

51%
Trzeciak A., Błasiak J., Wojewódzka M., Kowalik J., Department of Molecular Genetics U. o. L.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
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2001
|
vol. 15
EN
Pesticides are widely used in agriculture, food production and household. Due to the broad spectrum of their activity, their biological action is extensively investigated. We assessed the genotoxidty of methylparaoxon - the main metabolite of commonly used organophosphorus insecticide, methylparathion. Freshly isolated human peripheral blood lymphocytes were incubated for 1 h with methylparaoxon at 37° C, and then, were incubated in methylparaoxon-free medium to examine DNA repair. Alkaline single cell gel electrophoresis (the comet assay) was used to assess DNA damage and repair. Methylparaoxon induced moderate DNA damages that were almost completely repaired after 60 min. Obtained results suggest that methylparaoxon could induce single-strand breaks in DNA both directly and by methylathion of DNA bases.
10
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Effects of some organophosphorus in secticides on calcium, potassium and chloride effux from isolated pig lymphocytes

51%
Błasiak J., Walter Z., Gawrońska M., University of Łódź I. o. B.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1992
|
vol. 9
11
Publication available in full text mode
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The 4G /5G polymorphism in the promoter of the plasminogen activator in hibitor-1 (PAI-1) gene in subjects with cancer

51%
Błasiak J., Smolarz B., Piestrzeniewicz D., Pytel J., University of Łódź D. o. M. G.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1999
|
vol. 14
PL
Urokinazowy układ aktywacji plazminogenu zawiera enzymy proteolityczne mogące brać udział w inwazji komórek rakowych poprzez degradację macierzy zewnątrzkomórkowej i przerywaniu połączeń pomiędzy komórkami i macierzą. Wyniki znaczącej liczby eksperymentów wskazują, że zawartość przeciwciał dla jednego ze składników układu aktywacji plazminogenu inhibitora aktywatorów plazminogenu typu 1 (PAI-1), w ekstraktach z fragmentów pierwotnych guzów nowotworowych może mieć duże znaczenie prognostyczne: wysoki poziom PAI-1 źle rokuje dla pacjenta. Zademonstrowano także, że poziom PAI-1 w metastazie jest wyższy niż w guzach pierwotnych. Polimorfizm insercyjno/delecyjny 4G/5G w obszarze promotorowym genu PAI-1 może być związany z osoczowym poziomem PAI-1. W pracy badano ten polimorfizm we krwi 53 pacjentów cierpiących na różne rodzaje nowotworów (16 przypadków ra k a sutka, 12 jelita grubego, 9 żołądka, 9 czerniaków i 7 nowotworów głowy i szyi) oraz 53 odpowiednio dobranych osobników zdrowych. Częstości alleli 4G i 5G u chorych były odpowiednio: 0,53 i 0,47, podczas gdy w grupie kontrolnej wartości te wynosiły 0,43 i 0,57. Rozkłady genotypów w badanych grupach były znacząco różne - u chorych genotyp 4G/5G występował ze zwiększoną częstością niż w grupie kontrolnej. Konieczne są dalsze badania dla oceny częstości występowania danego genotypu polimorfizmu 4G/5G, jak również innych polimorfizmów, genu PAI-1 i stopniem ryzyka zapadnięcia na chorobę nowotworową.
12
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Urokinase plasminogen activation system and its role in cancer invasion and metastasis

51%
Błasiak J., Smolarz B., Piestrzeniewicz D., University of Łódź D. o. M. G.
Acta Universitatis Lodziensis. Folia Biochimica et Biophysica
|
1999
|
vol. 14
PL
Inwazyjność nowotworów i ich zdolność do przerzutowania są klinicznymi cechami progresji nowotworów i wymagają degradacji i migracji przez tkankę łączną przez komórki rakowe. Procesy te zależą od złożonego oddziaływania pomiędzy komórkami nowotworu i otaczającą macierzą zewnątrzkomórkową. Oddziaływania te są modyfikowane przez enzymy proteolityczne i ich receptory. Urokinazowy układ aktywacji plazminogenu odgrywa ważną rolę w inwazyjności nowotworów i ich zdolności do przerzutowania. Układ len zawiera urokinazowy aktywator plazminogenu (uPA), receptor urokinazowy (uPAR) i specyficzne inhibitory aktywatorów plazminogenu, PAI-1 i PAI-2. Receptor uPA może znajdować się na powierzchni komórek rakowych. uPA może być uwalniany zarówno przez komórki normalne jak i zmienione nowotworowo. Kompleks uPA-uPAR skupia aktywność proteolityczną na powierzchni komórek rakowych przez konwersję osoczowego białka plazminogenu d o proteazy serynowej plazminy. Plazmina degraduje macierz zewnątrzkomórkową w sąsiedztwie komórek rakowych ułatwiając w ten sposób inwazję nowotworów. uPA, uPAR i PAI-1 mogą być stosowane jak o markery prognostyczne w wielu typach raka.
13
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A comparison of the in vitro genotoxicity of anticancer drugs idarubicin and mitoxantrone.

