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Items 1 to 24 of about 24
1. Shimamura T, Royal RE, Kioi M, Nakajima A, Husain SR, Puri RK: Interleukin-4 cytotoxin therapy synergizes with gemcitabine in a mouse model of pancreatic ductal adenocarcinoma. Cancer Res; 2007 Oct 15;67(20):9903-12
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  • [Title] Interleukin-4 cytotoxin therapy synergizes with gemcitabine in a mouse model of pancreatic ductal adenocarcinoma.
  • Targeting cell surface receptors with cytotoxins or immunotoxins provides a unique opportunity for tumor therapy.
  • Here, we show the efficacy of the combination therapy of gemcitabine with an interleukin-4 (IL-4) cytotoxin composed of IL-4 and truncated Pseudomonas exotoxin in animal models of pancreatic ductal adenocarcinoma (PDA).
  • We have observed that 42 of 70 (60%) tumor samples from patients with PDA express moderate- to high-density surface IL-4 receptor (IL-4R), whereas normal pancreatic samples express no or low-density IL-4R.
  • IL-4 cytotoxin was specifically and highly cytotoxic [50% protein synthesis inhibition (IC50) ranging from >0.1 to 13 ng/mL] to six of eight pancreatic cancer cell lines, whereas no cytotoxicity (IC50>1,000 ng/mL) was observed in normal human pancreatic duct epithelium cells, fibroblasts, and human umbilical vein endothelial cells (HUVEC).
  • To confirm synergistic antitumor activity in vivo and monitor precise real-time disease progression, we used a novel metastatic and orthotopic mouse model using green fluorescent protein-transfected cancer cells and whole-body imaging system.
  • In addition, combined treatment significantly prolonged the survival of nude mice bearing day 14 advanced distant metastatic PDA tumors.
  • These results indicate that IL-4 cytotoxin combined with gemcitabine may provide effective therapy for the treatment of patients with PDA.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Deoxycytidine / analogs & derivatives. Interleukin-4 / administration & dosage. Interleukin-4 / metabolism. Leukocidins / administration & dosage. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Synergism. Green Fluorescent Proteins / genetics. Humans. Mice. Mice, Nude. Receptors, Interleukin-4 / biosynthesis. Receptors, Interleukin-4 / metabolism. Recombinant Fusion Proteins / administration & dosage. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / metabolism. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 17942922.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Leukocidins; 0 / Pseudomonas aeruginosa Cytotoxins; 0 / Receptors, Interleukin-4; 0 / Recombinant Fusion Proteins; 0W860991D6 / Deoxycytidine; 147336-22-9 / Green Fluorescent Proteins; 207137-56-2 / Interleukin-4; B76N6SBZ8R / gemcitabine
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2. Shimamura T, Fujisawa T, Husain SR, Joshi B, Puri RK: Interleukin 13 mediates signal transduction through interleukin 13 receptor alpha2 in pancreatic ductal adenocarcinoma: role of IL-13 Pseudomonas exotoxin in pancreatic cancer therapy. Clin Cancer Res; 2010 Jan 15;16(2):577-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Interleukin 13 mediates signal transduction through interleukin 13 receptor alpha2 in pancreatic ductal adenocarcinoma: role of IL-13 Pseudomonas exotoxin in pancreatic cancer therapy.
  • However, its significance and expression in pancreatic cancer is not known.
  • EXPERIMENTAL DESIGN: The expression of IL-13Ralpha2 was assessed in pancreatic cancer samples by immunohistochemistry and in cell lines by flow cytometry and reverse transcription-PCR.
  • The role of IL-13Ralpha2 was examined by IL-13-induced signaling in pancreatic cancer cell lines.
  • IL-13Ralpha2-positive tumors were targeted by IL-13PE cytotoxin in vitro and in vivo in an orthotopic murine model of human pancreatic cancer.
  • RESULTS: Of the pancreatic tumor samples 71% overexpressed moderate to high-density IL-13Ralpha2 chain compared with normal pancreatic samples.
  • In the orthotopic mouse model, IL13-PE significantly decreased tumor growth when assessed by whole-body imaging and prolonged the mean survival time.
