• International Journal of Stem Cells
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• v.17 no.3
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• pp.253-269
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• 2024

Pancreas serves endocrine and exocrine functions in the body; thus, their pathology can cause a broad range of irreparable consequences. Endocrine functions include the production of hormones such as insulin and glucagon, while exocrine functions involve the secretion of digestive enzymes. Disruption of these functions can lead to conditions like diabetes mellitus and exocrine pancreatic insufficiency. Also, the symptoms and causality of pancreatic cancer very greatly depends on their origin: pancreatic ductal adenocarcinoma is one of the most fatal cancer; however, most of tumor derived from endocrine part of pancreas are benign. Pancreatitis, an inflammation of the pancreatic tissues, is caused by excessive alcohol consumption, the bile duct obstruction by gallstones, and the premature activation of digestive enzymes in the pancreas. Hereditary pancreatic diseases, such as maturity-onset diabetes of the young and hereditary pancreatitis, can be a candidate for disease modeling using human pluripotent stem cells (hPSCs), due to their strong genetic influence. hPSC-derived pancreatic differentiation has been established for cell replacement therapy for diabetic patients and is robustly used for disease modeling. The disease modeling platform that allows interactions between immune cells and pancreatic cells is necessary to perform in-depth investigation of disease pathogenesis.

• Journal of Digestive Cancer Research
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• v.3 no.1
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• pp.17-20
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• 2015

Pancreatic cancer is an aggressive tumor and only 10-20% patients are considered candidates for curative resection at diagnosis. While surgery remains the only chance for cure, prognosis is poor even after surgery due to high rate of recurrence. A complementary chemotherapy and radiotherapy in a multimodal approach has been attempted to improved prognosis after surgery. Since adjuvant chemotherapy has yielded an only modest outcome improvement, various neoadjuvant approaches with chemotherapy, chemoradiation, or chemotherapy followed by chemoradiation have been attempted. In this article, current knowledge of the various neoadjuvant approaches for pancreatic cancer will be reviewed and the role of the neoadjuvant strategies will be discussed.

• Journal of Yeungnam Medical Science
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• v.33 no.2
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• pp.77-84
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• 2016

Pancreatic cancer, the 4th leading cause of cancer-related death in the United States, has a very poor prognosis. Cholangiocarcinoma originates from either intrahepatic or extrahepatic bile duct, and its incidence is gradually increasing worldwide. Endoscopic retrograde cholangiopancreatography with brush cytology has a high false-negative rate for the diagnosis of biliary malignancy. Recently, endoscopic ultrasonography (EUS) has emerged as the potential modality to detect pancreatic cancer. EUS-guided fine needle aspiration for cytologic analysis made it possible to overcome the obstacle in differentiating between benign and malignant lesions in the pancreatobiliary lesion, and it has been well established as a safe and effective procedure. Herein, the clinical application of EUS in the diagnosis of pancreatobiliary cancer was reviewed.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.9
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• pp.3805-3810
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• 2015

Arsenic trioxide (ATO) has been found to exert anti-cancer activity in various human malignancies. However, the molecular mechanisms by which ATO inhibits tumorigenesis are not fully elucidated. In the current study, we explored the molecular basis of ATO-mediated tumor growth inhibition in pancreatic cancer cells. We used multiple approaches such as MTT assay, wound healing assay, Transwell invasion assay, annexin V-FITC, cell cycle analysis, RT-PCR and Western blotting to achieve our goal. We found that ATO treatment effectively caused cell growth inhibition, suppressed clonogenic potential and induced G2-M cell cycle arrest and apoptosis in pancreatic cancer cells. Moreover, we observed a significant down-regulation of Skp2 after treatment with ATO. Furthermore, we revealed that ATO regulated Skp2 downstream genes such as FOXO1 and p53. These findings demonstrate that inhibition of Skp2 could be a novel strategy for the treatment of pancreatic cancer by ATO.

