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1. Borska S, Drag-Zalesinska M, Wysocka T, Sopel M, Dumanska M, Zabel M, Dziegiel P: Antiproliferative and pro-apoptotic effects of quercetin on human pancreatic carcinoma cell lines EPP85-181P and EPP85-181RDB. Folia Histochem Cytobiol; 2010 Jan;48(2):222-9
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  • [Title] Antiproliferative and pro-apoptotic effects of quercetin on human pancreatic carcinoma cell lines EPP85-181P and EPP85-181RDB.
  • Our studies aimed at evaluation of antiproliferative and pro-apoptotic effects of quercetin alone and in combinations with daunorubicin on cells of human pancreatic carcinoma lines.
  • Results of the studies confirmed that quercetin may probably break resistance of neoplastic cells to chemotherapy.
  • On the other side, studied flavonol augmented action of cytostatic drug in case of sensitive tumour cells what suggest, that it might allow to decrease dosage of cytostatic drugs and reduce negative side effects of the treatment.

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  • (PMID = 20675278.001).
  • [ISSN] 1897-5631
  • [Journal-full-title] Folia histochemica et cytobiologica
  • [ISO-abbreviation] Folia Histochem. Cytobiol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Poland
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Antioxidants; 9IKM0I5T1E / Quercetin; ZS7284E0ZP / Daunorubicin
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2. Turrini O, Cano C, Legoffic A, Delpero JR, Dagorn JC, Iovanna J: Genetic alterations in precancerous pancreatic lesions and their clinical implications. Gastroenterol Clin Biol; 2009 Oct-Nov;33(10-11):1028-35, e1-9
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  • [Title] Genetic alterations in precancerous pancreatic lesions and their clinical implications.
  • Pancreatic adenocarcinoma, with an incidence/death ratio of 0.99, has the worst prognosis of all cancers.
  • Risk factors associated with the sporadic form of pancreatic adenocarcinoma are unknown and less than 10% of patients receive curative treatment (surgery associated with radiation therapy or chemotherapy) with a low 5-year survival rate (10 to 20%).
  • Thus, a better understanding of the etiology of pancreatic cancer is essential to identify new prognostic markers and new therapeutic targets.
  • There is a wealth of data on the identification of genetic alterations associated with pancreatic cancer and their role in its development.
  • This review will focus on the current knowledge of genetic alterations associated with two pancreatic lesions that can potentially evolve into pancreatic adenocarcinoma, Pancreatic Intraepithelial Neoplasia (PanIN) and Intraductal Papillary Mucinous Neoplasm (IPMN).
  • These two lesions share a large panel of typical genetic alterations which are close to those found in pancreatic adenocarcinoma.
  • A better understanding of these alterations may lead to therapeutic targets that could help prevent the progression of PanIN and IPMN to cancer.
  • [MeSH-major] Pancreatic Neoplasms / genetics. Precancerous Conditions / genetics
  • [MeSH-minor] Adenocarcinoma, Mucinous / genetics. Carcinoma in Situ / genetics. Carcinoma, Papillary / genetics. Humans. Proto-Oncogene Proteins / genetics. Telomere / ultrastructure. Tumor Suppressor Proteins / genetics

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  • (PMID = 19766418.001).
  • [ISSN] 0399-8320
  • [Journal-full-title] Gastroentérologie clinique et biologique
  • [ISO-abbreviation] Gastroenterol. Clin. Biol.
  • [Language] eng; fre
  • [Publication-type] Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / Tumor Suppressor Proteins
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3. Sarela AI, Verbeke CS, Ramsdale J, Davies CL, Markham AF, Guillou PJ: Expression of survivin, a novel inhibitor of apoptosis and cell cycle regulatory protein, in pancreatic adenocarcinoma. Br J Cancer; 2002 Mar 18;86(6):886-92
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  • [Title] Expression of survivin, a novel inhibitor of apoptosis and cell cycle regulatory protein, in pancreatic adenocarcinoma.
  • It has been implicated in sensitisation to chemotherapy and as a prognostic marker in several common cancers.
  • Immunohistochemistry for Survivin, P53 and BCL-2 expression as well as cell proliferative index (Ki-67) and apoptosis index (TUNEL) was conducted on 52 pancreatic and 12 ampullary adenocarcinomas.
  • Survivin was detected in the cytoplasm of carcinoma cells in 46 (88%) of pancreatic tumours.
  • P53 and BCL-2 were detected in 54% and 12% of pancreatic tumours, respectively.
  • Ampullary carcinoma showed Survivin expression in 83% of cases.
  • However, unlike pancreatic carcinoma, there was no correlation between Survivin and P53 expression or proliferative index.
  • In conclusion, Survivin is expressed in the majority of pancreatic adenocarcinomas and correlates with both cellular proliferation and apoptosis.
  • Molecular manipulation of Survivin expression may enhance chemotherapy and radiation therapy for pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / chemistry. Apoptosis. Chromosomal Proteins, Non-Histone / analysis. Microtubule-Associated Proteins. Pancreatic Neoplasms / chemistry
  • [MeSH-minor] Aged. Cell Cycle / drug effects. Cell Division. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Inhibitor of Apoptosis Proteins. Male. Middle Aged. Neoplasm Proteins. Proto-Oncogene Proteins c-bcl-2 / analysis. Tumor Suppressor Protein p53 / analysis

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  • [Copyright] Copyright 2002 Cancer Research UK
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  • (PMID = 11953819.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / BIRC5 protein, human; 0 / Chromosomal Proteins, Non-Histone; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / Neoplasm Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC2364160
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4. Saif MW: Primary pancreatic lymphomas. JOP; 2006;7(3):262-73
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  • [Title] Primary pancreatic lymphomas.
  • Primary pancreatic lymphomas are extremely rare.
  • Clinically, primary pancreatic lymphomas usually present with symptoms of carcinoma of the pancreatic head.
  • Patients with primary pancreatic lymphomas are between 35 and 75 years of age and with a strong male predominance.
  • An accurate cytopathologic diagnosis by fine-needle aspiration (FNA) is imperative because the primary treatment is non-surgical.
  • FNA coupled with flow cytometry analysis appears to be highly accurate in the diagnosis of primary pancreatic lymphomas.
  • Fluorescence in-situ hybridisation technique has been established its role in the diagnosis of lymphoid malignancies, including primary pancreatic lymphomas.
  • The differential diagnoses of primary pancreatic lymphomas include secondary lymphoma, pancreatic endocrine neoplasm, and florid chronic pancreatitis.
  • Treatment usually consists of a combination of chemotherapy and radiation therapy, or stem cell transplantation.
  • Primary pancreatic lymphomas has a much better prognosis than adenocarcinoma of the pancreas.
  • [MeSH-major] Lymphoma / diagnosis. Pancreatic Neoplasms / diagnosis

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  • (PMID = 16685107.001).
  • [ISSN] 1590-8577
  • [Journal-full-title] JOP : Journal of the pancreas
  • [ISO-abbreviation] JOP
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 40
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5. Yan H, Wu J, Liu W, Zuo Y, Chen S, Zhang S, Zeng M, Huang W: MicroRNA-20a overexpression inhibited proliferation and metastasis of pancreatic carcinoma cells. Hum Gene Ther; 2010 Dec;21(12):1723-34
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  • [Title] MicroRNA-20a overexpression inhibited proliferation and metastasis of pancreatic carcinoma cells.
  • The aim of this study was to investigate the effect of microRNA-20a on pancreatic carcinoma cell proliferation and invasion and to find a new effective treatment strategy for pancreatic carcinoma.
  • MicroRNA-20a expression was determined in 10 matched normal pancreatic tissues and pancreatic carcinoma by in situ hybridization.
  • Quantitative real-time RT-PCR was used to evaluate the expression of microRNA-20a in two pancreatic carcinoma cell lines (BxPC-3 and Panc-1) and immortal human pancreatic duct epithelial cell line H6C7.
  • The pancreatic cancer cell lines (Panc-1 and BxPC-3) stably overexpressing microRNA-20a showed reduced proliferation and invasion capacity in vitro and in vivo, compared with parental cells or cells transfected with a control vector.
  • These results show that microRNA-20a regulates Stat3 at the post-transcriptional level, resulting in inhibition of cell proliferation and invasion of pancreatic carcinoma.
  • It may open a new perspective for the development of effective gene therapy for pancreatic carcinoma.
  • [MeSH-major] MicroRNAs / biosynthesis. Pancreatic Neoplasms / pathology
  • [MeSH-minor] 3' Untranslated Regions / drug effects. Animals. Base Sequence. Cell Cycle. Cell Line, Tumor. Cell Movement. Cell Proliferation. Down-Regulation. Female. Humans. Lung Neoplasms / secondary. Matrix Metalloproteinase 2 / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Molecular Sequence Data. Neoplasm Invasiveness. Neoplasm Metastasis. Neoplasm Transplantation. STAT3 Transcription Factor / genetics. STAT3 Transcription Factor / metabolism. Tumor Burden. Vascular Endothelial Growth Factor A / metabolism

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  • (PMID = 20583868.001).
  • [ISSN] 1557-7422
  • [Journal-full-title] Human gene therapy
  • [ISO-abbreviation] Hum. Gene Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 3' Untranslated Regions; 0 / MIRN20 microRNA, human; 0 / MicroRNAs; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 0 / Vascular Endothelial Growth Factor A; EC 3.4.24.24 / MMP2 protein, human; EC 3.4.24.24 / Matrix Metalloproteinase 2
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6. Hecht JR, Bedford R, Abbruzzese JL, Lahoti S, Reid TR, Soetikno RM, Kirn DH, Freeman SM: A phase I/II trial of intratumoral endoscopic ultrasound injection of ONYX-015 with intravenous gemcitabine in unresectable pancreatic carcinoma. Clin Cancer Res; 2003 Feb;9(2):555-61
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  • [Title] A phase I/II trial of intratumoral endoscopic ultrasound injection of ONYX-015 with intravenous gemcitabine in unresectable pancreatic carcinoma.
  • PURPOSE: Localized pancreatic carcinoma is rarely resectable and is resistant to conventional therapies.
  • Endoscopic ultrasound (EUS) has the potential to conveniently and accurately deliver local therapy to the pancreas.
  • Therefore, we undertook a trial of the feasibility, tolerability, and efficacy of EUS injection of ONYX-015 into unresectable pancreatic carcinomas.
  • EXPERIMENTAL DESIGN: Twenty-one patients with locally advanced adenocarcinoma of the pancreas or with metastatic disease, but minimal or absent liver metastases, underwent eight sessions of ONYX-015 delivered by EUS injection into the primary pancreatic tumor over 8 weeks.
  • The final four treatments were given in combination with gemcitabine (i.v., 1,000 mg/m(2)).
  • Patients received 2 x 10(10) (n = 3) or 2 x 10(11) (n = 18) virus particles/treatment.
  • RESULTS: After combination therapy, 2 patients had partial regressions of the injected tumor, 2 had minor responses, 6 had stable disease, and 11 had progressive disease or had to go off study because of treatment toxicity.
  • CONCLUSIONS: This study indicates that ONYX-015 injection via EUS into pancreatic carcinomas by the transgastic route with prophylactic antibiotics is feasible and generally well tolerated either alone or in combination with gemcitabine.
  • Transgastric EUS-guided injection is a new and practical method of delivering biological agents to pancreatic tumors.
  • [MeSH-major] Adenocarcinoma / drug therapy. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / ultrasonography. Viral Vaccines / adverse effects
  • [MeSH-minor] Adenoviridae / genetics. Adenoviridae / isolation & purification. Adult. Aged. Antimetabolites, Antineoplastic / therapeutic use. Combined Modality Therapy. Disease Progression. Feasibility Studies. Female. Humans. In Situ Hybridization. Injections, Intralesional. Male. Middle Aged. Neoplasm Metastasis. Patient Selection. Safety. Treatment Outcome

