• 한국비블리아학회지
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• 제26권1호
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• pp.217-231
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• 2015

본 연구에서는 췌장암의 유전자-단백질 상호작용 네트워크를 구성하고, 관련 연구에서 주요하게 언급되는 유전자-단백질의 유발관계 사슬을 파악함으로써, 췌장암의 원인을 규명하는 실증적인 연구로 이어질 수 있는 미발견 공공 지식을 제공하려 하였다. 이를 위하여 텍스트마이닝과 주경로 분석을 Swanson의 ABC 모델에 적용해 중간 개념인 B를 방향성을 가진 다단계 모델로 확장하고 가장 의미 있는 경로를 도출하였다. 본 연구의 주제가 된 췌장암의 사례처럼 시작점과 끝점조차 한정할 수 없는 미발견 공공 지식 추론에서 주경로 분석은 유용한 도구가 될 수 있을 것이다.

• IMMUNE NETWORK
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• 제12권6호
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• pp.247-252
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• 2012

Pancreatic cancer is the fourth commonest cause of cancer-related deaths in the world. However, no adequate therapy for pancreatic cancer has yet been found. In this study, the antitumor activity of cytokine-induced killer (CIK) cells against the human pancreatic cancer was evaluated in vitro and in vivo. Human peripheral blood mononuclear cells were cultured with IL-2-containing medium in anti-CD3 for 14 days. The resulting populations of CIK cells comprised 94% $CD3^+$, 4% $CD3^-CD56^+$, 41% $CD3^+CD56^+$, 11% $CD4^+$, and 73% $CD8^+$. This heterogeneous cell population was called cytokine-induced killer (CIK) cells. At an effector-target cell ratio of 100 : 1, CIK cells destroyed 51% of AsPC-1 human pancreatic cancer cells, as measured by the $^{51}Cr$-release assay. In addition, CIK cells at doses of 3 and 10 million cells per mouse inhibited 42% and 70% of AsPC-1 tumor growth in nude mouse xenograft assays, respectively. This study suggests that CIK cells may be used as an adoptive immunotherapy for pancreatic cancer patients.

• Journal of Yeungnam Medical Science
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• 제39권2호
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• pp.124-132
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• 2022

Background: Despite recent advances in first-line chemotherapy for advanced pancreatic cancer, standard treatment after the failure of initial chemotherapy has not been established. Hence, we aimed to retrospectively analyze the clinical characteristics and outcomes of second-line chemotherapy in patients with advanced pancreatic cancer. Methods: We reviewed the clinical data of patients with advanced pancreatic cancer who underwent palliative chemotherapy at Kosin University Gospel Hospital between January 2013 and October 2020. Results: Among 366 patients with advanced pancreatic cancer who had received palliative chemotherapy, 104 (28.4%) underwent at least one cycle of second-line chemotherapy. The median age of the patients at the time of initiating second-line treatment was 62 years (interquartile range, 57-62 years), and 58.7% (61 patients) of them were male. The common second-line chemotherapy regimens were 5-fluorouracil (FU) plus leucovorin, irinotecan, and oxaliplatin (33 patients, 31.7%); gemcitabine/nab-paclitaxel (29, 27.9%), gemcitabine±erlotinib (13, 12.5%); and oxaliplatin and 5-FU/leucovorin (12, 11.5%). The median overall survival (OS) and progression-free survival were 6.4 months (95% confidence interval [CI], 4.5-8.6 months) and 4.5 months (95% CI, 2.7-6.3 months), respectively. In a multivariate analysis, poor performance status (PS) (hazard ratio [HR], 2.247; p=0.021), metastatic disease (HR, 2.745; p=0.011), and elevated carcinoembryonic antigen (CEA) levels (HR, 1.939; p=0.030) at the beginning of second-line chemotherapy were associated with poor OS. Conclusion: The survival outcome of second-line chemotherapy for advanced pancreatic cancer remains poor. However, PS, disease extent (locally advanced or metastatic), and CEA level may help determine patients who could benefit from second-line treatment.

