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Tytuł:
Influence of G arrest on the cytotoxicity of DNA topoisomerase inhibitors toward human carcinoma cells with different p53 status.
Autorzy:
Bozko, Przemyslaw
Larsen, Annette
Raymond, Eric
Skladanowski, Andrzej
Powiązania:
https://bibliotekanauki.pl/articles/1043815.pdf
Data publikacji:
2002
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
cytotoxicity
UCN-01
p53
DNA topoisomerase inhibitors
G2 arrest
Opis:
We here report the influence of the cell cycle abrogator UCN-01 on RKO human colon carcinoma cells differing in p53 status following exposure to two DNA damaging agents, the topoisomerase inhibitors etoposide and camptothecin. Cells were treated with the two drugs at the IC90 concentration for 24 h followed by post-incubation in drug-free medium. RKO cells expressing wild-type, functional p53 arrested the cell cycle progression in both the G1 and G2 phases of the cell cycle whereas the RKO/E6 cells, which lack functional p53, only arrested in the G2 phase. Growth-arrested cells did not resume proliferation even after prolonged incubation in drug-free medium (up to 96 h). To evaluate the importance of the cell cycle arrest on cellular survival, a non-toxic dose of UCN-01 (100 nM) was added to the growth-arrested cells. The addition of UCN-01 was accompanied by mitotic entry as revealed by the appearance of condensed chromatin and the MPM-2 phosphoepitope, which is characteristic for mitotic cells. G2 exit and mitotic transit was accompanied by a rapid activation of caspase-3 and apoptotic cell death. The influence of UCN-01 on the long-term cytotoxic effects of the two drugs was also determined. Unexpectedly, abrogation of the G2 arrest had no influence on the overall cytotoxicity of either drug. In contrast, addition of UCN-01 to cisplatin-treated RKO and RKO/E6 cells greatly increased the cytotoxic effects of the alkylating agent. These results strongly suggest that even prolonged cell cycle arrest in the G2 phase of the cell cycle is not necessarily coupled to efficient DNA repair and enhanced cellular survival as generally believed.
Źródło:
Acta Biochimica Polonica; 2002, 49, 1; 109-119
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
The role of E2F2 in signaling pathways associated with cancer pathogenesis and potential treatment: A review of current studies
Autorzy:
Domańska, Julia
Poboży, Kamil
Domański, Paweł
Fudalej, Marta
Deptała, Andrzej
Badowska-Kozakiewicz, Anna
Powiązania:
https://bibliotekanauki.pl/articles/22792539.pdf
Data publikacji:
2023-07
Wydawca:
Medical Education
Tematy:
E2F2
E2F
cancer
transcription factor
oncology
p53
p21
Opis:
Introduction and objective. E2F transcription factor 2 (E2F2) protein is the transcription factor that plays an important role in tumorigenesis. E2F2 effects the cell cycle, tumor suppressor proteins, and can also be transformed by proteins of small DNA tumor viruses. The objective of the study is to provide a summary of the current knowledge on the neoplastic pathways that involve E2F2. State of knowledge. Numerous studies have demonstrated a role for E2F2 in various signaling pathways. Certain components of these pathways may serve as potential targets for oncological therapy. E2F2 has been shown to be associated with neoplasms of various locations and histological types (breast, colon, gastric, laryngeal, liver, lung, ovarian, pancreatic, and prostate cancers). Conclusions. Further investigations of E2F2 pathways are warranted for a clearer understanding of neoplastic processes and to identify novel pharmacological treatments.
Źródło:
OncoReview; 2023, 13, 2; 58-66
2450-6125
Pojawia się w:
OncoReview
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
GENTIAN VIOLET: WHAT WE KNOW AND WHAT IS AHEAD OF US
Autorzy:
Dragan, Jędrzej
Michalak, Sylwia S.