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  • (PMID = 12576418.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Clinical Trial, Phase II; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / ONYX015; 0 / Viral Vaccines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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7. Tomioka D, Maehara N, Kuba K, Mizumoto K, Tanaka M, Matsumoto K, Nakamura T: Inhibition of growth, invasion, and metastasis of human pancreatic carcinoma cells by NK4 in an orthotopic mouse model. Cancer Res; 2001 Oct 15;61(20):7518-24
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  • [Title] Inhibition of growth, invasion, and metastasis of human pancreatic carcinoma cells by NK4 in an orthotopic mouse model.
  • We have now determined whether blockade of the HGF-c-Met/HGF receptor pathway and tumor angiogenesis by administration of recombinant NK4 would inhibit growth, invasion, and metastasis of human pancreatic carcinoma implanted into the pancreas of nude mice.
  • When treatment with NK4 or anti-HGF neutralizing antibody was initiated from the third day after orthotopic injection of SUIT-2 human pancreatic cancer cells, both NK4 and anti-HGF antibody suppressed the conversion of orthotopic pancreatic tumors from carcinoma in situ to aberrantly invading cancers during days 3-14.
  • On the other hand, when the treatment was begun on day 10, a time when cancer cells were already invading surrounding tissues, NK4 but not anti-HGF antibody inhibited tumor growth, peritoneal dissemination, and ascites accumulation at 4 weeks after the inoculation.
  • Antitumor effects of NK4 correlated with decreased microvessel density in pancreatic tumors thereby indicating that the antiangiogenic activity of NK4 may have mainly contributed to its antitumor effects.
  • Moreover, although NK4-treatment was initiated from the end stage (day 24 after tumor inoculation), NK4 prolonged survival time of mice, and the suppression of peritoneal dissemination, ascites accumulation, and invasion of metastasized cancer cells into the peritoneal wall were remarkable.
  • We propose that simultaneous targeting of both tumor angiogenesis and the HGF-mediated invasion-metastasis may prove to be a new approach to treating patients with pancreatic cancer.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Hepatocyte Growth Factor / pharmacology. Mitogens. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Disease Progression. Growth Inhibitors / pharmacology. Humans. Male. Mice. Neoplasm Invasiveness. Neovascularization, Pathologic / drug therapy. Peritoneal Neoplasms / prevention & control. Peritoneal Neoplasms / secondary. Proto-Oncogene Proteins c-met / metabolism. Xenograft Model Antitumor Assays


8. Wang BL, Chen XP, Zhai SP, Chen DF: Clinical significance of mrp gene in primary hepatocellular carcinoma. Hepatobiliary Pancreat Dis Int; 2003 Aug;2(3):397-403
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  • [Title] Clinical significance of mrp gene in primary hepatocellular carcinoma.
  • OBJECTIVE: To study the relations among the expression of the multidrug resistance associated-protein (mrp) gene and clinicopathologic features, the influence of alpha-fetoprotein (AFP), and prognosis of patients who received adjuvant chemotherapy after resection of primary hepatocellular carcinoma (HCC).
  • METHODS: The expression of the mrp gene encoding MRP and mRNAmrp was determined in tissues from 54 untreated patients with HCC, adjacent tissues from 24 patients with HCC and archival paraffin-embedded tissues from 12 patients with posthepatic cirrhosis.
  • RESULTS: The percentage of positive expressions of MRP and mRNAmrp in the three kinds of tissues was 57.40%, 25.00%, 16.67%, and 72.22%, 37.50%, 33.33% respectively.
  • Significant difference was noted in the untreated HCC tissue, compared to the other two tissues (P<0.05).
  • Although no difference was seen in the 1-, 3-, 5-year survival rates of HCC patients (P>0.05), the mean survival time of postoperative HCC patients or the negative mrp gene expression group was longer than that of the positive group (P<0.05).
  • Detection of mrp gene expression is of great significance in accessing chemotherapeutic resistance of HCC, which provides evidence for reversing MDR in HCC.
  • The mrp gene may be a useful marker in detecting prognosis of HCC patients because its expression is correlated with tumor differention and mean survival time of the patients.
  • [MeSH-major] Carcinoma, Hepatocellular / pathology. Carcinoma, Hepatocellular / physiopathology. Liver Neoplasms / pathology. Liver Neoplasms / physiopathology. Multidrug Resistance-Associated Proteins / genetics
  • [MeSH-minor] Adult. Aged. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / genetics. Female. Gene Expression Regulation, Neoplastic. Hepatectomy. Humans. In Situ Hybridization. Male. Middle Aged. Postoperative Complications / mortality. Prognosis. alpha-Fetoproteins / metabolism

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  • (PMID = 14599947.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / Multidrug Resistance-Associated Proteins; 0 / alpha-Fetoproteins
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9. Eisold S, Antolovic D, Schmidt J, Wiessner R, Klar E, von Knebel-Doeberitz M, Linnebacher M: Effective antitumoral immune responses are not induced by cytosine deaminase suicide gene transfer in a syngeneic rat pancreatic carcinoma model. Eur Surg Res; 2006;38(6):513-21
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  • [Title] Effective antitumoral immune responses are not induced by cytosine deaminase suicide gene transfer in a syngeneic rat pancreatic carcinoma model.
  • METHODS: To analyze potential immunological effects, we used weakly immunogenic pancreatic carcinomas in syngeneic, immunocompetent Lewis rats and performed in situ adenoviral mediated cytosine deaminase (CD) gene transfer followed by administration of the prodrug, 5-fluorocytosine (5FC).
  • In order to reflect the clinical situation, such treated tumors were surgically resected and animals were rechallenged with parental DSL6A pancreatic tumor cells.
  • RESULTS: CD/5FC treatment of the DSL6A cells revealed significant induction of apoptosis in vitro and slowed down tumor progression in syngeneic hosts.
  • Analysis of T lymphocytes showed no specific cytotoxic activity against DSL6A cells.
  • CONCLUSIONS: Albeit the present study failed to induce protective antitumor immunity, the initial finding of reduced tumor growth argues for the development of multimodal therapeutic options to overcome negative impacts of advanced malignant disease or chemotherapy-related anergy and immunosuppression.
  • [MeSH-major] Cytosine Deaminase / genetics. Cytotoxicity, Immunologic. Flucytosine / therapeutic use. Genetic Therapy. Pancreatic Neoplasms / therapy

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  • [Copyright] Copyright 2006 S. Karger AG, Basel.
  • (PMID = 17028434.001).
  • [ISSN] 0014-312X
  • [Journal-full-title] European surgical research. Europäische chirurgische Forschung. Recherches chirurgicales européennes
  • [ISO-abbreviation] Eur Surg Res
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Switzerland
  • [Chemical-registry-number] D83282DT06 / Flucytosine; EC 3.5.4.1 / Cytosine Deaminase
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10. MacMillan-Crow LA, Greendorfer JS, Vickers SM, Thompson JA: Tyrosine nitration of c-SRC tyrosine kinase in human pancreatic ductal adenocarcinoma. Arch Biochem Biophys; 2000 May 15;377(2):350-6
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  • [Title] Tyrosine nitration of c-SRC tyrosine kinase in human pancreatic ductal adenocarcinoma.
  • During pancreatic tumorigenesis, the equilibrium between cell survival and cell death is altered, allowing aggressive neoplasia and resistance to radiation and chemotherapy.
  • Our recent in situ immunohistochemical studies demonstrated that levels of total nitrotyrosine, a footprint of the reactive nitrogen species peroxynitrite, are elevated in human pancreatic ductal adenocarcinomas.
  • In this study, quantitative HPLC-EC techniques demonstrated a 21- to 97-fold increase in the overall levels of nitrotyrosine of human pancreatic tumor extracts compared to normal pancreatic extracts.
  • Western blot analysis of human pancreatic tumor extracts showed that tyrosine nitration was restricted to a few specific proteins.
  • Peroxynitrite treatment of human pancreatic carcinoma cells in vitro resulted in increased tyrosine nitration and tyrosine phosphorylation of c-Src kinase, increased (>2-fold) c-Src kinase activity, and increased association between c-Src kinase and its downstream substrate cortactin.
  • Collectively, these observations suggest that peroxynitrite-mediated tyrosine nitration and tyrosine phosphorylation of c-Src kinase may lead to enhanced tyrosine kinase signaling observed during pancreatic ductal adenocarcinoma growth and metastasis.
  • [MeSH-major] Adenocarcinoma / enzymology. Pancreatic Neoplasms / enzymology. Proto-Oncogene Proteins pp60(c-src) / metabolism. Tyrosine / metabolism

