• Journal of Digestive Cancer Research
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• v.12 no.1
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• pp.51-52
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• 2024

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4689-4695
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• 2014

Background: A great number of studies have shown that cytochrome P450 1A1 (CYP1A1) genetic polymorphisms, CYP1A1 Msp I and CYP1A1 Ile/Val, might be risk factors for digestive tract cancers, including esophageal cancer (EC), gastric cancer (GC), hepatic carcinoma (HC), as well as colorectal cancer (CC), but the results are controversial. In this study, a meta-analysis of this literature aimed to clarify associations of CYP1A1 genetic polymorphisms with digestive tract cancers susceptibility in Chinese populations. Materials and Methods: Eligible case-control studies published until December 2013 were retrieved by systematic literature searches from PubMed, Embase, CBM, CNKI and other Chinese databases by two investigators independently. The associated literature was acquired through deliberate search and selection based on established inclusion criteria. Fixed-effects or random-effects models were used to estimate odds ratios (ORs and 95%CIs). The meta-analysis was conducted using Review Manager 5.2 and Stata 12.0 softwares with stability evaluated by both stratified and sensitivity analyses. Moreover, sensitivity analysis and publication bias diagnostics confirmed the reliability and stability. Results: Eighteen case-control studies with 1,747 cases and 2,923 controls were selected for CYP1A1 MspI polymorphisms, and twenty case-control studies with 3, 790 cases and 4, 907 controls for the CYP1A1 Ile/Val polymorphisms. Correlation associations between CYP1A1 Ile/Val polymorphisms and digestive tract cancers susceptibility were observed in four genetic models in the meta-analysis (GG vs AA:OR= 2.03, 95%CI =1.52- 2.72; AG vs AA: OR=1.26, 95%CI =1.07-1.48; [GG+AG vs AA] :OR =1.42, 95%CI=1.20-1.68, [GG vs AA+AG]:OR=1.80, 95%CI =1.40-2.31). There was no association between CYP1A1 Msp I polymorphisms and digestive tract cancers risk. Subgroup analysis for tumor type showed a significant association of CYP1A1 Ile/Val genetic polymorphisms with EC in China. However, available data collected by the study failed to reveal remarkable associations of GC or HC with CYP1A1 Ile/Val genetic polymorphisms and EC, GC or CC with CYP1A1 MspI genetic polymorphisms. Conclusions: Our results indicated that CYP1A1 Ile/Val genetic polymorphisms, but not CYP1A1 Msp I polymorphisms, are associated with an increased digestive tract cancers risk in Chinese populations. Additional well-designed studies, with larger sample size, focusing on different ethnicities and cancer types are now warranted to validate this finding.

• Proceedings of the Korean Nuclear Society Conference
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• 1996.11b
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• pp.629-635
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• 1996

The lifetime radiation-induced cancer mortality for Korean has been estimated for both single and continuous radiation exposure using the BEIR V method. In case of single exposure, a dominant cancer site for young and old ages was digestive and respiratory cancer, respectively. For Korean population, digestive cancer was the most dominant radiation-induced cancer site. In case of 1 mGy/yr continuous exposure from birth to death, the contribution of total radiation-induced cancer mortality was negligible as within 3% in comparison with total natural cancer mortality.

• Journal of Digestive Cancer Reports
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• v.5 no.2
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• pp.97-104
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• 2017

Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.

• Journal of Digestive Cancer Research
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• v.5 no.2
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• pp.97-104
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• 2017

Background: Cachexia is a multi-factorial syndrome presenting with chronic illness, decreases in body weight, and loss of adipose tissue and skeletal muscle, mostly in patients with advanced cancer and chronic wasting disease. Even after years of intensive researches, there remains no convincing therapy to prevent cancer cachexia. Methods: In this in vivo study, we have established C26 adenocarcinoma-induced cancer cachexia model in mice to explore the underlying core changes in cytokine, signal transduction, and muscle wasting. The ultimate aim of establishing animal model is to find optimal therapeutics to mitigate cancer cachexia. Results: We have administered C26 adenocarcinoma cells onto BALB/c mice and observed 4 weeks to assess the progression of cancer cachexia. Significant loss of weight accompanied with loss of appetite was noted. As C26 adenocarcinoma xenograft progressed, mortality was started from 3 weeks, accompanied with significant sarcopenia and decreased mice movement. Surges in TNF-α and IL-6 were noted with the commencement of cancer cachexia. Conclusion: Using C26 adenocarcinoma cancer cachexia model, we can screen the optimal therapeutics to mitigate cancer cachexia, in which agents to modulate IL-6, TNF-α, and NF-κB were essential.

• Korean Journal of Adult Nursing
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• v.28 no.3
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• pp.343-353
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• 2016

Purpose: This study aimed to identify the levels of oxaliplatin-induced peripheral neuropathy (OXLIPN) and the quality of life (QOL) related to OXLIPN in patients with digestive system cancer. Methods: A total of 83 patients with chemotherapy-induced peripheral neuropathy (CIPN)-related symptoms participated in this study. Data were collected through self-reported questionnaire which were constructed to include general and clinical characteristics, EORTC QLQ-C30, Patient Neurotoxicity Questionnaire (PNQ), and EORTC QLQ-CIPN20. Results: The average scores of OXLIPN upper and lower extremity scale were 30.01 and 29.16, respectively. The average scores of PNQ sensory and motor scale were 2.11 and 1.70, respectively. The mean score of the QLQ-C30 global health status was 54.85, and the range of mean score of the functional and symptom subdomains was 34.85~73.29 and 17.67~53.54, respectively. The CIPN-related symptoms positively correlated with the global health status scale and all subdomains of functional scale, respectively and negatively correlated with fatigue, pain, dyspnea, insomnia, and financial problem subdomains of the symptom scale, respectively. Conclusion: Oncology nurses should pay attention and provide remedies for CIPN symptoms reported by their patients. Nursing interventions should be developed for patients with digestive system cancer to alleviate CIPN and enhance their QOL.

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.11
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• pp.4563-4566
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• 2014

Background: To evaluate relationship between the cyclooxygenase-2 promoter 765G/C polymorphism and digestive cancer risk in China. Materials and Methods: A literature search through February 2014 was performed using PubMed, Chinese Biomedical Literature Database (CBM) and China National Knowledge Infrastructure (CNKI) databases, and a meta-analysis was performed with RevMan 5.2 software for odds ratios and 95%CIs. Results: In total, 9 articles with 3,263 cases and 4,858 controls were included in this meta-analysis. The pooled OR (95%CIs) in the co-dominant model (GC vs GG) was 1.56 [1.19, 2.06], and in the dominant model ((CC+GC) vs GG), the pooled OR was 1.59 [1.21, 2.09] in overall cancers. In the subgroup analysis, stratified by cancer type, significant associations were found that the-765C allele had increased pancreatic cancer and gastric risk. No significant liver cancer and colorectal cancer risk of COX-2 -765G/C polymorphism was found. Conclusions: These findings suggest that COX-2-765*C is related to cancer susceptibility and may increase gastric and pancreatic cancer risk.

• Journal of Digestive Cancer Reports
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• v.9 no.2
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• pp.75-77
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• 2021

• Journal of Digestive Cancer Research
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• v.3 no.1
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• pp.1-4
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• 2015

• Journal of Digestive Cancer Research
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• v.1 no.2
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• pp.67-72
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• 2013