Powiązania:
https://bibliotekanauki.pl/articles/895376.pdf
Data publikacji:
2019-06-28
Wydawca:
Polskie Towarzystwo Farmaceutyczne
Tematy:
p53
Crystal Violet
Gentian Violet
fungal infection
bacterial infection
Opis:
At present, the only active substance of Gentian Violet (GV) is methylrosaniline - a triphenylmethane dye of which amino group contains 2 methyl groups. GV can be used to treat uncomplicated bacterial and/or yeast infections, support antibiotic therapy of more severe infections, but also to protect medical equipment against colonization by microorganisms. In the light of recent studies, there are many new possibilities for GV application. It has been shown to be effective in the treatment of viral infections, some chronic skin diseases and oncology. GV can induce apoptosis of tumor cells among others by elevating caspase 8, inhibiting NADPH oxidases, decreasing mitochondrial thioredoxin 2 or inhibiting STAT3/SOX2 axis. Preclinical and in vitro studies have also demonstrated GV efficacy in the treatment of breast cancer, melanoma tumors and cutaneous T-cell lymphoma. There is no unambiguous evidence indicating the toxicity of GV, whereas its safety has been proven by its long history of use, its inclusion in numerous guidelines and its legal trade and distribution with no specific approval requested in many countries around the world. The article gathers the available knowledge about GV and its potential use in the future.
Źródło:
Acta Poloniae Pharmaceutica - Drug Research; 2019, 76, 3; 389-396
0001-6837
2353-5288
Pojawia się w:
Acta Poloniae Pharmaceutica - Drug Research
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
p53 codon 72 polymorphism in cervical cancer patients and healthy women from Poland.
Autorzy:
Dybikowska, Aleksandra
Dettlaff, Agnieszka
Konopa, Krzysztof
Podhajska, Anna
Powiązania:
https://bibliotekanauki.pl/articles/1044272.pdf
Data publikacji:
2000
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
p53 gene
codon 72 polymorphism
cervical carcinoma
Opis:
A polymorphism at codon 72 of gene p53 results in the presence of either arginine or proline at this position. We investigated the distribution of p53 codon 72 polymorphism in cervical cancer patients and a control group of healthy women from Poland. Our results do not confirm the hypothesis that the p53 codon polymorphism could play a role as a factor for squamous carcinoma of the cervix.
Źródło:
Acta Biochimica Polonica; 2000, 47, 4; 1179-1182
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Immunological and genotoxic effects of occupational exposure to α-cypermethrin pesticide
Autorzy:
El Okda, El-Sayed
Abdel-Hamid, Mona A.
Hamdy, Ahmed M.
Powiązania:
https://bibliotekanauki.pl/articles/2161902.pdf
Data publikacji:
2017-06-19
Wydawca:
Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
Tematy:
p53
pyrethroids
immunological
genotoxic
cypermethrin
Oxidative stress
Opis:
Objectives The aim of this work has been to find out the occupational oxidative stress, immunological and genotoxic health hazards among α-cypermethrin (CYP) pesticide-exposed workers. Material and Methods A cross-sectional study was performed including 200 workers divided into 3 groups according to the level of exposure: highly exposed group (50 workers), moderately exposed group (50 workers) and unexposed group (100 workers). All workers were subjected to detailed laboratory investigation for gene P53 mutations, immunological parameters as a cluster of differentiation into 3 percentage (CD3%), CD4% and CD8% in addition to peripheral blood total leukocytic and platelet counts that were measured. Spectrophotometer technique was used for detection of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx). Air samples were collected with a High Volume Small Surface Sampler for measurement of α-cypermethrin level. Results A highly exposed group to the α-cypermethrin had lower CD4/CD8 as compared to an unexposed group with statistically significant difference. As regards gene mutation, exons 5a and 6 were more frequent among the highly exposed group as compared to no mutation among moderately exposed and unexposed groups with significant difference. As regards antioxidants; SOD, CAT, GSH and GPx were higher among the unexposed group as compared to the highly and moderately exposed group with statistically significant difference. Significant negative correlation was found between working years and antioxidant parameters. Conclusions Repeated exposure to α-CYP may lead to gene mutations, immunological disturbances and oxidative stress. Strict safety precautions are required not only for workers but also for public users. Int J Occup Med Environ Health 2017;30(4):603–615
Źródło:
International Journal of Occupational Medicine and Environmental Health; 2017, 30, 4; 603-615
1232-1087
1896-494X
Pojawia się w:
International Journal of Occupational Medicine and Environmental Health
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Rola markerów aktywacji płytek krwi u pacjentów po udarze mózgu
The role of platelet activation markers in patient with ischemic stroke
Autorzy:
Gałka, Małgorzata
Powiązania:
https://bibliotekanauki.pl/articles/1061308.pdf
Data publikacji:
2006
Wydawca:
Medical Communications
Tematy:
P-selectin
glycoprotein 53
ischemic stroke
platelet activation
platelet-leukocyte complexes
kompleksy płytkowo-leukocytarne
udar niedokrwienny mózgu
aktywacja płytek
P-selektyna
glikoproteina 53
Opis:
Platelet activation plays an important role in atherothrombotic disease. Several glycoproteins are expressed on the platelet surface during platelet activation. One of them is P-selectin (CD62P), the more important platelet activation marker. P-selectin is transmembrane protein of the α-granules, which is translocated to the cell surface following activation. The interaction between platetel P-selectin and the specific ligand for P-selectin on leukocytes, P-selectin glycoprotein ligand-1 (PSGL-1), resulting in the formation of platelet-leukocyte complexes, and secretion cytokines and chemokines leading to aggravate the inflammatory processes. Glycoprotein 53 (CD63) which is present in lysosomal membranes also translocates to the plasma membrane during platelet activation. Platelet hyperactivation has been reported in patients with ischemic stroke. Several studies have suggested that platelets are excessively activated in the acute and chronic phases after cerebral ischemia. Therefore, finding platelet function test, could be the first step toward identifying patients who would benefit from antiplatelet treatment.
