open access

Vol 80, No 11 (2009)
ARTICLES
Get Citation

Is global DNA methylation in sporadic uterine adenocarcinomas in women a result of histological and clinical tumor advancement?

Magdalena Gałecka-Josse, Krzysztof Postawski, Włodzimierz Baranowski
Ginekol Pol 2009;80(11).

open access

Vol 80, No 11 (2009)
ARTICLES

Abstract

Aim: to find out the relationship, if any, between the extent of the overall genomic DNA methylation, and clinical and pathological features of the sporadic endometrial adenocarcinomas in women. Material: genomic DNA was isolated from 44 primary uterine cancer tissue specimens. There were eight G1, 24 G2 and twelve G3 tumors. Methods: m5dC level was estimated after enzymatic digestion of DNA into nucleotides, 32P-postlabelling, twodimensional thin-layer chromatography on cellulose plates and phosphorobioimaging. The overall m5dC of the uterine cancer DNAs expressed as a ratio: (pm5dC/pm5dC+pdC) x 100% was compared to results obtained for parallel investigated but published earlier normal human endometrium DNAs. Results: mean total cancer DNA methylation (3.48±0.46%) was significantly higher than that of the normal proliferative endometrium (2.94±0,4%, p=0.003) and lower than that of the secretory endometrium DNAs (3.75±0,47%, p=0.03). Among all endometrial cancer DNAs six were found to be hypomethylated, eight were hypermethylated, whereas the remaining 30 had m5dC within range of normal endometrium. Total DNA methylation was significantly higher in poorly differentiated (G3) than in lower grade neoplasms (3.94±0.46 vs. 3.3 ±0.32 %, p=0.025). Lower levels of DNA methylation seemed to be associated with diminished tumor invasiveness. Conclusions: our results suggest that alterations in overall DNA methylation seem to be a result of neoplastic transformation and could therefore be used as a prognostic molecular marker of endometrial cancer.

Abstract

Aim: to find out the relationship, if any, between the extent of the overall genomic DNA methylation, and clinical and pathological features of the sporadic endometrial adenocarcinomas in women. Material: genomic DNA was isolated from 44 primary uterine cancer tissue specimens. There were eight G1, 24 G2 and twelve G3 tumors. Methods: m5dC level was estimated after enzymatic digestion of DNA into nucleotides, 32P-postlabelling, twodimensional thin-layer chromatography on cellulose plates and phosphorobioimaging. The overall m5dC of the uterine cancer DNAs expressed as a ratio: (pm5dC/pm5dC+pdC) x 100% was compared to results obtained for parallel investigated but published earlier normal human endometrium DNAs. Results: mean total cancer DNA methylation (3.48±0.46%) was significantly higher than that of the normal proliferative endometrium (2.94±0,4%, p=0.003) and lower than that of the secretory endometrium DNAs (3.75±0,47%, p=0.03). Among all endometrial cancer DNAs six were found to be hypomethylated, eight were hypermethylated, whereas the remaining 30 had m5dC within range of normal endometrium. Total DNA methylation was significantly higher in poorly differentiated (G3) than in lower grade neoplasms (3.94±0.46 vs. 3.3 ±0.32 %, p=0.025). Lower levels of DNA methylation seemed to be associated with diminished tumor invasiveness. Conclusions: our results suggest that alterations in overall DNA methylation seem to be a result of neoplastic transformation and could therefore be used as a prognostic molecular marker of endometrial cancer.
Get Citation

Keywords

adenocarcinoma, DNA methylation, molecular epidemiology

About this article
Title

Is global DNA methylation in sporadic uterine adenocarcinomas in women a result of histological and clinical tumor advancement?

Journal

Ginekologia Polska

Issue

Vol 80, No 11 (2009)

Bibliographic record

Ginekol Pol 2009;80(11).

Keywords

adenocarcinoma
DNA methylation
molecular epidemiology

Authors

Magdalena Gałecka-Josse
Krzysztof Postawski
Włodzimierz Baranowski

Regulations

Important: This website uses cookies. More >>

The cookies allow us to identify your computer and find out details about your last visit. They remembering whether you've visited the site before, so that you remain logged in - or to help us work out how many new website visitors we get each month. Most internet browsers accept cookies automatically, but you can change the settings of your browser to erase cookies or prevent automatic acceptance if you prefer.

By "Via Medica sp. z o.o." sp.k., ul. Świętokrzyska 73, 80–180 Gdańsk
tel.:+48 58 320 94 94, faks:+48 58 320 94 60, e-mail:  viamedica@viamedica.pl