• Journal of Korean Traditional Oncology
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• v.27 no.1
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• pp.1-12
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• 2022

Objectives: To report recurrent pancreatic cancer treated by Korean medicine based-integrated oncology treatment, who is improved quality of life without progression of cancer Method: A 63-year-old female patient diagnosed with recurrent pancreatic cancer in April, 2022 received Chemotherapy with Korean medicine based integrative oncology treatment. Radiologic outcome was assessed by Abdomen Computed Tomography (CT) based on Response Evaluation Criteria In Solid Tumors (RECIST). Clinical outcomes were assessed by National Cancer Institute Common Terminology Criteria for Adverse Event (NCI-CTCAE), Eastern Cooperative Oncology Group (ECOG), Numeric Rating Scale (NRS) Result: During 2months of treatment, Cancer size was stable in Abdominal CT. Chief complaints, Abdominal pain and dyspepsia, were improved and ECOG score was improved from grade 2 to 1. There were no toxicity on laboratory test and no side effects of grade 3 or higher on NCI-CTCAE. Conclusion: This report shows that Korean medicine based integrative oncology treatment might contribute to synergetic effect to Chemotherapy and improvement of quality of life

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.4
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• pp.2453-2459
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• 2013

Bevacizumab has been approved for use in combination with chemotherapy to treat many types of cancer but associated neutropenic events, including febrile neutropenia, have been reported. To estimate the incidence and relative risk of neutropenic events in cancer patients treated with bevacizumab combination therapy, we searched PubMed, EMBASE, and Web of Science literature databases, as well as abstracts presented at the American Society of Clinical Oncology conferences, to identify relevant studies published from January 1966 to December 2011. Studies that compared bevacizumab plus chemotherapy or biological therapy with chemotherapy or biological therapy alone, and that had adequate safety data profiles, were selected for analysis. Statistical analyses were conducted to calculate the summary incidence rates, relative risks (RRs), and 95% confidence intervals (CIs) using fixed- or random-effects models. A total of 22 clinical trials involving 15,056 patients were included in the analysis. The summary incidences of high-grade neutropenia (HGN) and high-grade febrile neutropenia (HGFN) in patients receiving bevacizumab was 27.3% (95% CI: 26.4%-28.3%) and 3.91% (95% CI: 3.51%-4.37%), respectively. The risks of HGN (RR=1.10; 95% CI: 1.02-1.19; P=0.02) and HGFN (RR=1.31; 95% CI: 1.08-1.59; P=0.005) were significantly increased in bevacizumab-treated patients, compared to those who did not receive bevacizumab. The RR of bevacizumab-associated HGN, but not HGFN, varied significantly with tumor types (P=0.005). The increased risk of bevacizumab-associated neutropenic events was dose-dependent, as the RR was greater at a dose of 5 mg/kg/week than at 2.5 mg/kg/week. Our findings suggest that bevacizumab addition to cancer therapy significantly increases the risk of serious neutropenic events, and this risk may be dose-dependent.

• The Journal of Internal Korean Medicine
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• v.41 no.2
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• pp.166-176
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• 2020

Objectives: This study reports on the effect of Integrative Medicine Therapy (IMT) on a patient with pancreatic cancer with liver metastasis. Methods: One pancreatic cancer with liver metastasis patient was treated using IMT in conjunction with Gemcitabine/Abraxane since September 2019. The cycle was repeated every four weeks for a total of 11 times. At the same time, the patient was treated with IMT. Tumor size was measured by scanning with Computed Tomography (CT). Adverse events were evaluated using the National Cancer Institute Common Terminology Criteria for Adverse Events (NCI-CTCAE), version 5.0. Results: After treatment with Gemcitabine/Abraxane and IMT for eight months, the size of the body and tail of the cancer tumor and several hepatic metastatic regions decreased (partial response, [PR]), size, and number of multiple nodules in both lungs decreased. No evidence of newly developed metastatic lesions was found. The patient has maintained a good treatment outcome and has shown prolonged overall survival. Conclusions: This case demonstrates that treatment with IMT may have substantial benefits for patients with end-stage pancreatic cancer.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.10
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• pp.4387-4392
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• 2015

