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Statements

Subject Item
n2:RIV%2F00216208%3A11150%2F13%3A10195436%21RIV14-MSM-11150___
rdf:type
skos:Concept n17:Vysledek
rdfs:seeAlso
http://fb.cuni.cz/file/5707/FB2013A0034.pdf
dcterms:description
Cervical cancer affects women worldwide, especially in developing countries. Approximately 500,000 cases of this disease are diagnosed per year. The method of choice in the treatment of advanced cervical cancers (in accordance with the International Federation of Gynecology and Obstetrics staging system (FIGO) starting from stage JIB) is combined radiotherapy with concomitant chemotherapy. This treatment provides good tumour control, but it carries a risk of late complications in the irradiated area in 10-15 A of cases. Methylation is one of the methods of epigenetic control, which has an important role in gene expression. Aberrant methylation of normal CpG islands in promoters of tumour suppressor genes such as RB, p53 or DNA reparation genes ATM, BRCA1,2, and RAD51 gene family causes silencing of their function and cell cycle deregulation, which is one of the efficient ways of neoplastic transformation. The significantly decreased expression of molecules involved in DNA response may cause facilitated radiosensitivity in predisposed individuals. We looked for the relationship between hypermethylation of 18 DNA reparation genes and late toxicity occurrence in cervical cancer patients treated by chemoradiotherapy using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA). The cut-off value for the hypermethylation was set at 10 %. We confirmed significant association between promoter hypermethylation in the XRCC2 gene and occurrence of late grade toxicity in cervical cancer patients (P = 0.0357). This finding could be useful in the late toxicity prediction in radiotherapy-treated patients. Cervical cancer affects women worldwide, especially in developing countries. Approximately 500,000 cases of this disease are diagnosed per year. The method of choice in the treatment of advanced cervical cancers (in accordance with the International Federation of Gynecology and Obstetrics staging system (FIGO) starting from stage JIB) is combined radiotherapy with concomitant chemotherapy. This treatment provides good tumour control, but it carries a risk of late complications in the irradiated area in 10-15 A of cases. Methylation is one of the methods of epigenetic control, which has an important role in gene expression. Aberrant methylation of normal CpG islands in promoters of tumour suppressor genes such as RB, p53 or DNA reparation genes ATM, BRCA1,2, and RAD51 gene family causes silencing of their function and cell cycle deregulation, which is one of the efficient ways of neoplastic transformation. The significantly decreased expression of molecules involved in DNA response may cause facilitated radiosensitivity in predisposed individuals. We looked for the relationship between hypermethylation of 18 DNA reparation genes and late toxicity occurrence in cervical cancer patients treated by chemoradiotherapy using methylation-specific multiplex ligation-dependent probe amplification (MS-MLPA). The cut-off value for the hypermethylation was set at 10 %. We confirmed significant association between promoter hypermethylation in the XRCC2 gene and occurrence of late grade toxicity in cervical cancer patients (P = 0.0357). This finding could be useful in the late toxicity prediction in radiotherapy-treated patients.
dcterms:title
Hypermethylation of RAD51L3 and XRCC2 Genes to Predict Late Toxicity in Chemoradiotherapy-Treated Cervical Cancer Patients Hypermethylation of RAD51L3 and XRCC2 Genes to Predict Late Toxicity in Chemoradiotherapy-Treated Cervical Cancer Patients
skos:prefLabel
Hypermethylation of RAD51L3 and XRCC2 Genes to Predict Late Toxicity in Chemoradiotherapy-Treated Cervical Cancer Patients Hypermethylation of RAD51L3 and XRCC2 Genes to Predict Late Toxicity in Chemoradiotherapy-Treated Cervical Cancer Patients
skos:notation
RIV/00216208:11150/13:10195436!RIV14-MSM-11150___
n17:predkladatel
n18:orjk%3A11150
n3:aktivita
n7:P n7:I
n3:aktivity
I, P(NT11334)
n3:cisloPeriodika
6
n3:dodaniDat
n15:2014
n3:domaciTvurceVysledku
n4:3299643 n4:5460913 n4:6210554 n4:2010887 n4:3811115
n3:druhVysledku
n9:J
n3:duvernostUdaju
n19:S
n3:entitaPredkladatele
n10:predkladatel
n3:idSjednocenehoVysledku
78542
n3:idVysledku
RIV/00216208:11150/13:10195436
n3:jazykVysledku
n12:eng
n3:klicovaSlova
cells; family; proteins; microarray; radiotherapy; repair; radiation; recombination
n3:klicoveSlovo
n5:proteins n5:family n5:microarray n5:recombination n5:cells n5:radiotherapy n5:repair n5:radiation
n3:kodStatuVydavatele
CZ - Česká republika
n3:kontrolniKodProRIV
[D03AE2C53EFD]
n3:nazevZdroje
Folia Biologica
n3:obor
n20:FD
n3:pocetDomacichTvurcuVysledku
5
n3:pocetTvurcuVysledku
5
n3:projekt
n16:NT11334
n3:rokUplatneniVysledku
n15:2013
n3:svazekPeriodika
59
n3:tvurceVysledku
Chmelařová, Marcela Palička, Vladimír Paulík, Adam Paulíková, Simona Petera, Jiří
n3:wos
000330161600005
s:issn
0015-5500
s:numberOfPages
6
n13:organizacniJednotka
11150