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  • (PMID = 10845713.001).
  • [ISSN] 0003-9861
  • [Journal-full-title] Archives of biochemistry and biophysics
  • [ISO-abbreviation] Arch. Biochem. Biophys.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK51629; United States / NHLBI NIH HHS / HL / HL45990
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / CTTN protein, human; 0 / Cortactin; 0 / Microfilament Proteins; 0 / Nitrates; 21820-51-9 / Phosphotyrosine; 26404-66-0 / peroxynitric acid; 3604-79-3 / 3-nitrotyrosine; 42HK56048U / Tyrosine; EC 2.7.10.2 / Proto-Oncogene Proteins pp60(c-src)
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11. Bernhaus A, Ozsvar-Kozma M, Saiko P, Jaschke M, Lackner A, Grusch M, Horvath Z, Madlener S, Krupitza G, Handler N, Erker T, Jaeger W, Fritzer-Szekeres M, Szekeres T: Antitumor effects of KITC, a new resveratrol derivative, in AsPC-1 and BxPC-3 human pancreatic carcinoma cells. Invest New Drugs; 2009 Oct;27(5):393-401
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  • [Title] Antitumor effects of KITC, a new resveratrol derivative, in AsPC-1 and BxPC-3 human pancreatic carcinoma cells.
  • Pancreatic cancer is a very aggressive malignant disease due to lack of early diagnosis and chemotherapeutic resistance of the tumor cells.
  • There is distinct evidence that food derived polyphenols possess chemopreventive effects in the development of several cancers including pancreatic carcinoma.
  • The aim of our study was to evaluate the cytotoxic and biochemical effects of a newly synthesized polymethoxylated resveratrol analogue, N-hydroxy-N'-(3,4,5-trimethoxphenyl)-3,4,5-trimethoxy-benzamidine (KITC) in two human pancreatic cancer cell lines.
  • The human pancreatic cancer cell lines, AsPC-1 and BxPC-3 were used to test the potential inhibitory effect of the resveratrol derivative on cell proliferation and the underlying mechanisms of this effect.
  • KITC (40 microM) arrested cells in the G0/G1 phase and depleted cells in the S phase of the cell cycle (-105% and -35% of control, respectively).
  • KITC induced dose-dependent apoptosis in both pancreatic cancer cell lines and was found to significantly reduce the in situ activity of ribonucleotide reductase, the key enzyme of DNA synthesis.
  • In summary, we found that KITC exerted considerable antitumor activity against human pancreatic cancer cells and could be a promising candidate for further investigations to establish a new chemotherapeutic regimen.
  • [MeSH-major] Antineoplastic Agents, Phytogenic / pharmacology. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Proliferation / drug effects. Pancreatic Neoplasms / drug therapy. Stilbenes / pharmacology
  • [MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Antineoplastic Combined Chemotherapy Protocols. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Dose-Response Relationship, Drug. Drug Synergism. Humans. Molecular Structure. Ribonucleotide Reductases / antagonists & inhibitors. Ribonucleotide Reductases / metabolism. Tumor Cells, Cultured

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  • (PMID = 18841326.001).
  • [ISSN] 1573-0646
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents, Phytogenic; 0 / N-hydroxy-N'-(3,4,5-trimethoxyphenyl)-3,4,5-trimethoxy-benzamidine; 0 / Stilbenes; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases
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12. Bruns CJ, Shinohara H, Harbison MT, Davis DW, Nelkin G, Killion JJ, McConkey DJ, Dong Z, Fidler IJ: Therapy of human pancreatic carcinoma implants by irinotecan and the oral immunomodulator JBT 3002 is associated with enhanced expression of inducible nitric oxide synthase in tumor-infiltrating macrophages. Cancer Res; 2000 Jan 1;60(1):2-7
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  • [Title] Therapy of human pancreatic carcinoma implants by irinotecan and the oral immunomodulator JBT 3002 is associated with enhanced expression of inducible nitric oxide synthase in tumor-infiltrating macrophages.
  • We determined the therapeutic effect of irinotecan (CPT-11) combined with the immunomodulator JBT 3002, a synthetic bacterial lipopeptide (N-acylated derivative of psi-amino-C1-C3-alkane-sulfonic acid), against highly metastatic human pancreatic carcinoma cells injected into the pancreas of athymic nude mice.
  • Treatment with CPT-11 alone significantly decreased the median volume of pancreatic tumors and the incidence of metastasis, whereas treatment with only JBT 3002 did not.
  • The combination therapy of CPT-11 plus JBT 3002 decreased tumor volume and incidence of metastasis significantly more than CPT-11 alone.
  • The number of apoptotic cells (terminal deoxynucleotidyl transferase-mediated nick end labeling assay), the number of scavenger-receptor-positive macrophages, and expression level of inducible nitric oxide synthase (iNOS) within lesions directly correlated with therapeutic effects.
  • Collectively, these data demonstrate that the oral administration of the immunomodulator JBT 3002 combined with i.p. injection of CPT-11 can decrease the growth of human pancreatic carcinoma and the incidence of metastasis in nude mice by both a direct antitumor effect and the activation of iNOS in infiltrating macrophages.
  • [MeSH-major] Adjuvants, Immunologic / therapeutic use. Antineoplastic Agents, Phytogenic / therapeutic use. Camptothecin / analogs & derivatives. Lipoproteins / therapeutic use. Macrophages / enzymology. Nitric Oxide Synthase / metabolism. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Administration, Oral. Animals. Apoptosis. Drug Therapy, Combination. Humans. In Situ Nick-End Labeling. Injections, Intralesional. Lipopeptides. Liver Neoplasms / prevention & control. Liver Neoplasms / secondary. Lymph Nodes / pathology. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Nitric Oxide Synthase Type II. Proliferating Cell Nuclear Antigen / analysis. Transplantation, Heterologous. Tumor Cells, Cultured / drug effects

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  • (PMID = 10646841.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / R35-CA42107
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Adjuvants, Immunologic; 0 / Antineoplastic Agents, Phytogenic; 0 / JBT-3002; 0 / Lipopeptides; 0 / Lipoproteins; 0 / Proliferating Cell Nuclear Antigen; 7673326042 / irinotecan; EC 1.14.13.39 / NOS2 protein, human; EC 1.14.13.39 / Nitric Oxide Synthase; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; XT3Z54Z28A / Camptothecin
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13. Meggiato T, Calabrese F, De Cesare CM, Baliello E, Valente M, Del Favero G: C-JUN and CPP32 (CASPASE 3) in human pancreatic cancer: relation to cell proliferation and death. Pancreas; 2003 Jan;26(1):65-70
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  • [Title] C-JUN and CPP32 (CASPASE 3) in human pancreatic cancer: relation to cell proliferation and death.
  • AIMS: To ascertain the expression of c-Jun in specimens of pancreatic duct cancer and to evaluate its correlation with CPP32, apoptotic index, and proliferation index (MIB-1).
  • METHODS: Tissue samples were collected from 23 patients with pancreatic duct cancer who had not received chemotherapy nor radiation therapy before surgery.
  • Pancreatic cancer tissue with an increased percentage of proliferating tumor cells showed also a strong expression of c-Jun, which supports the hypothesis that this oncogene may be involved in the growth of pancreatic cancer.
  • [MeSH-major] Apoptosis. Carcinoma, Pancreatic Ductal / metabolism. Caspases / metabolism. Pancreatic Neoplasms / metabolism. Proto-Oncogene Proteins c-jun / metabolism
  • [MeSH-minor] Adult. Aged. Caspase 3. Cell Division. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / analysis. Ki-67 Antigen / immunology. Male. Middle Aged


14. Ishikawa O, Ohigashi H, Yamada T, Sasaki Y, Imaoka S, Nakaizumi A, Uehara H, Tanaka S, Takenaka A: Radical resection for pancreatic cancer. Acta Gastroenterol Belg; 2002 Jul-Sep;65(3):166-70
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  • [Title] Radical resection for pancreatic cancer.
  • Ductal adenocarcinoma of the pancreas is still characterized by (1) poor prognosis after surgery and (2) extreme difficulty in early diagnosis, and we need a breakthrough.
  • For the first problem, we have performed a wide range of lymphatic and connective tissue clearance (extended pancreatectomy) which has succeeded in improving the 5-year survival rate from 8% to 24% via decreasing the incidence of locoregional recurrence.
  • When liver perfusion chemotherapy via the hepatic artery and the portal vein was added to the patients who had received extended pancreatectomy, the 5-year survival rate was further elevated to 40% via decreasing the incidence of hepatic metastasis.
  • We conclude that pancreatic cancer should be treated by the better-balanced treatments between locoregional control and prevention of hepatic metastasis.
  • For the second problem, we have more actively collected pancreatic juice to perform cytodiagnosis even though no obvious tumor was delineated by the conventional imaging diagnoses.
  • When cancer cells were detected in the pancreatic juice, our method of intraoperative cytology was very useful in precisely locating the occult lesion indicating an appropriate range of pancreatectomy.
  • The resected pancreas was proven to have included borderline malignancy and in situ or minimally-invasive carcinoma by the postoperative histology, and disease-free 5-year survival rate was 100%.
  • In the future, we need to detect patients with a high risk of pancreatic cancer and develop a less-painful method to collect the pancreatic juice.
  • [MeSH-major] Adenocarcinoma / surgery. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Humans. Liver Neoplasms / secondary. Neoplasm Recurrence, Local. Pancreatectomy. Pancreatic Juice / cytology

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  • (PMID = 12420609.001).
  • [ISSN] 1784-3227
  • [Journal-full-title] Acta gastro-enterologica Belgica
  • [ISO-abbreviation] Acta Gastroenterol. Belg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Belgium
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15. Pan X, Li ZS, Xu GM, Cui L, Tu ZX: Adenovirus-mediated gene transfer in the treatment of pancreatic cancer. Pancreas; 2003 Apr;26(3):274-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Adenovirus-mediated gene transfer in the treatment of pancreatic cancer.
  • INTRODUCTION: Suicide gene therapy is a new experimental form of cancer chemotherapy that is currently being evaluated in human trials.
  • AIM: To evaluate the killing effects of the cytosine deaminase (CD) gene mediated by an adenovirus vector on human pancreatic carcinoma in vitro and in vivo.
  • The human pancreatic carcinoma cell line PaTu8988/SW1990 was infected with this virus, and then 5-fluorocytosine (5-FC) was added; XTT assay was used to estimate relative numbers of viable cells.
  • An in vivo model of pancreatic cancer was established by injecting 1.0 x 10(7) PaTu8988/SW1990 cells subcutaneously in Balb/c nude mice.
  • RESULTS: It was found that significant cytotoxic activities were possessed by 5-FC for CD gene-transduced PaTu8988/SW1990 cells, but there was little effect on the nontransduced pancreatic carcinoma cells.
  • The antitumor effect was observed in PaTu8988/SW1990 xenografts from nude mice with in situ CD gene transduction.
  • CONCLUSION: These results indicate that the CD gene mediated by adenovirus has a high level of infectivity and is efficient for gene therapy for pancreatic carcinoma.
  • [MeSH-major] Adenoviridae / genetics. Carcinoma / therapy. Cytosine Deaminase / genetics. Genetic Therapy. Pancreatic Neoplasms / therapy