Background: Tight junctions (TJs) organise paracellular permeability and they have an important role in epithelial and endothelial cell polarity and permanence of barrier function. It has been demonstrated that the Claudin family constitutes an important component of them. In this study, we assessed expression patterns of of Claudin1, 4 and 7 and whether they have any relation with prognosis in patients with pancreatic cancer. Materials and Methods: Expression patterns of Claudin 1,4 and 7 were examined by immunohistochemistry in 25 patients with a histopathological diagnosis of pancreatic cancer using a semiquantitative scoring of the extent and intensity of staining. After grouping the staining scores as low (final score 0-2) and high (final score 3-9) the relation between expression of Claudin 1,4 and 7 and survival was evaluated. Results: There was no significant relation between expression of Claudin 1,4 and 7 and gender and stage. No statistically significant relation was found between Claudin 1 and 4 expression and survival whereas a statistically significant relation was found between decrease in Claudin 7 expression and decrease in survival. Conclusions: Claudins have important functions other than their popular function known as adhesion. Supporting this hypothesis, we found a statistically significant relationship between increased Claudin 7 expression and increased survival time, and this suggests that Claudin 7 may exert different tumorigenic effects in pancreatic cancer other than its well-known adhesion effect.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.1917-1921
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• 2012

Background: Colorectal cancer is one of the leading causes of mortality worldwide. Genome wide analysis studies have identified sequence mutations causing loss-of-function that are associated with disease occurrence and severity. Epigenetic modifications, such DNA methylation, have also been implicated in many cancers but have yet to be examined in the East Asian population of colorectal cancer patients. Methods: Biopsies of tumors and matched non-cancerous tissue types were obtained and genomic DNA was isolated and subjected to the bisulphite conversion method for comparative DNA methylation analysis on the Illumina Infinium HumanMethylation27 BeadChip. Results: Totals of 258 and 74 genes were found to be hyper- and hypo-methylated as compared to the individual's matched control tissue. Interestingly, three genes that exhibited hypermethylation in their promoter regions, CMTM2, ECRG4, and SH3GL3, were shown to be significantly associated with colorectal cancer in previous studies. Using heatmap cluster analysis, eight hypermethylated and 10 hypomethylated genes were identified as significantly differentially methylated genes in the tumour tissues. Conclusions: Genome-wide methylation profiling facilitates rapid and simultaneous analysis of cancerous cells which may help to identify methylation markers with high sensitivity and specificity for diagnosis and prognosis. Our results show the promise of the microarray technology in identification of potential methylation biomarkers for colorectal cancers.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.5
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• pp.1793-1797
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• 2012

Objective: To analyze the capacity of neurotrophic artemin to promote the motility and invasiveness of MIA PaCa-2 pancreatic cancer cells. Methods: MIA PaCa-2 was cultured in vitro and studied using transwell chambers for motility and invasiveness on treatment with different concentrations of aArtemin or its receptor $GFR{\alpha}3$ were also determined. Expression of matrix metalloproteinase-2 (MMP-2) and epithelial cadherin (E-cadherin) was quantified using RT-PCR and Western blotting. Results: MIA PaCa-2 pancreatic cancer cell motility and invasiveness was significantly increased with artemin and its receptor $GFR{\alpha}3$ with dose dependence (P<0.01). MMP-2 production was also significantly increased (t = 6.35, t = 7.32), while E-cadherin was significantly lowered (t = 4.27, t = 5.61) (P <0.01). Conclusion: Artemin and its receptor $GFR{\alpha}3$ can promote pancreatic cancer cell motility and invasiveness and contribute to aggressive behavior. The mechanism may be related to increased expression of MMP-2 molecule and down-regulation of E-cadherin expression.