• Journal of Microbiology and Biotechnology
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• 제33권4호
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• pp.449-462
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• 2023

Previously, we confirmed that Mychonastes sp. 246 methanolic extract (ME) markedly reduced the viability of BxPC-3 human pancreatic cancer cells. However, the underlying mechanism ME remained unclear. Hence, we attempted to elucidate the anticancer effect of ME on BxPC-3 human pancreatic cancer cells. First, we investigated the components of ME and their cytotoxicity in normal cells. Then, we confirmed the G1 phase arrest mediated growth inhibitory effect of ME using a cell counting assay and cell cycle analysis. Moreover, we found that the migration-inhibitory effect of ME using a Transwell migration assay. Through RNA sequencing, Gene Ontology-based network analysis, and western blotting, we explored the intracellular mechanisms of ME in BxPC-3 cells. ME modulated the intracellular energy metabolism-related pathway by altering the mRNA levels of IGFBP3 and PPARGC1A in BxPC-3 cells and reduced PI3K and mTOR phosphorylation by upregulating IGFBP3 and 4E-BP1 expression. Finally, we verified that ME reduced the growth of three-dimensional (3D) pancreatic cancer spheroids. Our study demonstrates that ME suppresses pancreatic cancer proliferation through the IGFBP3-PI3K-mTOR signaling pathway. This is the first study on the anticancer effect of the ME against pancreatic cancer, suggesting therapeutic possibilities and the underlying mechanism of ME action.

• Journal of Digestive Cancer Research
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• 제7권1호
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• pp.18-21
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• 2019

Serine protease inhibitor Kazal-type 1 (SPINK1) is a gene expressed from pancreatic acinar cell which its mutation is known to be associated with chronic pancreatitis (CP) and pancreatic cancer. We report a case of a 47-years-old female with nausea and weight loss with yellow discoloration of skin. Initial imaging and endoscopic study led us to an impression of chronic pancreatitis with pancreatic cancer with common bile-duct dilation. Biopsy result was confirmed with pancreatic adenocarcinoma and additional imaging revealed lymph node and bone metastasis. Our genetic analysis revealed 194+2T>C mutation of SPINK1. Biliary obstruction was successfully decompressed by stent insertion and underwent chemotherapy and radiotherapy. Although there is accumulating evidence of association between SPINK1 mutation and CP, the relationship between SPINK1 mutation and pancreatic cancer in CP patient is an emerging concept. Genetic analysis should be considered in patients with young age especially when diagnosed with both CP and pancreatic cancer.

• Radiation Oncology Journal
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• 제34권2호
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• pp.156-159
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• 2016

Although carbohydrate antigen (CA) 19-9 is a useful tumor marker for pancreatic cancer, it can also become elevated from a variety of benign and malignant conditions. Herein we describe an unusual presentation of elevated CA 19-9 in an asymptomatic patient who had previously undergone adjuvant chemotherapy and radiation therapy for resected early stage pancreatic cancer. The rise in CA 19-9 might be due to delayed radiation-induced inflammation related to previous intra-abdominal radiation therapy with or without radiation recall induced by gemcitabine. After treatment with corticosteroids the CA 19-9 level decreased to normal, and the patient has not developed any evidence of recurrent cancer to date.

• 한국간담췌외과학회지
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• 제27권1호
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• pp.28-39
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• 2023

We aimed to compare resection and survival outcomes of neoadjuvant chemoradiotherapy (CRT) and immediate surgery in patients with resectable pancreatic cancer (RPC) or borderline resectable pancreatic cancer (BRPC). In compliance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement standards, a systematic review of randomized controlled trials (RCTs) was conducted. Random effects modeling was applied to calculate pooled outcome data. Likelihood of type 1 or 2 errors in the meta-analysis model was assessed by trial sequential analysis. A total of 400 patients from four RCTs were included. When RPC and BRPC were analyzed together, neoadjuvant CRT resulted in a higher R0 resection rate (risk ratio [RR]: 1.55, p = 0.004), longer overall survival (mean difference [MD]: 3.75 years, p = 0.009) but lower overall resection rate (RR: 0.83, p = 0.008) compared with immediate surgery. When RPC and BRPC were analyzed separately, neoadjuvant CRT improved R0 resection rate (RR: 3.72, p = 0.004) and overall survival (MD: 6.64, p = 0.004) of patients with BRPC. However, it did not improve R0 resection rate (RR: 1.18, p = 0.13) or overall survival (MD: 0.94, p = 0.57) of patients with RPC. Neoadjuvant CRT might be beneficial for patients with BRPC, but not for patients with RPC. Nevertheless, the best available evidence does not include contemporary chemotherapy regimens. Patients with RPC and those with BRPC should not be combined in the same cohort in future studies.