16. Bruns CJ, Harbison MT, Davis DW, Portera CA, Tsan R, McConkey DJ, Evans DB, Abbruzzese JL, Hicklin DJ, Radinsky R: Epidermal growth factor receptor blockade with C225 plus gemcitabine results in regression of human pancreatic carcinoma growing orthotopically in nude mice by antiangiogenic mechanisms. Clin Cancer Res; 2000 May;6(5):1936-48
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  • [Title] Epidermal growth factor receptor blockade with C225 plus gemcitabine results in regression of human pancreatic carcinoma growing orthotopically in nude mice by antiangiogenic mechanisms.
  • Both epidermal growth factor receptor (EGF-R) signaling mechanisms and angiogenesis have been evaluated as independent targets for therapy of human pancreatic carcinoma, but a link between the two processes has been identified only recently.
  • This study evaluated whether EGF-R blockade therapy with anti-EGF-R antibody C225 inhibits pancreatic carcinoma growth and metastasis in an orthotopic nude mouse model via tumor-mediated angiogenesis and whether gemcitabine potentiates this effect.
  • In vitro treatment of human pancreatic carcinoma L3.6pl cells with C225 inhibited EGF-R autophosphorylation, producing a maximum of 20% cytostasis.
  • Treatment with C225 plus gemcitabine resulted in additive cytotoxic effects that increased with increasing gemcitabine concentrations.
  • In L3.6pl tumors established in the pancreas of nude mice, systemic therapy with C225 alone and C225 in combination with gemcitabine resulted in growth inhibition, tumor regression, and abrogation of metastasis; median tumor volume was reduced from 538 to 0.3 and to 0 mm3, respectively.
  • Gemcitabine treatment alone reduced median tumor volume from 538 to 152 mm3.
  • No macroscopically visible liver metastases were observed in the combination treatment group.
  • As early as 11 days after C225 treatment, the median percentage of proliferating cell nuclear antigen-positive cells was substantially reduced compared with gemcitabine treatment alone (26% versus 73%, respectively) versus controls (92%), correlating with in vivo blockade of EGF-R activation.
  • Similarly after 11 days treatment, production of vascular endothelial growth factor and interleukin 8 was significantly lower in C225 and C225 plus gemcitabine-treated tumors versus gemcitabine-treated and control tumors.
  • Significant differences in microvessel density were observed 18 days after C225 or combination treatments (but not gemcitabine alone) in direct correlation with the difference in percentage of apoptotic endothelial cells, as visualized by double immunofluorescence microscopy.
  • These experiments indicate that therapeutic strategies targeting EGF-R have a significant antitumor effect on human L3.6pl pancreatic carcinoma growing in nude mice which is mediated in part by inhibition of tumor-induced angiogenesis, leading to tumor cell apoptosis and regression.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Neovascularization, Pathologic / prevention & control. Pancreatic Neoplasms / drug therapy. Receptor, Epidermal Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Antibodies, Monoclonal / administration & dosage. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal, Humanized. Antigens, CD31 / analysis. Apoptosis / drug effects. Cell Division / drug effects. Cetuximab. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Endothelial Growth Factors / metabolism. Endothelial Growth Factors / pharmacology. Epidermal Growth Factor / pharmacology. Fluorescent Antibody Technique. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Interleukin-8 / metabolism. Lymphokines / metabolism. Lymphokines / pharmacology. Male. Mice. Mice, Nude. Neoplasm Metastasis / prevention & control. Neoplasm Transplantation. Pancreas / drug effects. Pancreas / metabolism. Pancreas / pathology. Phosphorylation / drug effects. Proliferating Cell Nuclear Antigen / analysis. Transplantation, Heterologous. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 10815919.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 69676; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA67952
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antigens, CD31; 0 / Endothelial Growth Factors; 0 / Interleukin-8; 0 / Lymphokines; 0 / Proliferating Cell Nuclear Antigen; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 0W860991D6 / Deoxycytidine; 62229-50-9 / Epidermal Growth Factor; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; PQX0D8J21J / Cetuximab
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17. Valentich MA, Eynard AR, Barotto NN, Díaz MP, Bongiovanni GA: Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats. Food Chem Toxicol; 2006 Dec;44(12):2101-5
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  • [Title] Effect of the co-administration of phenobarbital, quercetin and mancozeb on nitrosomethylurea-induced pancreatic tumors in rats.
  • We have previously shown that a single i.p. injection of nitrosomethylurea (NMU) in 3-day-old rats orally treated with the pesticide mancozeb (MZ), the flavonoid quercetin (Q) or in combination (MZ-Q) induces hyperplasia, atypical acinar cell proliferation and carcinoma in situ (CIS) in the pancreas.
  • This work studies the effect of oral administration of phenobarbital (PB) on this model of pancreatic carcinogenesis.
  • CONCLUSION: Although PB, Q or MZ given alone enhance DYS lesions in NMU-treated rats, the MZ/Q/PB combined treatments may increase (mainly in males) or decrease (mainly in female) the DYS and CIS proportion.
  • [MeSH-major] Carcinogens / pharmacology. Carcinoma in Situ / chemically induced. Fungicides, Industrial / toxicity. Maneb / toxicity. Pancreatic Neoplasms / chemically induced. Phenobarbital / pharmacology. Quercetin / pharmacology. Zineb / toxicity
  • [MeSH-minor] Alkylating Agents / toxicity. Animals. Animals, Newborn. Disease Models, Animal. Drug Interactions. Drug Therapy, Combination. Female. Hyperplasia / chemically induced. Hyperplasia / pathology. Maternal Exposure. Maternal-Fetal Exchange. Methylnitrosourea / toxicity. Pregnancy. Rats. Rats, Wistar

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  • (PMID = 16965848.001).
  • [ISSN] 0278-6915
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Alkylating Agents; 0 / Carcinogens; 0 / Fungicides, Industrial; 12427-38-2 / Maneb; 684-93-5 / Methylnitrosourea; 9IKM0I5T1E / Quercetin; R0HY55EB9E / mancozeb; X1FSB1OZPT / Zineb; YQE403BP4D / Phenobarbital
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18. Yokoi K, Kim SJ, Thaker P, Yazici S, Nam DH, He J, Sasaki T, Chiao PJ, Sclabas GM, Abbruzzese JL, Hamilton SR, Fidler IJ: Induction of apoptosis in tumor-associated endothelial cells and therapy of orthotopic human pancreatic carcinoma in nude mice. Neoplasia; 2005 Jul;7(7):696-704
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  • [Title] Induction of apoptosis in tumor-associated endothelial cells and therapy of orthotopic human pancreatic carcinoma in nude mice.
  • Although gemcitabine has been accepted as the first-line chemotherapeutic reagent for advanced pancreatic cancer, improvement of response rate and survival is not sufficient and patients often develop resistance.
  • We hypothesized that the inhibition of phosphorylation of epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor (VEGFR) on tumor cells and tumor-associated endothelial cells, combined with gemcitabine, would overcome the resistance to gemcitabine in orthotopic pancreatic tumor animal model.
  • L3.6pl, human pancreatic cancer cells growing in the pancreas, and tumor-associated endothelial cells in microorgan environment highly expressed phosphorylated EGFR, VEGFR, and Akt, which regulates antiapoptotic mechanism.
  • Collectively, these data indicate that dual inhibition of phosphorylation of EGFR and VEGFR, in combination with gemcitabine, produces apoptosis of tumor-associated endothelial cells and significantly suppresses human pancreatic cancer in nude mice.

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  • (PMID = 16026649.001).
  • [ISSN] 1522-8002
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA90270; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P50 CA090270; United States / NCI NIH HHS / CA / CA10193-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AEE 788; 0 / Antigens, CD31; 0 / Proto-Oncogene Proteins; 0 / Purines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
  • [Other-IDs] NLM/ PMC1501424
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19. Yokoi K, Sasaki T, Bucana CD, Fan D, Baker CH, Kitadai Y, Kuwai T, Abbruzzese JL, Fidler IJ: Simultaneous inhibition of EGFR, VEGFR, and platelet-derived growth factor receptor signaling combined with gemcitabine produces therapy of human pancreatic carcinoma and prolongs survival in an orthotopic nude mouse model. Cancer Res; 2005 Nov 15;65(22):10371-80
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  • [Title] Simultaneous inhibition of EGFR, VEGFR, and platelet-derived growth factor receptor signaling combined with gemcitabine produces therapy of human pancreatic carcinoma and prolongs survival in an orthotopic nude mouse model.
  • Although gemcitabine has been approved as the first-line chemotherapeutic reagent for pancreatic cancer, its response rate is low and average survival duration is still only marginal.
  • Because epidermal growth factor receptor (EGFR), vascular endothelial growth factor receptor (VEGFR), and platelet-derived growth factor receptor (PDGFR) modulate tumor progression, we hypothesized that inhibition of phosphorylation of all three on tumor cells, tumor-associated endothelial cells, and stroma cells would improve the treatment efficacy of gemcitabine in an orthotopic pancreatic tumor model in nude mice and prolong survival.
  • We implanted L3.6pl, a human pancreatic cancer cell, in the pancreas of nude mice.
  • STI571 treatment also decreased pericyte coverage on tumor-associated endothelial cells.
  • Thus, inhibiting phosphorylation of EGFR, VEGFR, and PDGFR in combination with gemcitabine enhanced the efficacy of gemcitabine, resulting in inhibition of experimental human pancreatic cancer growth and significant prolongation of survival.

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  • (PMID = 16288027.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / CA90270; United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / P50 CA090270; United States / NCI NIH HHS / CA / P50 CA090270-050001; United States / NCI NIH HHS / CA / CA10193-06; United States / NCI NIH HHS / CA / P30 CA016672-279014
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AEE 788; 0 / Antigens, CD31; 0 / Benzamides; 0 / Piperazines; 0 / Purines; 0 / Pyrimidines; 0W860991D6 / Deoxycytidine; 8A1O1M485B / Imatinib Mesylate; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.10.1 / Receptors, Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
  • [Other-IDs] NLM/ NIHMS7796; NLM/ PMC1456803
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20. Lee WN, Guo P, Lim S, Bassilian S, Lee ST, Boren J, Cascante M, Go VL, Boros LG: Metabolic sensitivity of pancreatic tumour cell apoptosis to glycogen phosphorylase inhibitor treatment. Br J Cancer; 2004 Dec 13;91(12):2094-100
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  • [Title] Metabolic sensitivity of pancreatic tumour cell apoptosis to glycogen phosphorylase inhibitor treatment.
  • Here we demonstrate that restrained glycogen breakdown also inhibits cancer cell proliferation and induces apoptosis through limiting glucose oxidation, as well as nucleic acid and de novo fatty acid synthesis.
  • Increasing doses (50-100 microM) of the glycogen phosphorylase inhibitor CP-320626 inhibited [1,2-(13)C(2)]glucose stable isotope substrate re-distribution among glycolysis, pentose and de novo fatty acid synthesis in MIA pancreatic adenocarcinoma cells.
  • Limited oxidative pentose-phosphate synthesis, glucose contribution to acetyl CoA and de novo fatty acid synthesis closely correlated with decreased cell proliferation.
  • The stable isotope-based dynamic metabolic profile of MIA cells indicated a significant dose-dependent decrease in macromolecule synthesis, which was detected at lower drug doses and before the appearance of apoptosis markers.
  • This indicates that limiting carbon re-cycling and rapid substrate mobilisation from glycogen may be an effective and selective target site for new drug development in rapidly dividing cancer cells.
  • In conclusion, pancreatic cancer cell growth arrest and death are closely associated with a characteristic decrease in glycogen breakdown and glucose carbon re-distribution towards RNA/DNA and fatty acids during CP-320626 treatment.