  • Similar results were observed in mice xenografted with a surgically resected human pancreatic tumor sample.
  • CONCLUSIONS: These results indicate that IL-13Ralpha2 is a functional receptor as IL-13 mediates signaling in human pancreatic cancer cell lines.
  • In addition, IL13-PE cytotoxin may be an effective therapeutic agent for the treatment of pancreatic cancer.
  • [MeSH-major] ADP Ribose Transferases / therapeutic use. Bacterial Toxins / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Exotoxins / therapeutic use. Interleukin-13 / therapeutic use. Interleukin-13 Receptor alpha2 Subunit / physiology. Pancreatic Neoplasms / drug therapy. Virulence Factors / therapeutic use
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Mice, Nude. Mice, SCID. Signal Transduction / drug effects. Signal Transduction / genetics. Signal Transduction / physiology. Treatment Outcome. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 20068108.001).
  • [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
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Bacterial Toxins; 0 / Exotoxins; 0 / Interleukin-13; 0 / Interleukin-13 Receptor alpha2 Subunit; 0 / Virulence Factors; EC 2.4.2.- / ADP Ribose Transferases; EC 2.4.2.31 / toxA protein, Pseudomonas aeruginosa
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3. Liau SS, Whang E: HMGA1 is a molecular determinant of chemoresistance to gemcitabine in pancreatic adenocarcinoma. Clin Cancer Res; 2008 Mar 1;14(5):1470-7
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  • [Title] HMGA1 is a molecular determinant of chemoresistance to gemcitabine in pancreatic adenocarcinoma.
  • PURPOSE: HMGA1 proteins are architectural transcription factors that are overexpressed by pancreatic adenocarcinomas.
  • We previously have shown that RNA interference targeting the HMGA1 gene may represent a potential chemosensitizing strategy in pancreatic adenocarcinoma cells.
  • In this study, we tested the hypothesis that HMGA1 promotes chemoresistance to gemcitabine in pancreatic cancer cells.
  • Finally, HMGA1 silencing promoted chemosensitivity to gemcitabine in vivo in a nude mouse xenograft model of pancreatic adenocarcinoma.
  • Targeted therapies directed at HMGA1 represent a potential strategy for ameliorating chemoresistance in pancreatic adenocarcinoma.

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  • (PMID = 18316571.001).
  • [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 / CA114103-03; United States / NCI NIH HHS / CA / R01 CA114103-03
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 124544-67-8 / HMGA1a Protein; B76N6SBZ8R / gemcitabine; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 3.4.22.- / Caspase 3
  • [Other-IDs] NLM/ NIHMS84426; NLM/ PMC2652398
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4. Alves F, Borchers U, Padge B, Augustin H, Nebendahl K, Klöppel G, Tietze LF: Inhibitory effect of a matrix metalloproteinase inhibitor on growth and spread of human pancreatic ductal adenocarcinoma evaluated in an orthotopic severe combined immunodeficient (SCID) mouse model. Cancer Lett; 2001 Apr 26;165(2):161-70
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Inhibitory effect of a matrix metalloproteinase inhibitor on growth and spread of human pancreatic ductal adenocarcinoma evaluated in an orthotopic severe combined immunodeficient (SCID) mouse model.
  • The present study was aimed at evaluating the effect of the matrix metalloproteinase (MMP) inhibitor prinomastat (AG3340) on tumor progression using an orthotopic pancreatic carcinoma model in severe combined immunodeficient mice.
  • In controls, receiving vehicle only, the poorly differentiated ductal adenocarcinoma invaded into adjacent organs and metastasized to different sites in the abdomen and to the lungs.
  • Treatment with prinomastat, intraperitoneally twice daily for 21 days, reduced primary tumor volume significantly to 19.0 (+/-7.7)% of control, with induction of necrosis, differentiation, and fibrotic tissue in the pancreatic tumors.
  • We conclude that prinomastat is highly effective in inhibiting pancreatic carcinoma growth and progression in an orthotopic cancer model.
  • This model appears to be a valuable tool to investigate the potency of novel antimetastatic strategies in pancreatic ductal adenocarcinoma by specifically targeting certain MMPs.