51%
Błasiak J., Gloc E., Warszawski M.
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2002
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vol. 49
|
issue 1
145-155
EN
Idarubicin is an anthracycline antibiotic used in cancer therapy. Mitoxantrone is an anthracycline analog with presumed better antineoplastic activity and lesser toxicity. Using the alkaline comet assay we showed that the drugs at 0.01-10 μM induced DNA damage in normal human lymphocytes. The effect induced by idarubicin was more pronounced than by mitoxantrone (P < 0.001). The cells treated with mitoxantrone at 1 μM were able to repair damage to their DNA within a 30-min incubation, whereas the lymphocytes exposed to idarubicin needed 180 min. Since anthracyclines are known to produce free radicals, we checked whether reactive oxygen species might be involved in the observed DNA damage. Catalase, an enzyme inactivating hydrogen peroxide, decreased the extent of DNA damage induced by idarubicin, but did not affect the extent evoked by mitoxantrone. Lymphocytes exposed to the drugs and treated with endonuclease III or formamidopyrimidine-DNA glycosylase (Fpg), enzymes recognizing and nicking oxidized bases, displayed a higher level of DNA damage than the untreated ones. 3-Methyladenine-DNA glycosylase II (AlkA), an enzyme recognizing and nicking mainly methylated bases in DNA, increased the extent of DNA damage caused by idarubicin, but not that induced by mitoxantrone. Our results indicate that the induction of secondary malignancies should be taken into account as side effects of the two drugs. Direct strand breaks, oxidation and methylation of the DNA bases can underlie the DNA-damaging effect of idarubicin, whereas mitoxantrone can induce strand breaks and modification of the bases, including oxidation. The observed in normal lymphocytes much lesser genotoxicity of mitoxantrone compared to idarubicin should be taken into account in planning chemotherapeutic strategies.
14
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Changes in the fluidity of model lipid membranes evoked by the organophosphorus insecticide methylbromfenvinfos

50%
Błasiak J.
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|
vol. 40
|
issue 1
39-41
15
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Protective action of cholesterol against changes in membrane fluidity induced by methylparation

50%
Błasiak J.
|
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vol. 40
|
issue 1
35-38
16
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Expression of RUNX2 and its signaling partners TCF7, FGFR1/2 in cleidocranial dysplasia

45%
Pawłowska E., Wójcik K., Synowiec E., Szczepańska J., Błasiak J.
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2015
|
vol. 62
|
issue 1
123-126
EN
RUNX2 is a member of the PEBP2/CBF transcription factors family controlling the expression of genes whose products are essential for bone formation. Mutations in the RUNX2 gene may be associated with cleidocranial dysplasia (CCD), a rare skeletal disease characterized by stature aberrations, delayed closure of the cranial sutures, hypoplastic or aplastic clavicles, and multiple dental abnormalities. As RUNX2 is involved in many signaling pathways, we hypothesize that CCD may be associated with their changes. We determined the expression of RUNX2 and its signaling partners TCF7, involved in canonical Wnt signaling, and fibroblast growth factor receptors, FGFR1 and FGFR2 in periodontum of CCD patients and control individuals. We did not observe any differences between the level of RUNX2, TCF7 and FGFR1/2 mRNA, determined by real-time PCR, in CDD patients and controls. Therefore, RUNX2 signaling pathways with their partners TCF7 and FGFR1/2 may not be involved in CCD pathogenesis.
17
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The changes of osmotic fragility of pig erythrocytes induced by organophosphorus insecticides

45%
Błasiak J., Walter Z., Gawrońska M.
Acta Biochimica Polonica
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1991
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vol. 38
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issue 1
75-78
18
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Protective action of cholesterol against changes in membrane fluidity induced by malathion

45%
Błasiak J., Walter Z.
Acta Biochimica Polonica
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1992
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vol. 39
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issue 1
49-52
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TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.

39%
Gloc E., Warszawski M., Młynarski W., Stolarska M., Hoser G., Skorski T., Błasiak J.
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2002
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vol. 49
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issue 1
121-128
EN
The TEL/JAK2 chromosomal translocation (t(9;12)(p24;p13)) is associated with T cell childhood acute lymphoblastic leukemia. The TEL/JAK2 fusion protein contains the JAK2 catalytic domain and the TEL-specific oligomerization domain. TEL-mediated oligomerization of the TEL/JAK2 proteins results in the constitutive activation of the tyrosine kinase activity. Leukemia cells expressing TEL/JAK2 tyrosine kinase become resistant to anti-neoplastic drugs. Amifostine is a pro-drug which can selectively protect normal tissues against the toxicity of anticancer drugs and radiation. investigated the effects of amifostine on idarubicin-induced DNA damage and repair in murine pro-B lymphoid BaF3 cells and BaF3-TEL/JAK2-transformed cells using alkaline single cell gel electrophoresis (comet assay). Idarubicin induced DNA damage in both cell types but amifostine reduced its extent in control non-transformed BaF3 cells and enhanced it in TEL/JAK2-transformed cells. The transformed cells did not show measurable DNA repair after exposure to amifostine and idarubicin, but cells treated only with idarubicin were able to recover within a 60-min incubation. Because TEL/JAK2-transformed cells can be considered as model cells for certain human leukemias and lymphomas we anticipate an enhancement of idarubicin cytotoxicity by amifostine in these diseases. Moreover, TEL/JAK2 tyrosine kinase might be involved in cellular response to DNA damage. Amifostine could promote apoptosis or lower the threshold for apoptosis induction dependent on TEL/JAK2 activation.
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