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  • (PMID = 15599384.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCRR NIH HHS / RR / M01 RR000425; United States / NCI NIH HHS / CA / P01 CA042710; United States / NCRR NIH HHS / RR / M01-RR00425; United States / NCI NIH HHS / CA / P01-CA42710
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amides; 0 / CP 320626; 0 / Enzyme Inhibitors; 0 / Indoles; EC 2.4.1.- / Glycogen Phosphorylase
  • [Other-IDs] NLM/ PMC2409791
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21. Borgonovo G, Razzetta F, Assalino M, Varaldo E, Puglisi M, Ceppa P: Rectal hepatoid carcinoma with liver metastases in a patient affected by ulcerative colitis. Hepatobiliary Pancreat Dis Int; 2008 Oct;7(5):539-43
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  • [Title] Rectal hepatoid carcinoma with liver metastases in a patient affected by ulcerative colitis.
  • BACKGROUND: Hepatoid tumors (HTs) are rare extra-hepatic neoplasms with the histological features, biochemical profile and, sometimes, even clinical course of hepatocellular carcinoma.
  • Fine-needle biopsy revealed that liver masses were positive for hepatocellular carcinoma.
  • RESULTS: Immunohistochemistry and albumin mRNA in situ hybridization suggested that the nodules were metastases of a HT.
  • The patient was well during the first 6 months and refused any adjuvant chemotherapy.
  • CONCLUSIONS: HT is a rare colon cancer.
  • The prognosis is poor despite an aggressive and multimodal therapeutic strategy.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Hepatocellular / secondary. Colitis, Ulcerative / complications. Liver Neoplasms / secondary. Rectal Neoplasms / pathology
  • [MeSH-minor] Adult. Biopsy. Chemoembolization, Therapeutic. Diagnostic Errors. Fatal Outcome. Hepatectomy. Humans. Immunohistochemistry. Male. Neoplasm Staging. Proctocolectomy, Restorative. Tomography, X-Ray Computed

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  • (PMID = 18842504.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] China
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22. Walther DJ, Peter JU, Bader M: 7-Hydroxytryptophan, a novel, specific, cytotoxic agent for carcinoids and other serotonin-producing tumors. Cancer; 2002 Jun 15;94(12):3135-40
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  • Moreover, conventional chemotherapeutic agents, such as streptozocin, fluorouracil, cyclophosphamide, and doxorubicin, which target tumor cells directly, have produced disappointing results in the treatment of patients with these tumors in the advanced stage.
  • RESULTS: The authors chose tryptophan hydroxylase, the rate-limiting enzyme of serotonin biosynthesis, which is expressed highly in small cell lung carcinomas and carcinoids, as a target for the induction of cellular suicide by chemotherapy.
  • They found that this otherwise substrate specific enzyme was capable of metabolizing in situ a harmless tryptophan analogue, 7-hydroxytryptophan, to a potent toxin, 5,7-dihydroxytryptamine, a conversion blocked by the specific tryptophan hydroxylase inhibitor parachlorophenylalanine.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Carcinoid Tumor / drug therapy. Carcinoma, Small Cell / drug therapy. Lung Neoplasms / drug therapy. Serotonin / biosynthesis. Tryptophan / pharmacology
  • [MeSH-minor] 5,6-Dihydroxytryptamine / pharmacology. 5,7-Dihydroxytryptamine / pharmacology. Animals. COS Cells. Humans. Pancreatic Neoplasms / drug therapy. Tryptophan Hydroxylase / antagonists & inhibitors. Tumor Cells, Cultured

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  • [Copyright] Copyright 2002 American Cancer Society.
  • (PMID = 12115345.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 7-hydroxytryptophan; 0 / Antineoplastic Agents; 31363-74-3 / 5,7-Dihydroxytryptamine; 333DO1RDJY / Serotonin; 8DUH1N11BX / Tryptophan; EC 1.14.16.4 / Tryptophan Hydroxylase; W2QY253O8S / 5,6-Dihydroxytryptamine
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23. Lee KM, Cao D, Itami A, Pour PM, Hruban RH, Maitra A, Ouellette MM: Class III beta-tubulin, a marker of resistance to paclitaxel, is overexpressed in pancreatic ductal adenocarcinoma and intraepithelial neoplasia. Histopathology; 2007 Oct;51(4):539-46
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  • [Title] Class III beta-tubulin, a marker of resistance to paclitaxel, is overexpressed in pancreatic ductal adenocarcinoma and intraepithelial neoplasia.
  • Pancreatic ductal adenocarcinomas show limited responsiveness to taxanes, but little is known of the underlying mechanisms.
  • The aim of this study was to examine TUBB3 expression in pancreatic cancer cell lines, invasive pancreatic adenocarcinoma and pancreatic intraepithelial neoplasia (PanIN).
  • METHODS AND RESULTS: Reverse transcriptase-polymerase chain reaction and Western blot were used to study TUBB3 expression in pancreatic cancer cell lines.
  • Immunohistochemistry was employed to assess TUBB3 in pancreatic cancer specimens, including 75 invasive adenocarcinomas and 41 PanIN precursor lesions.
  • TUBB3 was undetectable in non-neoplastic ducts of the pancreas.
  • In contrast, the vast majority (78-93%) of pancreatic ductal adenocarcinomas demonstrated either diffuse or focal TUBB3 expression.
  • CONCLUSIONS: TUBB3 is expressed in most pancreatic ductal adenocarcinomas, possibly accounting for the suboptimal response of these tumours to microtubule-stabilizing agents.
  • TUBB3 immunohistochemistry could potentially help identify pancreatic cancer patients lacking TUBB3 expression who might benefit from taxane therapy.
  • [MeSH-major] Adenocarcinoma / metabolism. Antineoplastic Agents, Phytogenic / therapeutic use. Carcinoma in Situ / metabolism. Drug Resistance, Neoplasm. Paclitaxel / therapeutic use. Pancreatic Neoplasms / metabolism. Tubulin / metabolism

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  • (PMID = 17714470.001).
  • [ISSN] 0309-0167
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / U01 CA111294
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Biomarkers, Tumor; 0 / TUBB3 protein, human; 0 / Tubulin; P88XT4IS4D / Paclitaxel
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24. Liu WB, Wang XP, Wu K, Zhang RL: Effects of angiotensin II receptor antagonist, Losartan on the apoptosis, proliferation and migration of the human pancreatic stellate cells. World J Gastroenterol; 2005 Nov 7;11(41):6489-94
Hazardous Substances Data Bank. Losartan .

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  • [Title] Effects of angiotensin II receptor antagonist, Losartan on the apoptosis, proliferation and migration of the human pancreatic stellate cells.
  • AIM: To investigate the effects of AT1 (Type 1 angiotensin II receptor) antagonist (Losartan) on the apoptosis, proliferation and migration of the human pancreatic stellate cells (hPSCs).
  • METHODS: hPSCs were isolated from pancreatic sample of patients with pancreatic carcinoma using radioimmunoassay (RIA) technique to detect the concentration of AngII in culture media and cell homogenate.
  • Immunocytochemistry (ICC) and in situ hybridization (ISH) methods were utilized to test AT1 expression in hPSCs.
  • Immunofluorescence and Western blot were applied to quantify the expression of type I collagen in hPSCs.
  • Losartan induces cell apoptosis in a dose- and time-dependent manner (apparently at 10(-5) mol/L), no pro-proliferative effect was observed in the same condition.
  • Corresponding dosage of Losartan can also alleviate the motion capability and type I collagen content of hPSCs compared with AngII treatment and non-treatment control groups.
  • [MeSH-major] Angiotensin II Type 1 Receptor Blockers / pharmacology. Apoptosis / drug effects. Cell Movement / drug effects. Losartan / pharmacology. Pancreas, Exocrine / cytology
  • [MeSH-minor] Cell Division / drug effects. Cells, Cultured. Fibrosis. Humans. Pancreatitis, Chronic / drug therapy. Pancreatitis, Chronic / pathology

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  • (PMID = 16425421.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; JMS50MPO89 / Losartan
  • [Other-IDs] NLM/ PMC4355791
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25. Bruns CJ, Solorzano CC, Harbison MT, Ozawa S, Tsan R, Fan D, Abbruzzese J, Traxler P, Buchdunger E, Radinsky R, Fidler IJ: Blockade of the epidermal growth factor receptor signaling by a novel tyrosine kinase inhibitor leads to apoptosis of endothelial cells and therapy of human pancreatic carcinoma. Cancer Res; 2000 Jun 1;60(11):2926-35
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  • [Title] Blockade of the epidermal growth factor receptor signaling by a novel tyrosine kinase inhibitor leads to apoptosis of endothelial cells and therapy of human pancreatic carcinoma.
  • We determined whether down-regulation of the epidermal growth factor-receptor (EGF-R) signaling pathway by oral administration of a novel EGF-R tyrosine kinase inhibitor (PKI166) alone or in combination with gemcitabine (administered i.p.) can inhibit growth and metastasis of human pancreatic carcinoma cells implanted into the pancreas of nude mice.
  • Therapy beginning 7 days after orthotopic injection of L3.6pl human pancreatic cancer cells reduced the volume of pancreatic tumors by 59% in mice treated with gemcitabine only, by 45% in those treated with PKI166 only, and by 85% in those given both drugs.
  • The combination therapy also significantly inhibited lymph node and liver metastasis, which led to a significant increase in overall survival.
  • EGF-R activation was significantly blocked by therapy with PKI166 and was associated with significant reduction in tumor cell production of VEGF and IL-8, which in turn correlated with a significant decrease in microvessel density and an increase in apoptotic endothelial cells.
  • Collectively, our results demonstrate that oral administration of an EGF-R tyrosine kinase inhibitor decreased growth and metastasis of human pancreatic cancer growing orthotopically in nude mice and increased survival.
  • The therapeutic effects were mediated in part by inhibition of tumor-induced angiogenesis attributable to a decrease in production of proangiogenic molecules by tumor cells and increased apoptosis of tumor-associated endothelial cells.
  • [MeSH-major] Apoptosis / drug effects. Pancreatic Neoplasms / drug therapy. Protein-Tyrosine Kinases / antagonists & inhibitors. Pyrimidines / pharmacology. Pyrroles / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / metabolism. Signal Transduction / drug effects
  • [MeSH-minor] Administration, Oral. Animals. Antigens, CD31 / metabolism. Antineoplastic Combined Chemotherapy Protocols / pharmacology. Blotting, Western. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Down-Regulation. Endothelium / pathology. Fluorescent Antibody Technique. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Neoplasm Transplantation. Time Factors. Tumor Cells, Cultured