  • [MeSH-major] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Antineoplastic Agents / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / metabolism. Organic Chemicals. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Animals. Antigens, CD34 / biosynthesis. Cell Differentiation / drug effects. Female. Fibrosis. Humans. Immunohistochemistry. Male. Matrix Metalloproteinase Inhibitors. Mice. Mice, SCID. Necrosis. Neoplasm Invasiveness. Neoplasm Transplantation. Tumor Cells, Cultured

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  • (PMID = 11275365.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antigens, CD34; 0 / Antineoplastic Agents; 0 / Matrix Metalloproteinase Inhibitors; 0 / Organic Chemicals; 10T6626FRK / prinomastat
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5. Angel LP, Divino CM, Brower ST, Chen SH: A novel immunocytolytic factor secreted by pancreatic adenocarcinoma. J Surg Res; 2000 Jun 15;91(2):154-8
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel immunocytolytic factor secreted by pancreatic adenocarcinoma.
  • BACKGROUND: We have observed a putative immunocytolytic factor secreted by several pancreatic adenocarcinoma cell lines that mediates a potent cytolytic effect on lymphocytes.
  • MATERIALS AND METHODS: Coincubation assays with murine splenocytes and supernatants from various species of pancreatic adenocarcinoma cell lines were performed.
  • Pancreatic adenocarcinoma supernatant was coincubated with Fas-sensitive Jurkat cells and Western blotting for FasL was performed.
  • RESULTS: A marked reduction in the viability (%/control) of target splenocytes was observed after incubation with the conditioned media from hamster PAN-1 (14.7%), PC 1.0 (21.7%), Taka-1 p70 (12.4%), Taka-1 p79 (7.6%), murine PANCO2 (16.1%), and human Capan-1 (14.0%) pancreatic adenocarcinoma cell lines.
  • The cytolytic effect appeared to be specific for lymphocytes and was not observed with the conditioned media of other tumor cells or normal pancreatic ductal cells.
  • Pancreatic adenocarcinoma supernatant had no killing effect on Jurkat cells compared with control supernatant of TC-248 cells (87% vs 15%) and immunoblotting did not demonstrate soluble FasL.
  • CONCLUSIONS: These findings demonstrate that pancreatic adenocarcinoma cells secrete a potent cytolytic factor that induces apoptosis of lymphocytes and is not FasL-mediated.
  • [MeSH-major] Adenocarcinoma / immunology. Adenocarcinoma / secretion. Culture Media / pharmacology. Pancreatic Neoplasms / immunology. Pancreatic Neoplasms / secretion
  • [MeSH-minor] Animals. Apoptosis / physiology. Cell Line. Cricetinae. Fas Ligand Protein. Female. Humans. Immunoblotting. Lymphocytes / drug effects. Lymphocytes / physiology. Membrane Glycoproteins / physiology. Mice. Mice, Inbred C57BL. Spleen / cytology. Spleen / drug effects

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  • [Copyright] Copyright 2000 Academic Press.
  • (PMID = 10839965.001).
  • [ISSN] 0022-4804
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Grant] United States / PHS HHS / / R01-75175; United States / NCI NIH HHS / CA / R29CA70337
  • [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 / Culture Media; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Membrane Glycoproteins
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6. Morton JP, Karim SA, Graham K, Timpson P, Jamieson N, Athineos D, Doyle B, McKay C, Heung MY, Oien KA, Frame MC, Evans TR, Sansom OJ, Brunton VG: Dasatinib inhibits the development of metastases in a mouse model of pancreatic ductal adenocarcinoma. Gastroenterology; 2010 Jul;139(1):292-303
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  • [Title] Dasatinib inhibits the development of metastases in a mouse model of pancreatic ductal adenocarcinoma.
  • BACKGROUND & AIMS: Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive and metastatic disease for which conventional treatments are of limited efficacy.
  • The aim of this study was to assess the importance of Src in human PDAC and to use a genetically engineered mouse model of PDAC to determine the effects of dasatinib on PDAC progression.
  • Targeting expression of Trp53(R172H) and Kras(G12D) to the mouse pancreas results in the formation of invasive and metastatic PDAC.