Aktywacja płytek krwi odgrywa istotną rolę w chorobach pochodzenia zakrzepowo-zatorowego. Podczas aktywacji dochodzi na płytkach do ekspresji różnych glikoprotein powierzchniowych. Należy do nich m.in. P-selektyna, jeden z ważniejszych markerów aktywacji płytek. Jest to przezbłonowe białko α-ziarnistości, które w następstwie aktywacji ulega przemieszczeniu na powierzchnię płytek. P-selektyna pośredniczy w interakcji pomiędzy płytkami i leukocytami poprzez specyficzny ligand dla P-selektyny na leukocytach (PSGL-1). Konsekwencją tej reakcji jest tworzenie kompleksów leukocytarno-płytkowych oraz uwalnianie cytokin i chemokin, co prowadzi do nasilenia procesów zapalnych. Glikoproteina GP53 (CD63) jest obecna w błonach lizosomalnych i ulega również przemieszczeniu na powierzchnię błony plazmatycznej podczas aktywacji płytek. Nadmierna aktywność płytek krwi jest obserwowana u pacjentów z udarem niedokrwiennym mózgu. Różne badania wykazały, że płytki krwi wykazują nadmierną aktywację zarówno w ostrej, jak i przewlekłej fazie udaru. Dlatego też odnalezienie testu monitorującego funkcję płytek może okazać się pierwszym krokiem w kierunku identyfikacji pacjentów, którzy mogą osiągnąć korzyści z zastosowania terapii antypłytkowej.
Źródło:
Aktualności Neurologiczne; 2006, 6, 3; 153-158
1641-9227
2451-0696
Pojawia się w:
Aktualności Neurologiczne
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Indukowana fenobarbitalem hipermetylacja rejonu promotorowego genu p53 w watrobie szczurow szczepu Wistar
Phenobarbital-induced hypermethylation of the p53 promoter region in the liver of Wistar rats
Autorzy:
Kostka, G
Urbanek-Olejnik, K.
Wiadrowska, B.
Bankowski, R.
Powiązania:
https://bibliotekanauki.pl/articles/876498.pdf
Data publikacji:
2008
Wydawca:
Narodowy Instytut Zdrowia Publicznego. Państwowy Zakład Higieny
Tematy:
zwierzeta doswiadczalne
szczury
watroba
gen p53
hipermetylacja
fenobarbital
synteza DNA
metylotransferaza DNA
metylacja DNA
experimental animal
rat
liver
p53 gene
hypermethylation
phenobarbital
DNA synthesis
DNA methyltransferase
DNA methylation
Opis:
Indukowane niegenotoksycznymi kancerogenami (NGCs) zmiany metylacji DNA rozpatrywane są jako mechanizm ich toksycznego, w tym rakotwórczego działania. Zbadano wpływ fenobarbitalu (PB), na poziom metylacji regionu promotorowego genu p53 w wątrobie szczurów szczepu Wis tar. Zmiany metylacji genu p53 korelowano z syntezą DNA, aktywnością metylotransferaz DNA (DNMTs) oraz z masą wątroby. Samce szczurów szczepu Wistar otrzymywały PB w dawce wynoszącej 98,2 mg/ kg m.c. x dzień-1 jednorazowo, 3-krotnie i 14-krotnie. Wykazano, że PB wywoływał hipermetylację w badanych sekwencjach rejonu promotorowego genu p53. Indukowana PB hipermetylacja genu występowała w przebiegu całego okresu doświadczalnego. Stymulację syntezy DNA, która poprzedzała wzrost masy wątroby oraz indukcję DNMTs, wykazano tylko po 1 i 3 dawkach związku. Kontynuowanie narażenia zwierząt na PB (14 dawek) nie wywoływało zmian w syntezie DNA i aktywności DNMTs w porównaniu do kontroli. Przypuszcza się, że indukowana PB de novo metylacja rejonu promotorowego genu p53, nie była związana z aktywnością DNMTs.