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  • (PMID = 10850439.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / CA67952; United States / NCI NIH HHS / CA / R35-CA42107
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Antigens, CD31; 0 / PKI 166; 0 / Pyrimidines; 0 / Pyrroles; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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26. da Cunha Santos G, Dhani N, Tu D, Chin K, Ludkovski O, Kamel-Reid S, Squire J, Parulekar W, Moore MJ, Tsao MS: Molecular predictors of outcome in a phase 3 study of gemcitabine and erlotinib therapy in patients with advanced pancreatic cancer: National Cancer Institute of Canada Clinical Trials Group Study PA.3. Cancer; 2010 Dec 15;116(24):5599-607
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  • [Title] Molecular predictors of outcome in a phase 3 study of gemcitabine and erlotinib therapy in patients with advanced pancreatic cancer: National Cancer Institute of Canada Clinical Trials Group Study PA.3.
  • BACKGROUND: National Cancer Institute of Canada Clinical Trials Group PA.3 (NCIC CTG PA.3) was a phase 3 study (n = 569) that demonstrated benefits for overall survival and progression-free survival with the addition of the epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) erlotinib to gemcitabine in patients with advanced pancreatic carcinoma (APC).
  • METHODS: KRAS mutation status was evaluated by direct sequencing of exon 2, and EGFR GCN was determined by fluorescence in situ hybridization (FISH) analysis.
  • The hazard ratio of death between gemcitabine/erlotinib and gemcitabine/placebo was 0.66 (95% confidence interval [CI], 0.28-1.57) for patients with wild-type KRAS and 1.07 (95% CI, 0.68-1.66) for patients with mutant KRAS (P value for interaction = .38), and the hazard ratio was 0.6 (95% CI, 0.34-1.07) for FISH-negative patients and 0.90 (95% CI, 0.49-1.65) for FISH-positive patients (P value for interaction = .32).
  • CONCLUSIONS: In a molecular subset analysis of patients from NCIC CTG PA.3, EGFR GCN and KRAS mutation status were not identified as markers predictive of a survival benefit from the combination of erlotinib with gemcitabine for the first-line treatment of APC.
  • [MeSH-major] Biomarkers, Tumor / analysis. Deoxycytidine / analogs & derivatives. Pancreatic Neoplasms / drug therapy. Quinazolines / administration & dosage
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols. Canada. Disease-Free Survival. Erlotinib Hydrochloride. Gene Dosage. Humans. Mutation. Predictive Value of Tests. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins / genetics. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Receptor, Epidermal Growth Factor / genetics. Treatment Outcome. ras Proteins / analysis. ras Proteins / genetics

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  • [Copyright] Copyright © 2010 American Cancer Society.
  • (PMID = 20824720.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Clinical Trial, Phase III; Journal Article; Multicenter Study; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / KRAS protein, human; 0 / Proto-Oncogene Proteins; 0 / Quinazolines; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; DA87705X9K / Erlotinib Hydrochloride; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 3.6.5.2 / ras Proteins
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27. Corvera CU, Dunnican WJ, Blumgart LH, D'Angelica M: Recurrent invasive intraductal papillary mucinous carcinoma of the pancreas mimicking pott disease: review of the literature. Pancreas; 2006 Apr;32(3):321-4
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  • [Title] Recurrent invasive intraductal papillary mucinous carcinoma of the pancreas mimicking pott disease: review of the literature.
  • We report an unusual case of cancer recurrence in an 86-year-old woman who had undergone a pancreaticoduodenectomy for a large IPMN in the head of the pancreas.
  • Final pathological evaluation of the resected pancreas found a component of in situ and invasive ductal adenocarcinoma without lymph node involvement.
  • The patient did not receive postoperative chemotherapy and was monitored with transaxial imaging at regular intervals.
  • Nine years later, the patient developed a retroperitoneal psoas abscess that was misdiagnosed as tuberculous spondylitis (Pott disease) but was proven to be recurrent mucinous adenocarcinoma of pancreatic origin.
  • [MeSH-major] Adenocarcinoma, Mucinous / pathology. Carcinoma, Pancreatic Ductal / pathology. Carcinoma, Papillary / pathology. Neoplasm Recurrence, Local / pathology. Pancreatic Neoplasms / pathology. Tuberculosis, Spinal / diagnosis

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  • (PMID = 16628089.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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28. Solorzano CC, Baker CH, Bruns CJ, Killion JJ, Ellis LM, Wood J, Fidler IJ: Inhibition of growth and metastasis of human pancreatic cancer growing in nude mice by PTK 787/ZK222584, an inhibitor of the vascular endothelial growth factor receptor tyrosine kinases. Cancer Biother Radiopharm; 2001 Oct;16(5):359-70
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  • [Title] Inhibition of growth and metastasis of human pancreatic cancer growing in nude mice by PTK 787/ZK222584, an inhibitor of the vascular endothelial growth factor receptor tyrosine kinases.
  • Since vascular endothelial growth factor (VEGF) plays a major role in tumor angiogenesis, we determined whether blockage of VEGF receptor signaling using a novel tyrosine kinase inhibitor (PTK 787) decreases the growth and metastasis of human pancreatic carcinoma growing orthotopically in nude mice.
  • Human pancreatic L3.6pl cells were injected into the pancreas of nude mice.
  • Seven days later, groups of mice were given daily oral administrations of PTK 787 alone, twice weekly i.p. injections of gemcitabine, or combination therapy.
  • Therapy with PTK 787 alone, gemcitabine alone, or the combination of both agents produced respectively 60%, 70%, and 81% inhibition in the volume of pancreatic cancers.
  • The combination therapy significantly decreased the incidence of lymph node and liver metastasis, leading to a significant increase in survival.
  • Collectively, our results demonstrate that blockade of VEGF-R signaling may provide an additional approach to the therapy of pancreatic cancer.
  • [MeSH-major] Adenocarcinoma / drug therapy. Angiogenesis Inhibitors / therapeutic use. Deoxycytidine / analogs & derivatives. Enzyme Inhibitors / therapeutic use. Pancreatic Neoplasms / drug therapy. Phthalazines / therapeutic use. Pyridines. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Receptors, Growth Factor / antagonists & inhibitors
  • [MeSH-minor] Animals. Antigens, CD31 / analysis. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Humans. In Situ Nick-End Labeling. Male. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Metastasis. Neoplasm Proteins / analysis. Neoplasm Transplantation. Proliferating Cell Nuclear Antigen / analysis. Receptors, Vascular Endothelial Growth Factor. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 11776753.001).
  • [ISSN] 1084-9785
  • [Journal-full-title] Cancer biotherapy & radiopharmaceuticals
  • [ISO-abbreviation] Cancer Biother. Radiopharm.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA16672; United States / NCI NIH HHS / CA / R35-CA42107
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antigens, CD31; 0 / Enzyme Inhibitors; 0 / Neoplasm Proteins; 0 / Phthalazines; 0 / Proliferating Cell Nuclear Antigen; 0 / Pyridines; 0 / Receptors, Growth Factor; 0W860991D6 / Deoxycytidine; 5DX9U76296 / vatalanib; B76N6SBZ8R / gemcitabine; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptors, Vascular Endothelial Growth Factor
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29. Nio Y, Iguchi C, Yamasawa K, Sasaki S, Takamura M, Toga T, Dong M, Itakura M, Tamura K: Apoptosis and expression of Bcl-2 and Bax proteins in invasive ductal carcinoma of the pancreas. Pancreas; 2001 Apr;22(3):230-9
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  • [Title] Apoptosis and expression of Bcl-2 and Bax proteins in invasive ductal carcinoma of the pancreas.
  • The present study was designed to assess the clinicopathologic significance of apoptosis and the expression of the apoptosis-inhibitory Bcl-2 protein (pBcl-2) and the apoptosis-promoting Bax protein (pBax) in human invasive ductal carcinomas (IDCs) of the pancreas.
  • Apoptosis was assessed by the in situ nick end labeling method and pBcl-2 and pBax were stained immunohistochemically.
  • On the other hand, the survival curve of the adjuvant chemotherapy (ACT) group was also higher than that of the surgery alone (SA) group, with borderline statistical signfiicance.
  • [MeSH-major] Apoptosis. Carcinoma, Pancreatic Ductal / pathology. Pancreatic Neoplasms / pathology. Proto-Oncogene Proteins / analysis. Proto-Oncogene Proteins c-bcl-2 / analysis
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Antineoplastic Agents / therapeutic use. Chemotherapy, Adjuvant. Female. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Male. Middle Aged. Multivariate Analysis. Neoplasm Invasiveness. Pancreatectomy. Prognosis. Survival Rate. bcl-2-Associated X Protein