  • Cell lines were derived from mouse PDACs, and in vitro effects of dasatinib assessed.
  • CONCLUSIONS: This study confirms the importance of Src in human PDAC and shows the usefulness of a genetically engineered mouse model of PDAC for assessing the activity of potential antimetastatic agents and suggests that dasatinib should be evaluated further as monotherapy after resection of localized invasive PDAC.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / drug therapy. Pancreatic Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement / drug effects. Dasatinib. Disease Models, Animal. Female. Mice. Neoplasm Invasiveness. Neoplasm Metastasis

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20303350.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United Kingdom / Chief Scientist Office / / CAF/06/24; United Kingdom / Cancer Research UK / / C157/A9148; United Kingdom / Chief Scientist Office / / ; United Kingdom / Cancer Research UK / / C2193/A7603
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
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7. Olive KP, Jacobetz MA, Davidson CJ, Gopinathan A, McIntyre D, Honess D, Madhu B, Goldgraben MA, Caldwell ME, Allard D, Frese KK, Denicola G, Feig C, Combs C, Winter SP, Ireland-Zecchini H, Reichelt S, Howat WJ, Chang A, Dhara M, Wang L, Rückert F, Grützmann R, Pilarsky C, Izeradjene K, Hingorani SR, Huang P, Davies SE, Plunkett W, Egorin M, Hruban RH, Whitebread N, McGovern K, Adams J, Iacobuzio-Donahue C, Griffiths J, Tuveson DA: Inhibition of Hedgehog signaling enhances delivery of chemotherapy in a mouse model of pancreatic cancer. Science; 2009 Jun 12;324(5933):1457-61
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  • [Title] Inhibition of Hedgehog signaling enhances delivery of chemotherapy in a mouse model of pancreatic cancer.
  • Pancreatic ductal adenocarcinoma (PDA) is among the most lethal human cancers in part because it is insensitive to many chemotherapeutic drugs.
  • Studying a mouse model of PDA that is refractory to the clinically used drug gemcitabine, we found that the tumors in this model were poorly perfused and poorly vascularized, properties that are shared with human PDA.
  • We tested whether the delivery and efficacy of gemcitabine in the mice could be improved by coadministration of IPI-926, a drug that depletes tumor-associated stromal tissue by inhibition of the Hedgehog cellular signaling pathway.
  • The combination therapy produced a transient increase in intratumoral vascular density and intratumoral concentration of gemcitabine, leading to transient stabilization of disease.
  • Thus, inefficient drug delivery may be an important contributor to chemoresistance in pancreatic cancer.

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  • (PMID = 19460966.001).
  • [ISSN] 1095-9203
  • [Journal-full-title] Science (New York, N.Y.)
  • [ISO-abbreviation] Science
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA015704; United States / NCI NIH HHS / CA / CA111292; United States / NCI NIH HHS / CA / F32 CA123887; United States / NCI NIH HHS / CA / K08 CA106610; United States / NCI NIH HHS / CA / U01 CA084291; United States / NCI NIH HHS / CA / CA114028; United States / NCI NIH HHS / CA / CA084291; United States / NCI NIH HHS / CA / CA101973; United States / NCI NIH HHS / CA / CA123939-03X1; United States / NCI NIH HHS / CA / U01 CA105490; United States / NCI NIH HHS / CA / CA15704; United States / NCI NIH HHS / CA / F32 CA123939-03X1; United States / NCI NIH HHS / CA / F32 CA123939; United States / NCI NIH HHS / CA / F32CA123939-02; United States / NCI NIH HHS / CA / F32CA123887-01; United States / NCI NIH HHS / CA / CA105490; United States / NCI NIH HHS / CA / R01 CA101973
  • [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 / Antineoplastic Agents; 0 / Gli protein, mouse; 0 / Hedgehog Proteins; 0 / IPI-926; 0 / Kruppel-Like Transcription Factors; 0 / Receptors, G-Protein-Coupled; 0 / Smo protein, mouse; 0 / Veratrum Alkaloids; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ NIHMS228663; NLM/ PMC2998180
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8. Aikawa T, Gunn J, Spong SM, Klaus SJ, Korc M: Connective tissue growth factor-specific antibody attenuates tumor growth, metastasis, and angiogenesis in an orthotopic mouse model of pancreatic cancer. Mol Cancer Ther; 2006 May;5(5):1108-16
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  • [Title] Connective tissue growth factor-specific antibody attenuates tumor growth, metastasis, and angiogenesis in an orthotopic mouse model of pancreatic cancer.