Non-genotoxic carcinogens (NGCs)-induced changes of DNA methylation has been proposed as a mechanism of their toxicity, including carcinogenic action. The effect of phénobarbital (PB), a rodent liver carcinogen on the methylation level of the p53 promoter region in rat liver was studied. Changes in the methylation status of the p53 gene were correlated with changes in DNA synthesis, DNA methyltransferase (DNMTs) activity and liver weight. Male Wistar rats received PB in one, three or fourteen daily oral doses of 92.8 mg/kg b.w. x day-1. We have demonstrated that PB increased the methylation of the p53 gene. Cytosine hypermethylation in the analyzed CpG sites of the p53 gene promoter occurred during the whole period of study. However, an increase in DNA synthesis was only observed after 1 and 3 days of treatment with PB and it preceded liver growth. Treatment of rats with PB for 1 and 3 days also produced an increase in nuclear DNMTs activity. After prolonged administration (14 days), no changes in DNMTs activity nor DNA synthesis were observed. It is proposed that PB- induced de novo methylation of the p53 gene was not associated with DNMTs activity.
Źródło:
Roczniki Państwowego Zakładu Higieny; 2008, 59, 4; 455-465
0035-7715
Pojawia się w:
Roczniki Państwowego Zakładu Higieny
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Sequence-specific p53 gene damage by chloroacetaldehyde and its repair kinetics in Escherichia coli
Autorzy:
Kowalczyk, Paweł
Cieśla, Jarosław
Saparbaev, Murat
Laval, Jacques
Tudek, Barbara
Powiązania:
https://bibliotekanauki.pl/articles/1041247.pdf
Data publikacji:
2006
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
chloroacetaldehyde
p53
replication
exocyclic DNA adducts
vinyl chloride
LM-PCR
DNA repair
sequence-specific DNA damage
Opis:
Oxidative stress and certain environmental carcinogens, e.g. vinyl chloride and its metabolite chloroacetaldehyde (CAA), introduce promutagenic exocyclic adducts into DNA, among them 1,N6-ethenoadenine (εA), 3,N4-ethenocytosine (εC) and N2,3-ethenoguanine (εG). We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Analysis (DPFA), and identified sites of the highest sensitivity. CAA-induced DNA damage was more extensive in p53 regions which revealed secondary structure perturbations, and were localized in regions of mutation hot-spots. These perturbations inhibited DNA synthesis on undamaged template. We also studied the repair kinetics of CAA-induced DNA lesions in E. coli at nucleotide resolution level. A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5α strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent. Following transformation, plasmids were re-isolated from transformed cultures 35, 40, 50 min and 1-24 h after transformation, and further subjected to LM-PCR, using ANPG, MUG and Fpg glycosylases to identify the sites of DNA damage. In adaptive response-induced E. coli cells the majority of DNA lesions recognized by ANPG glycosylase were removed from plasmid DNA within 35 min, while MUG glycosylase excised base modifications only within 50 min, both in a sequence-dependent manner. In non-adapted cells resolution of plasmid topological forms was perturbed, suggesting inhibition of one or more bacterial topoisomerases by unrepaired ε-adducts. We also observed delayed consequences of DNA modification with CAA, manifesting as secondary DNA breaks, which appeared 3 h after transformation of damaged DNA into E. coli, and were repaired after 24 h.