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  • (PMID = 11291923.001).
  • [ISSN] 0885-3177
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein
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30. Ischenko I, Guba M, Yezhelyev M, Papyan A, Schmid G, Green T, Fennell M, Jauch KW, Bruns CJ: Effect of Src kinase inhibition on metastasis and tumor angiogenesis in human pancreatic cancer. Angiogenesis; 2007;10(3):167-82
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  • [Title] Effect of Src kinase inhibition on metastasis and tumor angiogenesis in human pancreatic cancer.
  • We hypothesized that decrease in pancreatic tumor growth due to inhibition of Src activity is associated with the inability of Src kinase to trigger a network of such signaling processes, which finally leads to endothelial cell death and angiogenesis-restricted tumor dormancy.
  • The therapeutic efficacy of Src kinase inhibitor AZM475271 was tested in nude mice orthotopically xenografted with L3.6pl pancreatic carcinoma cells.
  • No liver metastases and peritoneal carcinosis were detected and a significant effect on the average pancreatic tumor burden was observed following treatment with AZM475271, which in turn correlated with a decrease in cell proliferation and an increase in apoptotic endothelial cells.
  • In a rat aortic ring assay we could demonstrate as well inhibition of endothelial cell migration and sprouting following therapy with Src kinase inhibitor at similar doses.
  • Treatment with AZM475271 resulted in VEGF - dependent inhibition of tyrosine phosphorylation of FAK.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Neovascularization, Pathologic / enzymology. Pancreatic Neoplasms / blood supply. Pancreatic Neoplasms / drug therapy. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Proliferation / drug effects. Humans. Immunohistochemistry. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Mice. Mice, Inbred C57BL. Mice, Nude. Neoplasm Metastasis / prevention & control. Xenograft Model Antitumor Assays

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  • (PMID = 17486419.001).
  • [ISSN] 0969-6970
  • [Journal-full-title] Angiogenesis
  • [ISO-abbreviation] Angiogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; EC 2.7.10.2 / src-Family Kinases
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31. Kurihara K, Nagai H, Kasahara K, Kawai T, Saito K, Kanazawa K: Pleomorphic carcinoma of the pancreas with massive lymphocytic stromal infiltration and long-term survival after resection. Int J Pancreatol; 2000 Jun;27(3):241-8
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  • [Title] Pleomorphic carcinoma of the pancreas with massive lymphocytic stromal infiltration and long-term survival after resection.
  • BACKGROUND: Pleomorphic carcinoma of the pancreas is a rare tumor with an extremely poor prognosis.
  • The mean survival time is reported to be approx 3 mo.
  • CLINICAL AND HISTOLOGICAL FINDINGS: A 56-yr-old Japanese man presenting with general fatigue, loss of weight, and high fever was found to have a large hypervascular mass in the body of the pancreas with regional lymph node metastases.
  • In addition to distal pancreatectomy, splenectomy and lymph node dissection were performed.
  • Immunohistochemically, the infiltrating lymphocytes consisted of cytotoxic type of T cells.
  • In addition, in situ hybridization for Epstein-Barr virus-encoded RNA (EBAR-1) was not seen in the tumor cells or in lymphocytes.
  • After surgery the patient did not undergo chemotherapy or radiotherapy.
  • CONCLUSION: We report a case of pleomorphic carcinoma, possibly lymphoepithelioma-like carcinoma, of the pancreas with massive lymphocytic stromal infiltration and long-term survival after resection.
  • Cytokine responses and cellular immunoreactivity may have contributed to a long-term survival, which is unusual in the common type of pleomorphic carcinoma of the pancreas.
  • [MeSH-major] Carcinoma / pathology. Lymphocytes / pathology. Pancreatic Neoplasms / pathology

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  • (PMID = 10952407.001).
  • [ISSN] 0169-4197
  • [Journal-full-title] International journal of pancreatology : official journal of the International Association of Pancreatology
  • [ISO-abbreviation] Int. J. Pancreatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] UNITED STATES
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32. Wang W, Adachi M, Zhang R, Zhou J, Zhu D: A novel combination therapy with arsenic trioxide and parthenolide against pancreatic cancer cells. Pancreas; 2009 May;38(4):e114-23
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  • [Title] A novel combination therapy with arsenic trioxide and parthenolide against pancreatic cancer cells.
  • OBJECTIVES: To investigate the anticancer effect and potential mechanism of combination treatment with arsenic trioxide (ATO) and parthenolide (PTL) in human pancreatic cancer cells.
  • METHODS: The effects of PTL/ATO on 2 pancreatic carcinoma cell lines, PANC-1 and BxPC-3, were determined by trypan blue exclusion, annexin V/propidium iodide, 4',6-diamidino-2-phenylindole HCl, terminal deoxynucleotidyltransferase-mediated nick-end labeling, flow cytometry, Western blot, and clonogenic assay.
  • RESULTS: The combination of PTL and ATO inhibited the growth of pancreatic tumor cell lines much greater than each agent alone.
  • The PTL/ATO treatment induced apoptosis and reactive oxygen species generation.
  • The combination treatment significantly reduced tumor growth rates of PANC-1 xenografts compared with those treated with either PTL or ATO alone.
  • CONCLUSIONS: Combination therapy with ATO and PTL has an augmented anticancer effect on pancreatic cancer in vitro and in vivo, which provides a novel promising approach in the treatment of pancreatic cancer.
  • The mechanism of growth-suppressive effect of combination therapy was correlated with its ability to induce reactive oxygen species generation and apoptosis via the mitochondrial pathway.
  • [MeSH-major] Arsenicals / pharmacology. Oxides / pharmacology. Pancreatic Neoplasms / drug therapy. Sesquiterpenes / pharmacology
  • [MeSH-minor] Acetylcysteine / pharmacology. Animals. Anti-Inflammatory Agents, Non-Steroidal / administration & dosage. Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Blotting, Western. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Synergism. Flow Cytometry. Growth Inhibitors / administration & dosage. Growth Inhibitors / pharmacology. Humans. In Situ Nick-End Labeling. Membrane Potential, Mitochondrial / drug effects. Mice. Mice, Nude. Reactive Oxygen Species / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 19342982.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Arsenicals; 0 / Growth Inhibitors; 0 / Oxides; 0 / Reactive Oxygen Species; 0 / Sesquiterpenes; 2RDB26I5ZB / parthenolide; S7V92P67HO / arsenic trioxide; WYQ7N0BPYC / Acetylcysteine
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33. Yezhelyev MV, Koehl G, Guba M, Brabletz T, Jauch KW, Ryan A, Barge A, Green T, Fennell M, Bruns CJ: Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice. Clin Cancer Res; 2004 Dec 1;10(23):8028-36
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  • [Title] Inhibition of SRC tyrosine kinase as treatment for human pancreatic cancer growing orthotopically in nude mice.
  • Src kinases are overexpressed in a variety of human tumors, including cancer of the colon, breast, and pancreas, and they are an integral part of tumor cell signaling pathways associated with migration, proliferation, adhesion, and angiogenesis.
  • EXPERIMENTAL DESIGN: We investigated whether the blockade of Src kinase by daily oral administration of the novel Src tyrosine kinase inhibitor AZM475271 [kindly provided by AstraZeneca (Macclesfield, United Kingdom)], alone or in combination with intraperitoneal gemcitabine, can inhibit growth and metastasis of orthotopically implanted human pancreatic carcinoma cells in nude mice.
  • RESULTS: Treatment with AZM475271 alone reduced the primary pancreatic tumor volume by approximately 40%, whereas AZM475271 plus gemcitabine reduced tumor volume by 90%.
  • Furthermore, treatment with AZM475271 and gemcitabine significantly reduced metastasis: none of eight animals who received the combination treatment had lymph node or liver metastases, compared with five of five and three of five animals, respectively, in the control group (P = 0.001).
  • CONCLUSIONS: Src inhibition by AZM475271, either alone or in combination with gemcitabine, demonstrated significant antitumor and antimetastatic activity in an orthotopic nude mouse model for human pancreatic cancer.
  • [MeSH-major] Apoptosis / drug effects. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Enzyme Inhibitors / therapeutic use. Pancreatic Neoplasms / drug therapy. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Administration, Oral. Animals. Cell Movement / drug effects. Cell Proliferation / drug effects. Cells, Cultured. Drug Therapy, Combination. Flow Cytometry. Humans. In Situ Nick-End Labeling. Ki-67 Antigen / metabolism. Male. Mice. Mice, Nude. NIH 3T3 Cells. Ribonucleotide Reductases / antagonists & inhibitors

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  • (PMID = 15585638.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Ki-67 Antigen; 0 / Mki67 protein, mouse; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.17.4.- / Ribonucleotide Reductases; EC 2.7.10.2 / src-Family Kinases
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34. Toga T, Nio Y, Hashimoto K, Higami T, Maruyama R: The dissociated expression of protein and messenger RNA of DPC4 in human invasive ductal carcinoma of the pancreas and their implication for patient outcome. Anticancer Res; 2004 Mar-Apr;24(2C):1173-8
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  • [Title] The dissociated expression of protein and messenger RNA of DPC4 in human invasive ductal carcinoma of the pancreas and their implication for patient outcome.
  • BACKGROUND: The loss of expression of Dpc4 protein (pDpc4) has been demonstrated in about half of invasive ductal carcinoma (IDC) of the pancreas, but the expression of DPC4-mRNA remains to be evaluated.
  • The present study assessed the comparative expression of pDpc4 and DPC4-mRNA in pancreatic IDC and their implication for patient outcome.
  • MATERIALS AND METHODS: In the freshly separated specimens of 21 IDCs and the paraffin-embedded specimens of 88 resectable IDCs, the expression of mRNA was assessed by in situ hybridization and the expression of pDpc4 was assessed by immunohistochemistry.
  • Adjuvant chemotherapy (ACT) significantly improved the survival rate and, in the ACT group, pDpc4 (-) patients had a significantly lower survival rate than the pDpc4 (+) patients.
  • CONCLUSION: In human pancreatic IDC, although DPC4-mRNA was usually expressed, the expression of pDpc4 was lost.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / metabolism. DNA-Binding Proteins / biosynthesis. Pancreatic Neoplasms / metabolism. RNA, Messenger / biosynthesis. Trans-Activators / biosynthesis
  • [MeSH-minor] Aged. Chemotherapy, Adjuvant. Female. Humans. Immunohistochemistry. Male. Middle Aged. Neoplasm Invasiveness. Smad4 Protein. Treatment Outcome

