DNA methylation of selected tumor suppressor genes in endometrial hyperplasia
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00179906%3A_____%2F24%3A10481170" target="_blank" >RIV/00179906:_____/24:10481170 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/00216208:11150/24:10481170
Výsledek na webu
<a href="https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=DHzZhNSQWC" target="_blank" >https://verso.is.cuni.cz/pub/verso.fpl?fname=obd_publikace_handle&handle=DHzZhNSQWC</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.5507/bp.2022.053" target="_blank" >10.5507/bp.2022.053</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
DNA methylation of selected tumor suppressor genes in endometrial hyperplasia
Popis výsledku v původním jazyce
Aims. To investigate DNA methylation of specific gene promoters in endometrial hyperplasia compared to normal endometrial tissue.Materials and Methods. To search for epigenetic events, methylation-specific multiplex ligation-dependent probe amplification was employed to compare the methylation status of 64 tissue samples with atypical endometrial hyperplasia, 60 tissue samples with endometrial hyperplasia without atypia, and 40 control tissue samples with normal endometrium.Results. Differences in DNA methylation among the groups were found in PTEN, CDH13, and MSH6 promoters (PTEN: atypical hyperplasia 32%, benign hyperplasia 6.8%, normal endometrium 10%; P=0.004; CDH13: atypical hyperplasia, 50%; benign hyperplasia, 43%; normal endometrium 8.1%; P=0.003; MSH6 atypical hyperplasia 84%, benign hyperplasia, 62%; normal endometrium, 52%; P=0.008.) Higher rates of CDH13 promoter methylation were identified in the groups with both forms of endometrial hyperplasia when compared to the control group (atypical hyperplasia, P=0.003, benign hyperplasia, P=0.0002). A higher rate of DNA methylation of the PTEN and MSH6 promoters was observed in samples with atypical endometrial hyperplasia than in samples with benign endometrial hyperplasia (PTEN: P=0.02; MSH6: P=0.01) and samples with normal endometrial tissue (PTEN, P=0.04; MSH6, P=0.006).Conclusion. DNA methylation of CDH13, PTEN, and MSH6 appear to be involved in the development of endometrial hyperplasia.
Název v anglickém jazyce
DNA methylation of selected tumor suppressor genes in endometrial hyperplasia
Popis výsledku anglicky
Aims. To investigate DNA methylation of specific gene promoters in endometrial hyperplasia compared to normal endometrial tissue.Materials and Methods. To search for epigenetic events, methylation-specific multiplex ligation-dependent probe amplification was employed to compare the methylation status of 64 tissue samples with atypical endometrial hyperplasia, 60 tissue samples with endometrial hyperplasia without atypia, and 40 control tissue samples with normal endometrium.Results. Differences in DNA methylation among the groups were found in PTEN, CDH13, and MSH6 promoters (PTEN: atypical hyperplasia 32%, benign hyperplasia 6.8%, normal endometrium 10%; P=0.004; CDH13: atypical hyperplasia, 50%; benign hyperplasia, 43%; normal endometrium 8.1%; P=0.003; MSH6 atypical hyperplasia 84%, benign hyperplasia, 62%; normal endometrium, 52%; P=0.008.) Higher rates of CDH13 promoter methylation were identified in the groups with both forms of endometrial hyperplasia when compared to the control group (atypical hyperplasia, P=0.003, benign hyperplasia, P=0.0002). A higher rate of DNA methylation of the PTEN and MSH6 promoters was observed in samples with atypical endometrial hyperplasia than in samples with benign endometrial hyperplasia (PTEN: P=0.02; MSH6: P=0.01) and samples with normal endometrial tissue (PTEN, P=0.04; MSH6, P=0.006).Conclusion. DNA methylation of CDH13, PTEN, and MSH6 appear to be involved in the development of endometrial hyperplasia.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30214 - Obstetrics and gynaecology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2024
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Biomedical Papers
ISSN
1213-8118
e-ISSN
1804-7521
Svazek periodika
168
Číslo periodika v rámci svazku
1
Stát vydavatele periodika
CZ - Česká republika
Počet stran výsledku
6
Strana od-do
68-73
Kód UT WoS článku
000918605200001
EID výsledku v databázi Scopus
2-s2.0-85187623171