• Asian Pacific Journal of Cancer Prevention
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• 제16권9호
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• pp.3677-3683
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• 2015

Abnormally expressed microRNAs (miRNAs) and genes have been found to play key roles in esophageal squamous cell carcinoma (ESCC), but little is known about the underlying mechanisms. The aim of this paper was to assess inter-relationships and the regulatory mechanisms of ESCC through a network-based approach. We built three regulatory networks: an abnormally expressed network, a related network and a global network. Unlike previous examples, containing information only on genes or miRNAs, the prime focus was on relationships. It is worth noting that abnormally expressed network emerged as a fault map of ESCC. Theoretically, ESCC might be treated and prevented by correcting the included errors. In addition, the predicted transcription factors (TFs) obtained by the P-match method also warrant further study. Our results may further guide gene therapy researchers in the study of ESCC.

• Journal of Chest Surgery
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• 제23권4호
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• pp.825-830
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• 1990

Esophageal cancer is relatively uncommon except in isolated endemic areas, but it generally devastating to the patient. Usually, by the time the disease becomes clinically evident, it is incurable. The aim of treatment is then relegated to attempting to palliate the symptoms in the best possible manner with the least morbidity and mortality. Squamous cell carcinoma in by far the commonest type of malignancy involving the body of the esophagus, accounting for more than 95 percent of all esophageal malignancies. Because the tumor’s microscopic spread is much greater than its macroscopic extent, it is necessary to resect a sufficiently long segment of the esophagus. And second tumors may occur either in the esophagus as a manifestation of a field change or in other organs. Recently we had experienced a case with in situ carcinoma away from the invasive squamous cell carcinoma of the esophagus. A 58 year-old male was admitted with the chief complaint of swallowing difficulty for a month prior to admission. While we studied the esophagogram and chest CT, we found that the mass was protruded to the lumen of esophagus at the level of the 7th-9th thoracic vertebral columns. We performed esophagectomy with lymph node dissection and esophagogastrostomy by thoracic and abdominal approaches. The pathologic result showed separation of another in situ carcinoma away from the invasive squamous cell carcinoma of esophagus at the level of esophagogastric junctions. Postoperative course was uneventful. Now he is taking the postoperative irradiation at out patient department.

• Asian Pacific Journal of Cancer Prevention
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• 제15권2호
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• pp.763-767
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• 2014

Aim: To study the contribution of genetic variation in RAD51 to risk of esophageal squamous cell carcinoma (ESCC). Methods: Three single nucleotide polymorphisms (SNPs) in RAD51 (rs1801320, rs4144242 and rs4417527) were genotyped in 316 ESCC patients and 316 healthy controls in Anyang area of China using PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism). Demographic variables between cases and controls were statistically compared by T test and Chi-square test. Hardy-Weinberg equilibrium was evaluated by the Chi-square test. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to measure any association with ESCC. Haplotype frequencies were estimated by Phase 2.1. Result: The genotype frequencies of rs1801320, rs4144242 and rs4417527 in patients with ESCC demonstrated no significant differences from those in control group (P>0.05). When the haplotypes of these three SNPs were constructed and their relationships with ESCC risk investigated, however, CGG was observed to increase the risk (P=0.020, OR=2.289). Conclusions: There was no association between the three SNPs of RAD51 and ESCC susceptibility in our Chinese population. However, the CGG haplotype might be a risk factor.

• Journal of Digestive Cancer Reports
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• 제7권2호
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• pp.57-60
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• 2019

Definitive chemoradiotherapy (CRT) with its significant efficacy and safety in esophageal cancer is reserved for patients with unresectable tumor or those who decline surgery. However, the incidence of locoregional failure or recurrence after definitive CRT remains high. Although esophagectomy is the standard treatment for locoregional failure or recurrence, this approach is associated with high mortality and morbidity. A 56-year-old man diagnosed with esophageal squamous cell carcinoma who refused to undergo surgery received definitive CRT. An endoscopy for response assessment performed after 2 months revealed a residual lesion, which was completely resected by salvage endoscopic submucosal dissection. To the best of our knowledge, endoscopic resection in locoregional failure or recurrence after definitive CRT is very rarely reported, and there are no guidelines or consensus to date. Here, we report a case of successful salvage endoscopic resection of residual lesion after definitive CRT.