Źródło:
Acta Biochimica Polonica; 2006, 53, 2; 337-347
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
p53-dependent suppression of the human calcyclin gene (S100A6): the role of Sp1 and of NFκB
Autorzy:
Króliczak, Weronika
Pietrzak, Maciej
Puzianowska-Kuznicka, Monika
Powiązania:
https://bibliotekanauki.pl/articles/1040715.pdf
Data publikacji:
2008
Wydawca:
Polskie Towarzystwo Biochemiczne
Tematy:
gene suppression
wild type and mutant p53
Sp1
calcyclin gene (S100A6)
NFκB
Opis:
Calcyclin (S100A6) is believed to participate in cell cycle control. It was, however, unclear if its expression depends on p53, a key regulator of apoptosis and cell cycle. We therefore performed transcription regulation assays in HeLa cells and found that wild type p53 suppressed the S100A6 promoter up to 12-fold in a dose-dependent manner. In contrast, the well-characterized V143A, R175H, R249S, and L344A p53 mutants cloned from human cancers suppressed this promoter with a 6 to 9-fold lower efficiency. All the sites mediating the p53-dependent suppression were contained in the -167 to +134 fragment of the S100A6 promoter. Separate overexpression of either Sp1 or of NFκB only partially counteracted the p53 inhibitory effect on the S100A6 promoter, while simultaneous overexpression of both these transactivators resulted in a complete abolishment of the p53 inhibitory effect on this promoter. Sp1 and NFκB binding to the probes resembling their putative binding sites present in the S100A6 promoter was decreased in the presence of wild type p53. We propose that the suppression of S100A6 is yet another mechanism by which p53 inhibits proliferation. Insufficient suppression of this gene by p53 mutants could well be responsible for calcyclin overexpression and cell cycle deregulation observed in cancer tissues.
Źródło:
Acta Biochimica Polonica; 2008, 55, 3; 559-570
0001-527X
Pojawia się w:
Acta Biochimica Polonica
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Single stranded-DNA detection: the role of Wip1 in ATR-dependent pathway
Autorzy:
Kurpas, Monika
Jonak, Katarzyna
Puszynski, Krzysztof
Powiązania:
https://bibliotekanauki.pl/articles/747336.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Matematyczne
Tematy:
ATR
Wip1
mathematical model
UV
p53
ATR, Wip1, model matematyczny, UV, p53.
Opis:
Obszary pojedynczonciowego DNA (ssDNA) powstaja w komórkachw wyniku ekspozycji na stres na przykład- promieniowanie UVC-lub podczas naprawy podwójnoniciowych pekniec DNA. ATR (ataxia telangiectasia mutated and Rad3-related) jest odpowiedzialne za wykrywanie ssDNA. Niedawno wykazano kluczowa role fosfatazy Wip1, która inaktywuje główne elementy szlaków odpowiedzi na uszkodzenia DNA. Opracowalismy matematyczny model sciezki ATR i połaczylismygo z modelem szlaku supresora nowotworowego p53, odpowiadajacego za aktywacje genów zaangazowanych w reakcje komórki na uszkodzenie materiału genetycznego (naprawe DNA/apoptoze). Co wiecej, dodalismy fosfataze Wip1, jako główny czynnik odpowiedzialny za wyłaczenie sciezek sygnałowych uruchamianych w ramach reakcji na uszkodzenie. Uzyskane wyniki pokazuja, ze dzieki prawidłowo dobranej dawce UVC i wyciszeniu lub zablokowaniu aktywnosci Wip1, mozliwe jest skierowanie komórek nowotworowych na szlak apoptotyczny
Single-stranded DNA (ssDNA) areas arise in cells as a result of exposure to stress agents - like UVC - or during repair of DNA double-strand breaks. ATR(ataxia telangiectasia mutated and Rad3-related) is responsible for detecting ssDNA. Recently, it has been shown that one of the most important components of cellular response to the damage is Wip1 phosphatase, which inactivates main elements of DNA damage response (DDR) pathways. We developed a mathematical model of ATR detector system, connected to p53 tumor suppressor responsible for activation of genes involved in cellular response to the damage (DNA repair/apoptosis). Moreover, we added Wip1 phosphatase, as a main agent responsible for turning o DDR. Our results show that the apoptotic threshold, where more than half of cells die, is equal to 20 J/m2. The threshold shifts when activity of the specied proteins involved in the pathway is blocked or reduced. Moreover with accurate dose of UVC and silenced or blocked Wip1, it may be possible to drive cancer cells to apoptotic pathway.
