• Title/Summary/Keyword: Cancer, Pancreatic

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Clinical Effects of Gemcitabine and 5-Fluorouracil Combination therapy and Epirubicin. Cisplatin. and 5-Fluorouracil Combination therapy for patients with Pancreatic Cancer

  • Her, Sook;Lee, Suk-Hyung;Kang, Jin-Hyoung
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.428.1-428.1
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    • 2002
  • Gemcitabine demonstrated modest activity in locally advanced and metastatic pancreatic cancer with difficulty early diagnosis and poor prognisis. The purpose of this study was to evaluate the efficacy and toxicity of gemcitabine and 5-fluorouracil(GF) combination theraphy and epirubicin. cisplatin. and 5-fluorouracil(ECF) combination theraphy for the patients with locally advanced or metaststic pancreatic cancer. Between January 1996 and December 2001. (omitted)

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In vivo multiplex gene targeting with Streptococcus pyogens and Campylobacter jejuni Cas9 for pancreatic cancer modeling in wild-type animal

  • Chang, Yoo Jin;Bae, Jihyeon;Zhao, Yang;Lee, Geonseong;Han, Jeongpil;Lee, Yoon Hoo;Koo, Ok Jae;Seo, Sunmin;Choi, Yang-Kyu;Yeom, Su Cheong
    • Journal of Veterinary Science
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    • v.21 no.2
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    • pp.26.1-26.14
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    • 2020
  • Pancreatic ductal adenocarcinoma is a lethal cancer type that is associated with multiple gene mutations in somatic cells. Genetically engineered mouse is hardly applicable for developing a pancreatic cancer model, and the xenograft model poses a limitation in the reflection of early stage pancreatic cancer. Thus, in vivo somatic cell gene engineering with clustered regularly interspaced short palindromic repeats is drawing increasing attention for generating an animal model of pancreatic cancer. In this study, we selected Kras, Trp53, Ink4a, Smad4, and Brca2 as target genes, and applied Campylobacter jejuni Cas9 (CjCas9) and Streptococcus pyogens Cas9 (SpCas9) for developing pancreatic cancer using adeno associated virus (AAV) transduction. After confirming multifocal and diffuse transduction of AAV2, we generated SpCas9 overexpression mice, which exhibited high double-strand DNA breakage (DSB) in target genes and pancreatic intraepithelial neoplasia (PanIN) lesions with two AAV transductions; however, wild-type (WT) mice with three AAV transductions did not develop PanIN. Furthermore, small-sized Cjcas9 was applied to WT mice with two AAV system, which, in addition, developed high extensive DSB and PanIN lesions. Histological changes and expression of cancer markers such as Ki67, cytokeratin, Mucin5a, alpha smooth muscle actin in duct and islet cells were observed. In addition, the study revealed several findings such as 1) multiple DSB potential of AAV-CjCas9, 2) peri-ductal lymphocyte infiltration, 3) multi-focal cancer marker expression, and 4) requirement of > 12 months for initiation of PanIN in AAV mediated targeting. In this study, we present a useful tool for in vivo cancer modeling that would be applicable for other disease models as well.

GATA2-Mediated Transcriptional Activation of Notch3 Promotes Pancreatic Cancer Liver Metastasis

  • Lin, Heng;Hu Peng;Zhang, Hongyu;Deng, Yong;Yang, Zhiqing;Zhang, Leida
    • Molecules and Cells
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    • v.45 no.5
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    • pp.329-342
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    • 2022
  • The liver is the predominant metastatic site for pancreatic cancer. However, the factors that determine the liver metastasis and the specific molecular mechanisms are still unclear. In this study, we used human pancreatic cancer cell line Hs766T to establish Hs766T-L3, a subline of Hs766T with stable liver metastatic ability. We performed RNA sequencing of Hs766T-L3 and its parental cell line Hs766T, and revealed huge differences in gene expression patterns and pathway activation between these two cell lines. We correlated the difference in pathway activation with the expression of the four core transcriptional factors including STAT1, NR2F2, GATA2, and SMAD4. Using the TCGA database, we examined the relative expression of these transcription factors (TFs) in pan-cancer and their relationship with the prognosis of the pancreatic cancer. Among these TFs, we considered GATA2 is closely involved in tumor metastasis and may serve as a potential metastatic driver. Further in vitro and in vivo experiments confirmed that GATA2-mediated transcriptional activation of Notch3 promotes the liver metastasis of Hs766T-L3, and knockdown of either GATA2 or Notch3 reduces the metastatic ability of Hs766T-L3. Therefore, we claim that GATA2 may serve as a metastatic driver of pancreatic cancer and a potential therapeutic target to treat liver metastasis of pancreatic cancer.