• Asian Pacific Journal of Cancer Prevention
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• 제14권3호
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• pp.1911-1918
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• 2013

This meta-analysis was conducted to evaluate the association between intake of carotenoids and risk of esophageal cancer. A systematic search using PubMed, Cochrane Library, Web of Science, Scopus, CNKI, and CBM (updated to 6 May 2012) identified ten articles meeting the inclusion criteria with 1,958 cases of esophageal cancer and 4,529 controls. Higher intake of beta-carotene, alpha-carotene, lycopene, beta-cryptoxanthin, lutein, and zeaxanthin reduced esophageal cancer risk with pooled ORs of 0.58 (95% CI 0.44, 0.77), 0.81 (95% CI 0.70, 0.94), 0.75 (95% CI 0.64, 0.86), 0.80 (95% CI 0.66, 0.97), and 0.71 (95% CI 0.59, 0.87), respectively. In subgroup analyses, beta-carotene showed protective effects against esophageal adenocarcinoma in studies located in Europe and North America. Alpha-carotene, lycopene, and beta-cryptoxanthin showed protection against esophageal squamous cell cancer. This meta-analysis suggested that higher intake of carotenoids (beta-carotene, alpha-carotene, lycopene, beta-cryptoxanthin, lutein, and zeaxanthin) is associated with lower risk of esophageal cancer. Further research with large-sample studies need to be conducted to better clarify the potentially protective mechanisms of carotenoid associations risk of different types of esophageal cancer.

• Asian Pacific Journal of Cancer Prevention
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• 제14권5호
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• pp.3183-3186
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• 2013

Purpose: The 7th edition of the American Joint Committee on Cancer Staging Manual for esophageal cancer (EC) categorizes N stage according to the number of metastatic lymph nodes (LNs), irrespective of the site. The aim of this study was to determine the prognostic value of subcarinal LN metastasis in patients undergoing esophagectomy for esophageal squamous cell carcinoma (ESCC). Methods: A retrospective analysis of 507 consecutive patients with ESCC was conducted. Potential clinicopathological factors that could influence subcarinal LN metastasis were statistically analyzed. Univariate and multivariate analyses were also performed to evaluate the prognostic parameters for survival. Results: The frequency of subcarinal LN metastasis was 22.9% (116/507). Logistic regression analysis showed that tumor length (>3cm vs ${\leq}3cm$; P=0.027), tumor location (lower vs upper/middle; P=0.009), vessel involvement (Yes vs No; P=0.001) and depth of invasion (T3-4a vs T1-2; P=0.012) were associated with 2.085-, 1.810-, 2.535- and 2.201- fold increases, respectively, for risk of subcarinal LN metastasis. Multivariate analyses showed that differentiation (poor vs well/moderate; P=0.001), subcarinal LN metastasis (yes vs no; P=0.033), depth of invasion (T3-4a vs T1-2; P=0.014) and N staging (N1-3 vs N0; P=0.001) were independent prognostic factors. In addition, patients with subcarinal LN metastasis had a significantly lower 5-year cumulative survival rate than those without (26.7% vs 60.9%; P<0.001). Conclusions: Subcarinal LN metastasis is a predictive factor for long-term survival in patients with ESCC.

• Asian Pacific Journal of Cancer Prevention
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• 제15권15호
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• pp.6021-6024
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• 2014

Background: The STK15 gene located on chromosome 20q13.2 encodes a centrosome-associated kinase critical for regulated chromosome segregation and cytokinesis. Recent studies have demonstrated STK15 to be significantly associated with many tumors, with aberrant expression obseved in many human malignancies. The purpose of this study was to investigate expression of STK15 in esophageal squamous cell carcinomas (ESCCs) in a Mongolian population. Methods: Two non-synonymous single nucleotide polymorphisms in the coding region of STK15, rs2273535 (Phe31Ile) and rs1047972 (Val57Ile) were assessed in 380 ESCC patients and 380 healthy controls. We also detected STK15 mRNA expression in 39 esophageal squamous cell carcinomas and corresponding adjacent tissues by real time PCR. Results: rs2273535 showed a significant association with ESCC in our Mongolian population (rs227353, P allele = 0.0447, OR (95%CI) = 1.259 (1.005~1.578)). Real time PCR analysis of ESCC tissues showed that expression of STK15 mRNA in cancer tissues was higher than in normal tissues (p = 0.013). Conclusions: Our study showed that functional SNPs in the STK15 gene are associated with ESCC in a Mongolian population and up-regulation of STK15 mRNAoccurs in ESCC tumors compared adjacent normal tissues. STK15 may thus have an important role in the prognosis of ESCC and be a potential therapeutic target.

