• Title, Summary, Keyword: gemcitabine

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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.

Gemcitabine-Induced Radiation Recall Dermato-Myositis (Gemcitabine 투여 후 발생한 방사선 회귀 피부, 근육염)

  • No, Hee Sun;Lim, Hee Hwan;Kim, Jung Hoon;Cho, Jang Hyun;Huh, Jeong Kwon;Cho, Sung In;Yoo, Ji Young;Kim, Cheol Hyeon;Lee, Jae Cheol
    • Tuberculosis and Respiratory Diseases
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    • v.61 no.2
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    • pp.167-170
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    • 2006
  • A radiation recall reaction refers to an inflammatory reaction at previous irradiated areas subsequent to the administration of a variety of pharmacological agents. The skin is the major site of radiation recall reactons with the muscle and internal organs being less commonly affected. These reactions usually occur days to weeks after exposure to the causative agents. We report a case of gemcitabine-induced radiation recall dermato-myositis the developed in a female patient with a metastatic non-small cell lung cancer. She had received a palliative radiation therapy of 3900 cGy to the metastatic lesion on the femur shaft prior to chemotherapy. The pain, swelling and erythema of the left thigh resolved after the cessation of gemcitabine and the use of a systemic steroid.

Predictive and Prognostic Roles of Ribonucleotide Reductase M1 in Patients with Pancreatic Cancer Treated with Gemcitabine: A Meta-analysis

  • Zhang, Xiong;Jin, Fen-Shu;Zhang, Li-Guo;Chen, Rui-Xue;Zhao, Jin-Hui;Wang, Yan-Nan;Wang, En-Fu;Jiang, Zhen-Dong
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.7
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    • pp.4261-4265
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    • 2013
  • Increasing scientific evidence suggests that ribonucleotide reductase M1 (RRM1) may be a powerful predictor of survival in patients with pancreatic cancer treated with adjuvant gemcitabine-based chemotherapy after operative resection, but many existing studies have yielded inconclusive results. This meta-analysis aimed to assess the prognostic role of RRM1 in predicting survival in patients with pancreatic cancer treated with gemcitabine. An extensive literature search for relevant studies was conducted on PubMed, Embase, Web of Science, Cochrane Library, and CBM databases from their inception through May 1st, 2013. This meta-analysis was performed using the STATA 12.0 software and crude hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated. Eight clinical studies were included in this meta-analysis with a total of 665 pancreatic cancer patients treated with adjuvant gemcitabine-based chemotherapy, including 373 patients in the high RRM1 expression group and 292 patients in the low RRM1 expression group. Our meta-analysis revealed that high RRM1 expression was associated with improved overall survival (OS) of pancreatic cancer patients (HR=1.56, 95%CI=0.95-2.17, P<0.001). High RRM1 expression also was linked to longer disease-free survival (DFS) than low RRM1 expression (HR=1.37, 95%CI=0.25-2.48, P=0.016). In conclusion, our meta-analysis suggests that high RRM1 expression may be associated with improved OS and DFS of pancreatic cancer patients treated with adjuvant gemcitabine-based chemotherapy. Detection of RRM1 expression may be a promising biomarker for gemcitabine response and prognosis in pancreatic cancer patients.

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 of Hemolytic Uremic Syndrome in a Lung Cancer Patient Treated with Gemcitabine (Gemcitabine을 사용한 폐암환자에서 발생한 용혈성 요독증후군 1예)

  • Park, Youn-Jung;Yang, Keun-Suk;Jung, Hong-Soon;Nam, Hee-Chul;Jung, Seung-Hye;Kim, Boo-Gyoung;Kim, Ka-Young;Kim, Jung-Ho;Kim, Young-Ok;Yun, Yu-Seon
    • Tuberculosis and Respiratory Diseases
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    • v.72 no.2
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    • pp.207-211
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    • 2012
  • Hemolytic uremic syndrome (HUS) is a rare disorder characterized by the triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure. HUS arises from a wide spectrum of conditions, and chemotherapeutic agents have been reported to be associated with HUS, including Mitomycin, Cisplatin, Bleomycin, and Gemcitabine. A 76-year-old man treated with Gemcitabine due to non-small cell lung cancer developed clinical and laboratory findings compatible with HUS. Gemcitabine was ceased and hemodialysis and plasma exchange were utilized and he recovered. A high level of suspicion for HUS is necessary when cancer patients are treated with Gemcitabine, and prompt recognition and treatment are also essential.

Integrative Meta-Analysis of Multiple Gene Expression Profiles in Acquired Gemcitabine-Resistant Cancer Cell Lines to Identify Novel Therapeutic Biomarkers

  • Lee, Young Seok;Kim, Jin Ki;Ryu, Seoung Won;Bae, Se Jong;Kwon, Kang;Noh, Yun Hee;Kim, Sung Young
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.7
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    • pp.2793-2800
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    • 2015
  • In molecular-targeted cancer therapy, acquired resistance to gemcitabine is a major clinical problem that reduces its effectiveness, resulting in recurrence and metastasis of cancers. In spite of great efforts to reveal the overall mechanism of acquired gemcitabine resistance, no definitive genetic factors have been identified that are absolutely responsible for the resistance process. Therefore, we performed a cross-platform meta-analysis of three publically available microarray datasets for cancer cell lines with acquired gemcitabine resistance, using the R-based RankProd algorithm, and were able to identify a total of 158 differentially expressed genes (DEGs; 76 up- and 82 down-regulated) that are potentially involved in acquired resistance to gemcitabine. Indeed, the top 20 up- and down-regulated DEGs are largely associated with a common process of carcinogenesis in many cells. For the top 50 up- and down-regulated DEGs, we conducted integrated analyses of a gene regulatory network, a gene co-expression network, and a protein-protein interaction network. The identified DEGs were functionally enriched via Gene Ontology hierarchy and Kyoto Encyclopedia of Genes and Genomes pathway analyses. By systemic combinational analysis of the three molecular networks, we could condense the total number of DEGs to final seven genes. Notably, GJA1, LEF1, and CCND2 were contained within the lists of the top 20 up- or down-regulated DEGs. Our study represents a comprehensive overview of the gene expression patterns associated with acquired gemcitabine resistance and theoretical support for further clinical therapeutic studies.

