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1. Differential Expression of RUNX Genes in Human Esophageal Squamous Cell Carcinoma: Downregulation of RUNX3 Worsens Patient Prognosis. Oncology Vol. 73, No. 5-6, 2007& T9 o# Y: `# I; u" p
http://content.karger.com/produk ... &file=0001353508 B2 M: D$ q# V" W3 `4 `6 g- g
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2. Methylation Profiling of Archived Non–Small Cell Lung Cancer: A Promising Prognostic System. Clinical Cancer Research 2005* j; N$ @" S* v3 K' w# @& W, c
http://clincancerres.aacrjournals.org/content/11/12/4400.full% F6 j/ n( a/ I, q8 S
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3. Epigenetic dysregulation of Wnt signaling pathway in multiple myeloma. Leukemia (2007) 21, 2527–25362 h$ L( ]/ n# q7 B: U$ F
http://www.nature.com/leu/journal/v21/n12/abs/2404939a.html
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4. Reduced representation bisulfite sequencing for comparative high-resolution DNA methylation analysis. Nucleic Acids Research 2005 33(18):5868-5877
* s' M2 P/ f' Q: d2 h6 yhttp://nar.oxfordjournals.org/cgi/content/abstract/33/18/5868
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5. Promoter Hypermethylation Is Associated With Tumor Location, Stage, and Subsequent Progression in Transitional Cell Carcinoma. Journal of Clinical Oncology, Vol 23, No 13 (May 1), 2005: pp. 2903-2910
+ T, R3 G" _' O$ F9 u: @http://www.jcojournal.org/cgi/content/abstract/23/13/2903- Y+ v9 y, f0 v+ a
r6 s6 s1 W+ Y3 [6. Methylation of cyclin-dependent kinase inhibitors, XAF1, JUNB, CDH13 and soluble Wnt inhibitors in essential thrombocythaemia. J Clin Pathol 2010;63:518-521% D' c9 x% A) F, ^8 n5 j5 \0 R+ \
http://jcp.bmj.com/content/63/6/518.abstract
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7. Aberrant Gene Methylation in the Lymph Nodes Provides a Possible Marker for Diagnosing Micrometastasis in Gastric Cancer. Annals of Surgical Oncology, Volume 17, Number 4 / 2010
! J' f" e+ @9 F9 ]http://www.springerlink.com/content/k233x8n27343t0gk/! D, D0 b |# F% | [, J* }7 V
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8. Mouse Meningiocytes Express Sox2 and Yield High Efficiency of Chimeras after Nuclear Reprogramming with Exogenous Factors. Journal of Biological Chemistry, 283, 33730 - 33735. : A5 h+ Z! o6 C0 X" L
http://www.jbc.org/content/283/48/33730.short * {* B. R" q' D
Expression of beta-catenin and its mechanism of delocalization in intestinal-type early gastric cancer based on mucin expression.$ e4 b7 {$ e) Q' B; k
Histology and histopathology, 24 31-8 (2009)
% u2 `& Z' x4 X2 Z5 G0 u- gPub Med ID:19475529
3 S6 m0 I$ R" k f u* ahttp://www.ncbi.nlm.nih.gov/pubmed/19475529/ e# F) c/ _: i- y% y9 `0 l
! h- [) y8 l+ W; B. B0 L' z# lAbstract
/ m' T/ O7 v O3 a* }The biological characteristics of intestinal-type early gastric cancers (ICs) differ based on mucin phenotypes. Beta-catenin delocalization is a predictive marker of aggressive biological behavior (submucosal invasion and lymph node metastasis) of ICs. The presumptive causative genetic alterations leading to delocalization of beta-catenin in ICs are still controversial, and there are only a few reports regarding beta-catenin expression in gastric cancer based on mucin phenotypes. Therefore, in the current study, the expression and mechanisms of delocalization of beta-catenin were elucidated on the basis of mucin phenotypes in 109 cases of ICs. There was increased cytoplasmic and nuclear beta-catenin expression (delocalization) in ICs with a predominant intestinal mucin phenotype (ICIP; 46.3% [25/54 cases]) compared to ICs with a predominant gastric mucin phenotype (ICGP; 20% [11/55 cases]). There were no beta-catenin or APC mutations in ICs. APC promoter hypermethylation was present in 49 of 105 (46.7%) cases of ICs. There was a significant relationship between APC promoter hypermethylation and beta-catenin delocalization in ICs, especially in ICIPs. There was no relationship between beta-catenin delocalization and APC gene loss of heterozygosity in ICs. In conclusion, we showed that beta-catenin delocalization was more evident in ICIPs, and APC promoter hypermethylation might play a role in delocalization of beta-catenin, especially in ICIPs. |
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