4.7 Article

Decreased expression of ten-eleven translocation 1 protein is associated with some clinicopathological features in gastric cancer

Journal

BIOMEDICINE & PHARMACOTHERAPY
Volume 68, Issue 2, Pages 209-212

Publisher

ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER
DOI: 10.1016/j.biopha.2013.12.011

Keywords

Gastric cancer; TET1; 5-Hydroxymethylcytosine (5hmC)

Funding

  1. Poznan University of Medical Sciences, Poland [502-01-01124182-07474]

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A decrease in ten-eleven translocation 1 (TET1) transcript and 5-Hydroxymethylcytosine (5hmC) levels has recently been demonstrated in primary gastric cancer (GC). However, little is known about TET1 protein levels in gastric tumoral and nontumoral tissue. Therefore, using reverse transcription, real-time quantitative polymerase chain reaction and western blotting analysis, we determined the TET1 transcript and protein levels in tumoral and nontumoral tissue from 38 patients with GC. We also assessed the association between the decrease in TET1 transcript and protein levels and some clinicopathological features in primary GC. We found significantly decreased levels of TET1 transcript (P = 0.0023) and protein (P = 0.00024) in primary tumoral tissues as compared to nontumoral tissues in patients with GC. Moreover, we also observed significantly lower amounts of TET1 transcript (P = 0.03) and protein (P = 0.00018) in tumoral tissues in patients aged > 60. We also found significant lowered TET1 protein levels in male patients (P = 0.0014), stomach (P = 0.044) and cardia (P = 0.013) tumor localization, T3 depth of invasion (P = 0.019), N1 (P = 0.012) and N3 lymph node metastasis (P = 0.013) and G3 histological grade (P = 0.0012). There were also significant decreases in TET1 transcript levels in female patients (P = 0.042), intestinal histological types (P = 0.0079) and T4 depth of invasion (P = 0.037). Our results demonstrated that a decrease in TET1 transcript and protein levels is associated with some clinicopathological features in GC. (C) 2014 Published by Elsevier Masson SAS.

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