No Relationship between the Amount of DNA Damage and the Level of hMLH1 and RASSF1A Gene Expression in Bladder Cancer Cells Treated with Cisplatin and Gemcitabine

  • de Camargo, Elaine Aparecida;da Silva, Glenda Nicioli;Gobette, Camila Pereira;de Castro Marcondes, Joao Paulo;Salvadori, Daisy Maria Favero
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.10
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    • pp.5941-5948
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    • 2013
  • Tumor response to antineoplastic drugs is not always predictable. This is also true for bladder carcinoma, a highly recurrent neoplasia. Currently, the combination of cisplatin and gemcitabine is well accepted as a standard protocol for treating bladder carcinoma. However, in some cases, this treatment protocol causes harmful side effects. Therefore, we investigated the roles of the genes TP53, RASSF1A (a tumor suppressor gene) and hMLH1 (a gene involved in the mismatch repair pathway) in cell susceptibility to cisplatin/gemcitabine treatment. Two bladder transitional carcinoma cell (TCC) lines, RT4 (wild-type TP53) and 5637 (mutated TP53), were used in this study. First, we evaluated whether the genotoxic potential of cisplatin/gemcitabine was dependent on TP53 status. Then, we evaluated whether the two antineoplastic drugs modulated RASSF1A and hMLH1 expression in the two cell lines. Increased DNA damage was observed in both cell lines after treatment with cisplatin or gemcitabine and with the two drugs simultaneously, as depicted by the comet assay. A lack of RASSF1A expression and hypermethylation of its promoter were observed before and after treatment in both cell lines. On the other hand, hMLH1 downregulation, unrelated to methylation status, was observed in RT4 cells after treatment with cisplatin or with cisplatin and gemcitabine simultaneously (wild-type TP53); in 5637 cells, hMLH1 was upregulated only after treatment with gemcitabine. In conclusion, the three treatment protocols were genotoxic, independent of TP53 status. However, cisplatin was the most effective, causing the highest level of DNA damage in both wild-type and mutated TP53 cells. Gemcitabine was the least genotoxic agent in both cell lines. Furthermore, no relationship was observed between the amount of DNA damage and the level of hMLH1 and RASSF1A expression. Therefore, other alternative pathways might be involved in cisplatin and gemcitabine genotoxicity in these two bladder cancer cell lines.

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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    • pp.428.1-428
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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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CR 2945-Conjugated Liposomes for Targeting of Human Pancreatic Cancer Cells

  • Yoon, Na-Young;Kim, Jin-Seok
    • Journal of Pharmaceutical Investigation
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    • v.34 no.6
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    • pp.459-463
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    • 2004
  • CR 2945, a $gastrin/CCK_B$ receptor antagonist, was conjugated to liposome and tested for the targeting of pancreatic cancer cells in vitro. Successful conjugation was confirmed by FTIR and NMR. The size of CR 2945-conjugated liposome was about 500 nm in diameter, with the zeta-potential being -16.5 mV. In vitro anti-cancer activity of this formulation with or without gemcitabine encapsulated was tested on human pancreatic cancer cells, PANC-1. The growth inhibitory effect of gemcitabine-encapsulating CR 2945-conjugated liposome was found to be 10-fold more potent than that of gemcitabine-encapsulating non-conjugated liposome, suggesting that CR 2945 could be used as a potential cancer targeting moiety by conjugating into liposome.

Gemcitabine-based Concurrent Chemoradiotherapy Versus Chemotherapy Alone in Patients with Locally Advanced Pancreatic Cancer

  • Wang, Bu-Hai;Cao, Wen-Miao;Yu, Jie;Wang, Xiao-Lei
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.5
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    • pp.2129-2132
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    • 2012
  • Objective: To explore improved treatment by retrospectively comparing survival time of gemcitabine-based concurrent chemoradiotherapy (GemRT) versus chemotherapy (Gem) alone in patients with locally advanced pancreatic cancer (LAPC). Methods: From January 2005 to June 2010, 56 patients with LAPC from Subei People's Hospital were treated either with Gem (n=21) or GemRT (n=35). Gem consisted of 4-6 cycles gemcitabine alone (1000 mg/m2 on Days 1, 8, 15, 28-day a cycle). GemRT consisted of 50.4Gy/28F radiotherapy with concurrent 2 cycles of gemcitabine (1000 $mg/m^2$ on days of radiation 1, 8, 15, 21-day a cycle). Radiation was delivered to the gross tumor volume plus 1-1.5 cm by use of a three-dimensional conformal technique. The follow-up time was calculated from the time of diagnosis to the date of death or last contact. Kaplan-Meier methodology wes used to evaluate survival. Results: Patient characteristics were not significantly different between treatment groups. The disease control rate and the objective response rate of GemRT versus Gem was 97.1% vs 71.4%, 74.3% vs 38.1%. The overall survival (OS) was significantly better for GemRT compared to Gem (median 13 months versus 8 months; 51.4% versus 14.3% at 1 year, respectively). Conclusion: Radiation therapy at 50.4Gy with 2 concurrent cycles of gemcitabine results in favorable rates of OS. Concurrent chemoradiotherapy should be the first choice for patients with LAPC.