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J Cancer Metastasis Treat 2019;5:31 I http://dx.doi.org/10.20517/2394-4722.2019.21 Page 34 of 36

term follow-up. The ESRP1 participates in the epithelial-mesenchymal transition, a necessary prelude to
disease progression in prostate cancer (PC). The prognostic role of ESRP1 has been studied in various
human primary tumor tissues and has been described to be tumor-specific. However, little is known about
the prognostic value of ESPR1 in PC. A preliminary investigation into the clinical significance of ESRP1
was conducted using The Cancer Genome Atlas PC dataset. Tissue microarrays of radical prostatectomy
specimens from 514 PC patients at the National Cancer Center of Korea were immunohistochemically
stained for ESRP1. PC samples were grouped into high and low expression of ESRP1 based on the
immunohistochemistry results. The median follow-up period was 91.2 months. The immunohistochemistry
was interpreted semi-quantitatively using H-score, defined by the intensity (0, 1, 2 and 3), and the
percentage of expressed areas (0-100%). The prognostic significance of ESRP1 expression was analyzed
using the Cox proportional-hazards model (P < 0.05). After adjusting for clinicopathological variables, high
expression of ESRP1 was significantly associated with worse biochemical recurrence-free survival [hazard
ratio (HR): 1.37; 95% confidence interval (CI): 1.02-1.83; P = 0.037] and shorter cancer-specific survival (HR:
3.43; 95% CI: 1.12-10.54; P = 0.031). PC patients with high expression of ESRP1 appear to have increased
risk of biochemical recurrence and cancer-specific death. The expression of ESRP1 in patients with poor
survival outcomes indicates that there may be an opportunity to predict response to androgen deprivation
therapy based on ESRP1 expression.

Biography
Dr. Kang Hyun Lee has completed his MD and PhD from Seoul National University, College of Medicine,
Seoul, Korea. He is a Tenure Chief Scientist in the Division of Precision Medicine and Specialist in Center
for Prostate cancer, National Cancer Center of Korea. He is also the Emeritus Professor of GCSP and
he has published more than 130 papers in academic journals and had been serving as 6th President of
National Cancer Center of Korea.

45. Gene-specific methylation as a molecular biomarker in gastric cancer

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1
1
Fernanda Wisnieski , Leonardo Caires Santos , Jaqueline Cruz Geraldis , Mariana Ferreira Leal , Ana
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1
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1
1
Carolina Anauate Pereira , Danielle Queiroz Calcagno , Carolina Oliveira Gigek , Elizabeth Suchi Chen ,
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4
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Sâmia Demachki , Ricardo Artigiani , Paulo Pimentel Assumpção , Laércio Gomes Lourenço , Rommel
5
Rodríguez Burbano , Marília Cardoso Smith 1
1 Disciplina de Genética, Departamento de Morfologia e Genética, Universidade Federal de São Paulo, Sao
Paolo 04021-001, Brazil.
2 Núcleo de Pesquisas em Oncologia, Hospital Universitário João de Barros Barreto, Guamá, Belem 66073-
000, Brazil.
3 Departamento de Patologia, Universidade Federal de São Paulo, Sao Paolo 04021-001, Brazil.
4 Disciplina de Gastroenterologia Cirúrgica, Departamento de Cirurgia, Universidade Federal de São Paulo,
Sao Paolo 04021-001, Brazil.
5 Instituto de Ciências Biológicas, Universidade Federal do Pará, Guamá, Belem 66073-000, Brazil.
Despite the fact that overall rates of gastric cancer (GC) continue to decline worldwide, the majority of
patients are still diagnosed with advanced disease in Western countries. New strategies for early diagnosis
and new therapeutic methods in GC need to be explored. Epigenetic control using inhibitors of DNA
methylation, such as 5-aza-2’-deoxycytidine (also known as Decitabine), may offer new possibilities in GC
therapy. Our research group previously identified 86 differentially expressed genes (DEGs) by microarray
analysis comparing GC cell lines treated with Decitabine and non-treated cells. Among the upregulated