Laparoscopic radical distal pancreatosplenectomy with celiac axis excision following neoadjuvant chemotherapy for locally advanced pancreatic cancer

  • Yeon Su Kim;Ji Su Kim;Sung Hyun Kim;Ho Kyoung Hwang;Woo Jung Lee;Chang Moo Kang
    • Annals of Hepato-Biliary-Pancreatic Surgery
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    • v.26 no.1
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    • pp.118-123
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    • 2022
  • A recent successful prospective randomized control study comparing open distal pancreatectomy with laparoscopic distal pancreatectomy (LDP) has shown that LDP is a safe and effective surgical modality in treating left-sided pancreatic pathological conditions requiring surgical extirpation. With the accumulating surgical experiences and improved surgical techniques, we recently reported several cases of successful LDP in advanced pancreatic cancer following neoadjuvant chemotherapy. Herein, we report a case of LDP with celiac axis resection (LDP-CAR) in locally advanced pancreatic cancer (LAPC) following neoadjuvant chemotherapy. A 58-yearold female with LAPC was referred to our institution. Computed tomography (CT) findings revealed a 24-mm mass in the pancreatic body that showed celiac artery (CA), common hepatic artery abutment. There was no abutment with superior mesenteric artery, superior mesenteric vein, and portal vein. From these findings, Neoadjuvant chemotherapy (FORFIRINOX) was performed biweekly. After 8 cycles of chemotherapy, the tumor size was slightly decreased (24 mm to 16 mm), but still abutting to CA. After 14 cycles of chemotherapy, CT revealed the same tumor size (16 mm) still abutting to CA. LDP-CAR was performed. Intraoperative ultrasonography gastric perfusion and hepatic perfusion were confirmed using indocyanine green. The patient recovered without complications and was discharged from the hospital nine days after the surgery.

Clinical Effects of Gemcitabine/5-FU Theraphy vs. Epirubicin/Cisplatin/5-FU in Pancreatic Cancer

  • Huh, Sook;Lee, Suk-Hyang;Kang, Jin-Hyoung;Lee, Kyung-Sick;Lee, Myung-A
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.431.1-431.1
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    • 2002
  • Gemcitabine demonstrated modest activity in locally advanced and metastatic pancreatic cancer with difficulty early diagnosis and poor prognisis. The purpose of this study was to evaluate the efficacy and toxicity of gemcitabine and 5-fluorouracil(GF) combination theraphy and epirubiciil, cisplatin. and 5-fluorouracil(ECF) combination theraphy for the patients with locally advanced or metaststic pancreatic cancer. Between January 1996 and December 2001, Patients with locally advanced or metastatic pancreatic cancer were selected and reviewed retrospectively at Kangnam St. Mary's Hospital. (omitted)

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Comparative Proteomic Profiling of Pancreatic Ductal Adenocarcinoma Cell Lines

  • Kim, Yikwon;Han, Dohyun;Min, Hophil;Jin, Jonghwa;Yi, Eugene C.;Kim, Youngsoo
    • Molecules and Cells
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    • v.37 no.12
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    • pp.888-898
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    • 2014
  • Pancreatic cancer is one of the most fatal cancers and is associated with limited diagnostic and therapeutic modalities. Currently, gemcitabine is the only effective drug and represents the preferred first-line treatment for chemotherapy. However, a high level of intrinsic or acquired resistance of pancreatic cancer to gemcitabine can contribute to the failure of gemcitabine treatment. To investigate the underlying molecular mechanisms for gemcitabine resistance in pancreatic cancer, we performed label-free quantification of protein expression in intrinsic gemcitabine-resistant and -sensitive human pancreatic adenocarcinoma cell lines using our improved proteomic strategy, combined with filter-aided sample preparation, single-shot liquid chromatography-mass spectrometry, enhanced spectral counting, and a statistical method based on a power law global error model. We identified 1931 proteins and quantified 787 differentially expressed proteins in the BxPC3, PANC-1, and HPDE cell lines. Bioinformatics analysis identified 15 epithelial to mesenchymal transition (EMT) markers and 13 EMT-related proteins that were closely associated with drug resistance were differentially expressed. Interestingly, 8 of these proteins were involved in glutathione and cysteine/methionine metabolism. These results suggest that proteins related to the EMT and glutathione metabolism play important roles in the development of intrinsic gemcitabine resistance by pancreatic cancer cell lines.