Źródło:
Mathematica Applicanda; 2018, 46, 1
1730-2668
2299-4009
Pojawia się w:
Mathematica Applicanda
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Polymorphisms in the p53 pathway genes and micronucleus occurrence in Chinese vinyl chloride-exposed workers
Autorzy:
Li, Yong
Feng, Nan-Nan
Zhang, Guang-Hui
Wang, Qi
Hao, Yan-Hui
Nanzhang, Ya
Long, Changxu
Li, Yongliang
Brandt-Rauf, Paul W.
Xia, Zhao-Lin
Powiązania:
https://bibliotekanauki.pl/articles/2179059.pdf
Data publikacji:
2013-12-01
Wydawca:
Instytut Medycyny Pracy im. prof. dra Jerzego Nofera w Łodzi
Tematy:
VC
occupational exposure
p53 pathway genes
genetic polymorphism
Opis:
Objectives: To investigate the association between polymorphisms in the p53 pathway genes and chromosomal damage in vinyl chloride (VC)-exposed workers. Materials and Methods: Cytokinesis block micronucleus test was performed in 310 VC-exposed workers and 149 non-exposed workers to determine chromosomal damage. The polymerase chain reaction and restriction fragment length polymorphism technique were used to detect six SNPs in the p53 pathway genes involved in the cell cycle. Results: There was a highly significant dose-response relationship between VC exposure and chromosomal damage. Individuals carrying the variant genotypes were at higher risk for chromosomal damage compared with their wild type genotype: p53rs1042522, MDM2 Del1518rs3730485, MDM2rs2279744 and GADD45Ars532446. On the other hand, individuals possessing the variant genotype of CDKN2A rs3088440 had significantly decreased risk compared with the corresponding wild-type. Conclusions: Genetic polymorphisms in P53 pathway genes may have an impact on VC-induced chromosomal damage.
Źródło:
International Journal of Occupational Medicine and Environmental Health; 2013, 26, 6; 825-836
1232-1087
1896-494X
Pojawia się w:
International Journal of Occupational Medicine and Environmental Health
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Strongly Time-Consistent Core in Differential Games with Discrete Distribution of Random Time Horizon
Silnie zgodny w czasie rdze« gry ró»niczkowej z dyskretnym losowym horyzontem
Autorzy:
Malakhova, Anastasiya Pavlovna
Gromova, Ekaterina Victorovna
Powiązania:
https://bibliotekanauki.pl/articles/953387.pdf
Data publikacji:
2018
Wydawca:
Polskie Towarzystwo Matematyczne
Tematy:
differential games
random time horizon
cooperative solution
strong time-consistency
core
discrete distribution
imputation distribution procedure
atr
wip1
model matematyczny
uv
p53
Opis:
In this paper we investigate the problem of strong time-consistency of the core for a particular class of differential games with random time horizon, namely, it is assumed that there exists a set of probabilities of the end of the game at discrete time instants. A condition guaranteeing the strong time consistency of the core is presented.
Źródło:
Mathematica Applicanda; 2018, 46, 2
1730-2668
2299-4009
Pojawia się w:
Mathematica Applicanda
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Prognostic significance of p53 protein accumulation in cancer cells obtained from selected group of patients with sporadic colorectal cancer
Autorzy:
Paluszkiewicz, P
Karski, J.
Berbec, H.
Pawlowska-Wakowicz, B.
Cybulski, M.
Karski, M.
Paszkowska, A.