• Asian Pacific Journal of Cancer Prevention
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• 제14권5호
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• pp.2851-2857
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• 2013

Objective: REPS2 plays important roles in inhibiting cell proliferation, migration and in inducing apoptosis of cancer cells, now being identified as a useful biomarker for favorable prognosis in prostate and breast cancers. The purpose of this study was to assess REPS2 expression and to explore its role in esophageal squamous cell carcinoma (ESCC). Methods: Protein expression of REPS2 in ESCCs and adjacent non-cancerous tissues from 120 patients was analyzed by immunohistochemistry and correlated with clinicopathological parameters and patient outcome. Additionally, thirty paired ESCC tissues and four ESCC cell lines and one normal human esophageal epithelial cell line were evaluated for REPS2 mRNA and protein expression levels by quantitative RT-PCR and Western blotting. Results: REPS2 mRNA and protein expression levels were down-regulated in ESCC tissues and cell lines. Low protein levels were significantly associated with primary tumour, TNM stage, lymph node metastasis and recurrence (all, P < 0.05). Survival analysis demonstrated that decreased REPS2 expression was significantly associated with shorter overall survival and disease-free survival (both, P < 0.001), especially in early stage ESCC patients. When REPS2 expression and lymph node metastasis status were combined, patients with low REPS2 expression/lymph node (+) had both poorer overall and disease-free survival than others (both, P < 0.001). Cox multivariate regression analysis further revealed REPS2 to be an independent prognostic factor for ESCC patients. Conclusions: Our findings demonstrate that downregulation of REPS2 may contribute to malignant progression of ESCC and represent a novel prognostic marker and a potential therapeutic target for ESCC patients.

• Asian Pacific Journal of Cancer Prevention
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• 제15권13호
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• pp.5437-5442
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• 2014

Esophageal squamous cell carcinoma (ESCC) is one of the most malignancies with a poor prognosis. The phospholipase $C{\varepsilon}$ gene (PLCE1) encodes a novel ras-related protein effector mediating the effects of R-Ras on the actin cytoskeleton and membrane protrusion. However, molecular mechanisms pertinent to ESCC are unclear. We therefore designed PLCE1-special small interfering RNA and transfected to esophageal squamous cell (EC) 9706 cells to investigat the effects of PLCE1 gene silencing on the cell cycle and apoptosis of ESCC and indicate its important role in the development of ESCC. Esophageal cancer tissue specimens and normal esophageal mucosa were obtained and assayed by immunohistochemical staining to confirm overexpression of PLCE1 in neoplasias. Fluorescence microscopy was used to examine transfection efficiency, while the result of PLCE1 silencing was examined by reverse transcription (RT-PCR). Flow cytometry and annexin V apoptosis assays were used to assess the cell cycle and apoptosis, respectively. Expression of cyclin D1 and caspase-3 was detected by Western-blotting. The level of PLCE1 protein in esophageal cancer tissue was significantly higher than that in normal tissue. After transfection, the expression of PLCE1 mRNA in EC 9706 was significantly reduced, compared with the control group. Furthermore, flow cytometry results suggested that the PLCE1 gene silencing arrested the cell cycle in the G0/G1 phase; apoptosis was significantly higher than in the negative control group and mock group. PLCE1 gene silencing by RNAi resulted in decreased expression of cyclin D1 and increased expression of caspase-3. Our study suggests that PLCE1 may be an oncogene and play an important role in esophageal carcinogenesis through regulating proteins which control cell cycling and apoptosis.

• Asian Pacific Journal of Cancer Prevention
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• 제15권22호
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• pp.9955-9960
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• 2014

Background: Promoter hypermethylation is a common event in human cancer. O6-methylguanine-DNA methyltransferase (MGMT) is a gene involved in DNA repair, which is methylated in a variety of cancers. We aimed to explore the methylation status of MGMT gene among the North Eastern population where esophageal cancer incidence and exposure to carcinogens like nitrosamines is high. Materials and Methods: A total of 100 newly diagnosed esophageal cancer cases along with equal number of age, sex and ethnicity matched controls were included in this study. Methylation specific PCR was used to determine the MGMT methylation status in serum samples. Results: Aberrant promoter methylation of the MGMT gene was detected in 70% of esophageal cancer cases. Hypermethylation of MGMT gene was found to be influenced by environmental factors like betel quid and tobacco which contain potent carcinogens like nitrosamines. Tobacco chewing and tobacco smoking habit synergistically with MGMT methylation elevated the risk for esophageal cancer development [adjusted OR=5.02, 95% CI=1.35-18.74; p=0.010 for tobacco chewing and Adjusted OR=3.00, 95% CI=1.22-7.36; p=0.014 for tobacco smoking]. Conclusions: Results suggest that the DNA hypermethylation of MGMT is an important mechanism for MGMT gene silencing resulting in esophageal cancer development and is influenced by the environmental factors. Thus MGMT hypermethylation can be used as a biomarker for esophageal cancer in high incidence region of North East India.