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  • (PMID = 15154643.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / RNA, Messenger; 0 / SMAD4 protein, human; 0 / Smad4 Protein; 0 / Trans-Activators
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35. Kirstein MN, Brundage RC, Moore MM, Williams BW, Hillman LA, Dagit JW, Fisher JE, Marker PH, Kratzke RA, Yee D: Pharmacodynamic characterization of gemcitabine cytotoxicity in an in vitro cell culture bioreactor system. Cancer Chemother Pharmacol; 2008 Feb;61(2):291-9
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  • PURPOSE: Gemcitabine, a pyrimidine nucleoside, is approved for the treatment of non-small cell lung cancer, pancreatic carcinoma, and breast cancer.
  • Chemotherapy regimens are determined experimentally with static tissue culture systems, animal models, and in Phase I clinical trials.
  • The aim of this study was to assess for gemcitabine-induced cell death following infusion of drug under clinically-relevant conditions of infusion rate and drug exposure in an in vitro bioreactor system.
  • METHODS: To estimate an appropriate harvest time for cells from the bioreactor after drug treatment, we estimated the temporal relationship between gemcitabine treatment for 1 h and cell death at a later time point with monolayer growth assays (i.e., static culture).
  • Afterward, 5.3 mg gemcitabine was infused over 0.5 h in the bioreactor, followed by mono-exponential decay, simulating patient concentration-time profiles (n = 4).
  • Controls were run with drug-free media (n = 4).
  • Cells were harvested from the bioreactor at a later time point and assessed for cell death by flow cytometry.
  • RESULTS: According to monolayer growth assay results, cytotoxicity became more apparent with increasing time.
  • The E Max for cells 48 h after treatment was 50% and after 144 h, 93% (P = 0.022; t test), while flow cytometry showed complete DNA degradation by 120 h.
  • The gemcitabine area under the concentration-time curve (AUC) was 56.4 microM h and the maximum concentration was 87.5 +/- 2.65 microM.
  • CONCLUSIONS: The in vitro bioreactor system will be expanded to test additional cell lines, and will serve as a useful model system for assessing the role of drug pharmacokinetics in delivery of optimized anticancer treatment.
  • [MeSH-minor] Area Under Curve. Bioreactors. Cell Cycle / drug effects. Cell Death / drug effects. Cell Line, Tumor. DNA, Neoplasm / metabolism. Flow Cytometry. Humans. In Situ Nick-End Labeling. Tetrazolium Salts. Thiazoles

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  • (PMID = 17429628.001).
  • [ISSN] 0344-5704
  • [Journal-full-title] Cancer chemotherapy and pharmacology
  • [ISO-abbreviation] Cancer Chemother. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / Tetrazolium Salts; 0 / Thiazoles; 0W860991D6 / Deoxycytidine; 298-93-1 / thiazolyl blue; B76N6SBZ8R / gemcitabine
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36. Park SC, Yoon JH, Kim W, Gwak GY, Kim KM, Lee SH, Lee SM, Lee HS: Eupatilin attenuates bile acid-induced hepatocyte apoptosis. J Gastroenterol; 2006 Aug;41(8):772-8
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  • Eupatilin (5,7-dihydroxy-3,4,6-trimethoxyflavone) is a pharmacologically active ingredient found in Artemisia asiatica and exhibits cytoprotective effects against experimentally induced gastrointestinal, pancreatic, and hepatic damage.
  • METHODS: Huh-BAT cells, a human hepatocellular carcinoma cell line stably transfected with a bile acid transporter, were used in this study.
  • Eupatilin's in vivo effect on bile acid-induced hepatocyte apoptosis was explored in bile duct-ligated rats.
  • Moreover, eupatilin diminished hepatocyte apoptosis in bile duct-ligated rats.
  • [MeSH-major] Apoptosis / drug effects. Flavonoids / pharmacology. Hepatocytes / drug effects. MAP Kinase Signaling System / drug effects
  • [MeSH-minor] Animals. Caspase 8 / metabolism. Cell Line, Tumor. Cholestasis / drug therapy. Deoxycholic Acid / pharmacology. Humans. Immunoblotting. In Situ Nick-End Labeling. JNK Mitogen-Activated Protein Kinases / metabolism. Male. Microscopy, Fluorescence. Models, Animal. Rats. Rats, Sprague-Dawley. p38 Mitogen-Activated Protein Kinases / metabolism

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  • [CommentIn] J Gastroenterol. 2006 Aug;41(8):818-9 [16988777.001]
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  • (PMID = 16988766.001).
  • [ISSN] 0944-1174
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Flavonoids; 005990WHZZ / Deoxycholic Acid; 4D58O05490 / eupatilin; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.4.22.- / Caspase 8
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37. Gadi VK, Alexander SD, Waud WR, Allan PW, Parker WB, Sorscher EJ: A long-acting suicide gene toxin, 6-methylpurine, inhibits slow growing tumors after a single administration. J Pharmacol Exp Ther; 2003 Mar;304(3):1280-4
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  • We have demonstrated antitumor activity against refractory human glioma and pancreatic tumors with 6-methylpurine (MeP) using either a suicide gene therapy strategy to selectively release 6-methylpurine in tumor cells or direct intratumoral injection of 6-methylpurine itself.
  • A single i.p. injection in mice of the prodrug 9-beta-D-[2-deoxyribofuranosyl]-6-methylpurine (MeP-dR; 134 mg/kg) caused sustained regression lasting over 70 days of D54 (human glioma) tumors transduced with the Escherichia coli purine nucleoside phosphorylase (PNP), and a single intratumoral injection of 6-methylpurine (5-10 mg/kg) elicited prolonged delays of the growth of D54 tumors and CFPAC human pancreatic carcinoma.
  • Because the D54 tumor doubling time is >15 days, the experiments indicate that prodrug activation by E. coli PNP engenders destruction of both dividing and nondividing tumor compartments in vivo and, therefore, address a fundamental barrier that has limited the development of suicide gene strategies in the past.
  • A prolonged retention time of 6-methylpurine metabolites in tumors was noted in vivo (T(1/2) >24 h compared with a serum half-life of <1 h).
  • These experiments point to new endpoints for monitoring E. coli PNP suicide gene therapy, including intratumoral enzymatic activity, in situ (intratumoral) prodrug conversion, and tumor regressions after direct injection of a suicide gene toxin.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Neoplasms, Experimental / drug therapy. Purines / therapeutic use
  • [MeSH-minor] Animals. Disease Models, Animal. Glioma / pathology. Humans. Mice. Mice, SCID. Neoplasm Transplantation. Treatment Outcome. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12604707.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 5 U19 CA67763-05; United States / NIDDK NIH HHS / DK / P30 DK54781
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Purines; 2004-03-7 / 6-methylpurine
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38. Wang BL, Zhai HY, Chen BY, Zhai SP, Yang HY, Chen XP, Zhao WT, Meng L: Clinical relationship between MDR1 gene and gallbladder cancer. Hepatobiliary Pancreat Dis Int; 2004 May;3(2):296-9
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  • [Title] Clinical relationship between MDR1 gene and gallbladder cancer.
  • BACKGROUND: The most common mechanisms of multidrug resistance (MDR) in cancer cells is the expression of an energy-dependent exfflux pump.
  • It is a major therapeutic problem in cancer chemotherapy.
  • The aim of this study is to study the expression of MDR1 gene encoding P-gp and MDRl mRNA in primary gallbladder carcinoma, and analyze its clinical significance.
  • METHODS: Immunohistochemistry (IHC) S-P method and in situ polymerase chain reaction (ISPCR) were used to detect the expression of P-gp and MDR1 mRNA in 53 cases of untreated primary gallbladder carcinoma and 12 cases of cholecystitis (archival paraffin-embedded tissues).
  • RESULTS: The positive expression rates of P-gp and MDR1 mRNA in the 53 cases and 12 cases were 60.38%, 71.69% and 25.00%, 33.33%, respectively.
  • The positive expression rate of P-gp and MDR1mRNA were 69.44%, 83.33% and 41.18%, 47.06% respectively in tissues in stage of Nevin I-III against Nevin IV, V (P<0.05).
  • In well, moderately differentiated gallbladder carcinoma tissues, their expressions were 79.49%, 69.23% against 50.00%, 35.71% in low, undifferentiated tissues (P<0.05).
  • CONCLUSIONS: MDR to gallbladder carcinoma is closely related to the intrinsic MDR and it provides an important evidence to reverse the MDR by detection of the MDR1 gene.
  • Meanwhile, MDR1 gene expression in gallbladder carcinoma is correlated with some biological characteristics, takes part in the carcinogenesis of gallbladder tissues, and acts as a valuable biomarker of prognosis.
  • [MeSH-major] Biomarkers, Tumor / genetics. Carcinoma / genetics. Gallbladder Neoplasms / genetics. Genes, MDR / genetics. P-Glycoprotein / genetics
  • [MeSH-minor] Adult. Aged. Cell Transformation, Neoplastic / genetics. Drug Resistance, Neoplasm / genetics. Female. Humans. Male. Middle Aged. Prognosis. RNA, Messenger / genetics

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  • (PMID = 15138130.001).
  • [ISSN] 1499-3872
  • [Journal-full-title] Hepatobiliary & pancreatic diseases international : HBPD INT
  • [ISO-abbreviation] HBPD INT
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / P-Glycoprotein; 0 / RNA, Messenger
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39. El-Salhy M, Tjomsland V, Theodorsson E: Effects of triple treatment with octreotide, galanin and serotonin on a human pancreas cancer cell line in xenografts. Histol Histopathol; 2005 07;20(3):745-52
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  • [Title] Effects of triple treatment with octreotide, galanin and serotonin on a human pancreas cancer cell line in xenografts.
  • Human pancreas cancer cells were implanted s.c. in nude mice.
  • The first group received sterile saline solution and the second received triple therapy containing octreotide, galanin and serotonin, 40 microg/kg/day as a continuous i.p. infusion via an implanted osmotic pump for 14 days.
  • Triple therapy prolonged the survival rate of the mice bearing human pancreatic carcinoma.
  • Both the volume and weight of tumours in mice given triple therapy were less than in controls (not statistically significant).
  • The proliferation index and the labelling index for epidermal growth factor (EGF) increased significantly in mice given triple therapy vis-a-vis controls.
  • Identifying the agent(s) inducing pancreatic cancer cell proliferation may be useful in combining a new treatment, as antagonists to these bioactive substances are available.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Xenograft Model Antitumor Assays / methods
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blood Vessels / drug effects. Blood Vessels / pathology. Cell Line, Tumor. Cell Proliferation / drug effects. Epidermal Growth Factor / metabolism. Female. Galanin / administration & dosage. Humans. In Situ Nick-End Labeling. Infusions, Parenteral. Mice. Mice, Inbred C57BL. Mice, Nude. Neoplasms, Experimental / blood supply. Neoplasms, Experimental / mortality. Neoplasms, Experimental / prevention & control. Octreotide / administration & dosage. Receptor, Epidermal Growth Factor / metabolism. Serotonin / administration & dosage. Survival Rate. Treatment Outcome

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  • (PMID = 15944923.001).
  • [ISSN] 0213-3911
  • [Journal-full-title] Histology and histopathology
  • [ISO-abbreviation] Histol. Histopathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Spain
  • [Chemical-registry-number] 333DO1RDJY / Serotonin; 62229-50-9 / Epidermal Growth Factor; 88813-36-9 / Galanin; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; RWM8CCW8GP / Octreotide
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