Powiązania:
https://bibliotekanauki.pl/articles/2043897.pdf
Data publikacji:
1999
Wydawca:
Polska Akademia Nauk. Czytelnia Czasopism PAN
Tematy:
patient
cancer cell
monoclonal antibody
p53 protein
cancer prognosis
immunohistochemistry
sporadic colorectal cancer
accumulation
colorectal cancer
Źródło:
Journal of Applied Genetics; 1999, 40, 2; 135-144
1234-1983
Pojawia się w:
Journal of Applied Genetics
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Proinflammatory cytokines (IL-6, IL-18) and apoptotic factors (HP 53, survivin) in patients with alcoholic liver cirrhosis
Autorzy:
Prystupa, Andrzej
Kiciński, Paweł
Sak, Jarosław
Grzybowski, Andrzej
Boguszewska-Czubara, Anna
Toruń-Jurkowska, Anna
Niedziałek, Jarosław
Załuska, Wojciech
Powiązania:
https://bibliotekanauki.pl/articles/972717.pdf
Data publikacji:
2017
Wydawca:
Instytut Medycyny Wsi
Tematy:
survivin
alcoholic liver cirrhosis
proinflammatory cytokines
apoptosis
human protein p53
Opis:
Background. Apoptosis is involved in the pathogenesis of alcoholic liver cirrhosis. Its development can be triggered by an inflammatory process. In the present study, levels of apoptotic factors – survivin human protein p53 (HP 53) and IL-6, IL-18 were determined according to the stage of liver cirrhosis. Material and methods. Seventy patients with alcoholic liver cirrhosis, treated in various hospitals of the Lublin region, Poland were included in the study. Serum levels of IL-6, IL-18, HP53 and survivin were determined by the enzyme-linked immunosorbent assay (ELISA) technique. Results. The serum level of survivin in patients with alcoholic liver cirrhosis was not statistically different from that found in the control group. The level of HP53 was significantly higher in the group of patients with alcoholic liver cirrhosis compared to the control group (16.53±22.69 vs. 0.39±1.31 U/ml; p<0.001). Likewise, the level of IL-6 was significantly higher in the group of patients with alcoholic liver cirrhosis compared to the control group (33.83±41.78 vs. 0.88 ± 0.56 pg/ml; p<0.001). Moreover, the level of IL-18 was significantly higher in the group of patients with liver cirrhosis compared to the control group (23.96±31.07 vs. 5.3±8.6 pg/ml; p<0.001). Conclusion. In conclusion, increased serum levels of IL-6 and IL-18 were demonstrated in patients with alcoholic liver cirrhosis. Moreover, the liver cirrhosis patients had elevated levels of HP53, which is a marker of apoptosis. Our results did not demonstrate the correlation between the levels of apoptosis markers (survivin, HP53) and the levels of cytokines (IL-6, IL-18) in the blood serum.
Źródło:
Journal of Pre-Clinical and Clinical Research; 2017, 11, 1; 1-5
1898-2395
Pojawia się w:
Journal of Pre-Clinical and Clinical Research
Dostawca treści:
Biblioteka Nauki
Artykuł
Tytuł:
Regulation of p53 by siRNA in radiation treated cells: Simulation studies
Autorzy:
Puszyński, K.
Jaksik, R.
Świerniak, A.
Powiązania:
https://bibliotekanauki.pl/articles/331259.pdf
Data publikacji:
2012
Wydawca:
Uniwersytet Zielonogórski. Oficyna Wydawnicza
Tematy:
siRNA
p53
terapia skojarzona
combined therapy
Opis:
Ionizing radiation activates a large variety of intracellular mechanisms responsible for maintaining appropriate cell functionality or activation of apoptosis which eliminates damaged cells from the population. The mechanism of such induced cellular death is widely used in radiotherapy in order to eliminate cancer cells, although in some cases it is highly limited by increased cellular radio-resistance due to aberrations in molecular regulation mechanisms of malignant cells. Despite the positive correlation between the radiation dose and the number of apoptotic cancer cells, radiation has to be limited because of extensive side effects. Therefore, additional control signals whose role will be to maximize the cancer cells death-ratio while minimizing the radiation dose and by that the potential side effects are worth considering. In this work we present the results of simulation studies showing possibilities of single gene regulation by small interfering RNA (siRNA) that can increase radio-sensitivity of malignant cells showing aberrations in the p53 signaling pathway, responsible for DNA damage-dependant apoptosis. By blocking the production of the p53 inhibitor Mdm2, radiation treated cancer cells are pushed into the apoptotic state on a level normally achievable only with high radiation doses. The presented approach, based on a simulation study originating from experimentally validated regulatory events, concerns one of the basic problems of radiotherapy dosage limitations, which, as will be shown, can be partially avoided by using the appropriate siRNA based control mechanism.
Źródło:
International Journal of Applied Mathematics and Computer Science; 2012, 22, 4; 1011-1018
1641-876X
2083-8492
Pojawia się w:
International Journal of Applied Mathematics and Computer Science
Dostawca treści:
Biblioteka Nauki
Artykuł
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