A Case Report of Patient with Metastatic Pancreatic Cancer Treated with modified Bangam-tang and Gunchil-dan in conjunction with Gemcitabine (전이 췌장암 환자의 Gemcitabine과 방암탕 가감방 및 건칠단 병용투여 치험 1례)

  • Kim, Eun Hye;Yoon, Sung Soo;Lee, Jee Young;Yoon, Seong Woo
    • Journal of Korean Traditional Oncology
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    • v.23 no.2
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    • pp.1-9
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    • 2018
  • Objectives: This study was aimed to report a patient with metastatic pancreatic cancer treated with modified Bangam-tang and Gunchil-dan in conjunction with gemcitabine. There were better survival-related outcomes compared to gemcitabine alone. Methods: The patient with metastatic pancreatic cancer received gemcitabine as palliative chemotherapy since June 2016 concurrent with modified Bangam-tang and Gunchil-dan since October 2016 to October 2017. To evaluate the effect of treatment, tumor markers (carbohydrate antigen 19-9 (CA19-9) and carcinoembryonic antigen (CEA)), Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1, and overall survival were checked. Adverse events were evaluated according to the Common Terminology Criteria for Adverse Events (CTCAE) version 5.0. Results: After 12 months with the combination treatment, levels of CA19-9 were decreased from 8747 to 265.7 ng/ml and CEA from 42.2 to 6.5 U/ml. Clinical partial response state was shown until May 2, 2017 and stable disease state was maintained from August 4, 2017. In March 2018, the patient got an operation including pancreatectomy and diagnosed with no evidence of disease state in September, 2018. In conclusion, it showed the overall survival of 29 months from June, 2016 to November, 2018. Serious adverse events were not identified. Conclusions: This study suggested that combined treatment with modified Bangam-tang and Gunchil-dan may show better outcome in patient with metastatic pancreatic cancer than gemcitabine alone.

Study of SUVm Cut-off Value for the Distinction of Pancreatic Cancer In PET/CT Exam (PET/CT 검사에서 췌장암 판별을 위한 SUVm 경계값 연구)

  • Chang, Boseok;Kim, Jae Ho;Liu, Guoxu;Jang, Eun Sung
    • The Journal of the Korea Contents Association
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    • v.17 no.10
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    • pp.567-575
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    • 2017
  • In this study, when diagnosis pancreatic cancer by dual time point PET/CT, we propose SUVm 2.52 as the threshold value for performing the dual time point PET/CT exam. The hypothesis of normal distribution was adopted through data conversion of 60 pancreatic diseases. The proposed SUVm2.52 boundary value showed a significance level that could be applied to both 120 and 180 minutes of delay time scan for pancreatic cancer determination (p<0.05). C-value variation shows that delay time 2 hour test is more useful than delay time 3 hour test. When the SUVm 2.52 is set to the boundary value and the double-time point PET/CT exam is performed, the probability of distinguishing cancer from inflammation in the delayed image is 95%. When the delayed test is performed with the proposed boundary value SUVm 2.52, Compared with general PET / CT scans, it is thought that it may be helpful to distinguish pancreatic cancer.

Optimal Scan time Analysis for Pancreatic Cancer Distinction in Dual time PET-CT Exam (이중시간 PET/CT 검사에서 췌장암 판별을 위한 최적의 Scan time 분석)

  • Chang, Boseok
    • Journal of the Korean Society of Radiology
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    • v.13 no.2
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    • pp.305-311
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    • 2019
  • In this study, present the most useful delay scan time by statistical analysis of SUVm data for 30 suspected pancreatic cancer patients. Two statistical analysis and a mathematical model was applied to the theoretical formula by glucose and insulin mechanics, and a mathematical model was created. Statistical analysis was performed via Metlab p/g. Optimal delay scan time was suggested by Metlab p/g for the change of SUV value over time.In this study, for diagnosis pancreatic cancer by dual time point PET/CT, propose optimal delay scan time 131.5 minuts. The proposed delay scan time showed statistical reliability applicable to the diagnosis of pancreatic cancer (p<0.05). Delayed scanning with the suggested delay scan time of 131.5 minutes is considered to be useful for the diagnosis of pancreatic cancer compared to general PET / CT scan.hen the delayed test is performed with the proposed delay scan time 131.5 minuts, Compared with general PET/CT scans.

Pancreatic Diseases: Genetics and Modeling Using Human Pluripotent Stem Cells

  • Yuri Lee;Kihyun Lee
    • 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.