ABSTRACT
BACKGROUND/AIMS: To identify the risk factors for metachronous gastric neoplasms in patients who underwent an endoscopic resection of a gastric neoplasm. METHODS: We prospectively collected clinicopathologic data and measured the methylation levels of HAND1, THBD, APC, and MOS in the gastric mucosa by methylation-specific real-time polymerase chain reaction in patients who underwent endoscopic resection of gastric neoplasms. RESULTS: A total of 257 patients with gastric neoplasms (113 low-grade dysplasias, 25 high-grade dysplasias, and 119 early gastric cancers) were enrolled. Metachronous gastric neoplasm developed in 7.4% of patients during a mean follow-up of 52 months. The 5-year cumulative incidence of metachronous gastric neoplasm was 4.8%. Multivariate analysis showed that moderate/severe corpus intestinal metaplasia and family history of gastric cancer were independent risk factors for metachronous gastric neoplasm development; the hazard ratios were 4.12 (95% confidence interval [CI], 1.23 to 13.87; p=0.022) and 3.52 (95% CI, 1.09 to 11.40; p=0.036), respectively. The methylation level of MOS was significantly elevated in patients with metachronous gastric neoplasms compared age- and sex-matched patients without metachronous gastric neoplasms (p=0.020). CONCLUSIONS: In patients who underwent endoscopic resection of gastric neoplasms, moderate/severe corpus intestinal metaplasia and a family history of gastric cancer were independent risk factors for metachronous gastric neoplasm, and MOS was significantly hypermethylated in patients with metachronous gastric neoplasms.
Subject(s)
Aged , Female , Humans , Male , Middle Aged , Basic Helix-Loop-Helix Transcription Factors/genetics , DNA Methylation , Gastrectomy/methods , Genes, APC/physiology , Genes, mos/genetics , Incidence , Multivariate Analysis , Neoplasms, Second Primary/epidemiology , Proportional Hazards Models , Risk Factors , Stomach Neoplasms/genetics , Thrombomodulin/geneticsABSTRACT
<p><b>AIM</b>To immunolocalize the c-mos gene product and to investigate its spatial and temporal expression in mouse testis during postnatal development.</p><p><b>METHODS</b>Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization techniques were used to examine c-mos mRNA and indirect immunofluorescence was used to localize c-Mos protein in mouse testis on postnatal days 14, 21, 25, 28, 30, 35, 49 and 70.</p><p><b>RESULTS</b>c-mos mRNA remained low on postnatal days 14-21, increased abruptly from day 25 and peaked on day 30. Its levels decreased a little on day 35 and became almost stable thereafter until day 70. c-mos mRNA was localized in the nucleus and cytoplasm of the spermatocytes and round spermatids. The nuclear staining was much stronger than the cytoplasmic staining. Using a polyclonal anti-c-Mos antibody, Western blotting detected a single band at 43 kDa in testis lysate. c-Mos protein was exclusively localized to the elongating spermatids and was first detected on postnatal day 30. The number of c-Mos-positive spermatids increased progressively till day 49 and stabilized thereafter.</p><p><b>CONCLUSION</b>The c-mos gene displays a spatial and temporal expression pattern in the mouse testis during postnatal development at both the mRNA and protein level. This suggests that c-mos might play important roles in spermatogenesis.</p>
Subject(s)
Animals , Male , Mice , Fluorescent Antibody Technique, Indirect , Gene Expression , Genes, mos , Genetics , Reverse Transcriptase Polymerase Chain Reaction , Spermatocytes , Metabolism , Spermatogenesis , Genetics , Testis , MetabolismABSTRACT
Early in the development of many animals, before transcription begins, any change in the pattern of protein synthesis is attributed to a change in the translational activity or stability of mRNA in the egg and early embryo. As a result, translational control is critical for a variety of developmental decisions, including oocyte maturation and initiation of preimplantation development. In this study, using real-time RT-PCR method, we defined the time course of degradation and deadenylation of an oocyte specific gene [c-mos] more precisely and a gene that is re-synthesized after ZGA [cyclin A2]. Our data indicate that oocyte-specific transcript, c-mos, degrades rapidly while cyclin A2 mRNA does not and the deadenylation of c-mos mRNA precedes the process of degradation. Our findings suggest that time-dependent elimination of different maternal mRNA is a way for regulation of translation in early development of mouse embryos