• Asian Pacific Journal of Cancer Prevention
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• 제16권4호
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• pp.1651-1655
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• 2015

UGT1A play important roles in the glucuronidation of a variety of endogenous and exogenous compounds. UGT1A isoforms are expressed tissue specifically. The aim of this study was to examine the relationship between UGT1A3 and UGT1A7 mRNA expression and pancreatic cancer. Paired healthy and tumor tissue samples of 43 patients with pancreatic cancer were included in this study. UGT1A3 and UGT1A7 mRNA expressions were analyzed by real time-PCR. In the result of study, UGT1A3 and UGT1A7 mRNA expressions were significantly higher in tumor tissue than normal tissue of pancreatic cancer patients (p<0.05). In addition, high mRNA expression of UGT1A3 and UGT1A7 was significantly associated with larger tumor size (p<0.05). The data suggested that UGT1A3 and UGT1A7 may play roles in the progression of pancreatic cancer. Consequently, UGT1A3 and UGT1A7 are potential prognostic indicators.

• Asian Pacific Journal of Cancer Prevention
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• 제13권5호
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• pp.2249-2252
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• 2012

Objective: Methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms have been reported to be associated with pancreatic cancer, but the published studies had yielded inconsistent results.We therefore performed the present meta-analysis. Methods: A search of Google scholar, PubMed, Cochrane Library and CNKI databases before April 2012 was conducted to summarize associations of MTHFR polymorphisms with pancreatic cancer risk. Assessment was with odds ratios (ORs) and 95% confidence intervals (CIs). Publication bias were also calculated. Results: Four relative studies on MTHFR gene polymorphisms (C667T and A1298C) were involved in this meta-analysis. Overall, C667T(TT vs. CC : OR = 1.61, 95%CI = 0.78 - 3.34; TT vs. CT : OR = 1.41, 95%CI = 0.88-2.25; dominant model: OR = 0.68, 95%CI = 0.40-1.17; recessive model: OR = 0.82, 95%CI = 0.52-1.30) and A1298C(CC vs. AA:OR=1.01, 95%CI=0.47-2.17; CC vs. AC: OR=0.99,95%CI=0.46-2.14; dominant model: OR=1.01, 95%CI = 0.47-2.20; recessive model: OR = 1.01, 95%CI = 0.80-1.26) did not increase pancreatic cancer risk. Conclusion: This meta-analysis indicated that MTHFR polymorphisms (C667T and A1298C) were not associated with pancreatic cancer risk.

• Journal of Digestive Cancer Research
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• 제3권2호
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• pp.105-107
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• 2015

췌장암은 예후가 매우 불량한 암으로 수술적 절제술을 시행하여도 대부분의 경우 재발을 한다고 알려져 있다. 재발을 하는 경우 대개 항암화학요법을 시행하게 되나, 그 반응 또한 좋지 않은 것으로 알려져 있다. 간에 국소적으로 재발을 했을 경우 종양절제술을 시행하는 것에 대해서는 몇몇 보고가 있는 정도이며, 생존율을 향상시킬 수 있는지에 대해서는 연구가 거의 없는 상태이다. 본 증례는 유문보존 췌십이지장 절제술 시행 후 간에 국소적으로 재발한 췌장암에 대하여 gemcitabine 및 capecitabine과 oxaliplatin 병합 항암화학요법을 시행하였으나 크기가 증가하였고, 이에 종양절제술을 시행하였으며, 이후 장기생존을 보였던 경우로 매우 드문 증례를 경험하였기에 보고하는 바이다.