  • Connective tissue growth factor (CTGF) plays an important role in fibrosis by modulating cell migration and cell growth but may also modify tumor growth and metastasis.
  • Because CTGF is overexpressed in pancreatic ductal adenocarcinoma, we investigated the in vitro effects of CTGF on the proliferation and invasiveness of PANC-1 pancreatic cancer cells and examined the consequences of its in vivo inhibition on the growth and metastasis of these cells using a fully human CTGF-specific monoclonal antibody (FG-3019) in an orthotopic nude mouse model.
  • These findings suggest that CTGF may contribute to aberrant autocrine and paracrine pathways that promote pancreatic cancer cell growth, invasion, metastasis, and angiogenesis.
  • Therefore, blocking CTGF actions with FG-3019 may represent a novel therapeutic approach in pancreatic ductal adenocarcinoma.
  • [MeSH-major] Antibodies, Monoclonal / therapeutic use. Antineoplastic Agents / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Immediate-Early Proteins / antagonists & inhibitors. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Proliferation / drug effects. Connective Tissue Growth Factor. Disease Models, Animal. Female. Humans. Intercellular Signaling Peptides and Proteins / immunology. Intercellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Nude. Neoplasm Metastasis. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 16731742.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-75059
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antineoplastic Agents; 0 / CTGF protein, human; 0 / Ctgf protein, mouse; 0 / Immediate-Early Proteins; 0 / Intercellular Signaling Peptides and Proteins; 0 / Recombinant Proteins; 139568-91-5 / Connective Tissue Growth Factor
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9. Cook N, Olive KP, Frese K, Tuveson DA: K-Ras-driven pancreatic cancer mouse model for anticancer inhibitor analyses. Methods Enzymol; 2008;439:73-85
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  • [Title] K-Ras-driven pancreatic cancer mouse model for anticancer inhibitor analyses.
  • Genetically engineered mouse (GEM) models of cancer have progressively improved in technical sophistication and accurately recapitulating the cognate human condition and have had a measurable impact upon our knowledge of tumorigenesis.
  • However, the application of such models toward the development of innovative therapeutic and diagnostic approaches has lagged behind.
  • Our laboratory has established accurate mouse models of early and advanced ductal pancreatic cancer by conditionally expressing mutant K-ras and Trp53 alleles from their endogenous promoters in pancreatic progenitor cells.
  • These K-Ras-dependent preclinical models provide valuable information on the cell types and pathways involved in the development of pancreatic cancer.
  • Furthermore, they can be used to investigate the molecular, cellular, pharmacokinetic, and radiological characteristics of drug response to classical chemotherapeutics and to targeted agents.
  • This chapter reviews the methods used to explore issues of drug delivery, imaging, and preclinical trial design in our GEM models for pancreatic cancer.
  • We hypothesize that results of our preclinical studies will inform the design of clinical trials for pancreatic cancer patients.
  • [MeSH-major] Adenocarcinoma / drug therapy. Carcinoma, Pancreatic Ductal / drug therapy. Disease Models, Animal. Genes, ras / physiology. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor / methods. Mice

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  • (PMID = 18374157.001).
  • [ISSN] 0076-6879
  • [Journal-full-title] Methods in enzymology
  • [ISO-abbreviation] Meth. Enzymol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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10. DeRosier LC, Huang ZQ, Sellers JC, Buchsbaum DJ, Vickers SM: Treatment with gemcitabine and TRA-8 anti-death receptor-5 mAb reduces pancreatic adenocarcinoma cell viability in vitro and growth in vivo. J Gastrointest Surg; 2006 Nov;10(9):1291-300; discussion 1300
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  • [Title] Treatment with gemcitabine and TRA-8 anti-death receptor-5 mAb reduces pancreatic adenocarcinoma cell viability in vitro and growth in vivo.
  • Gemcitabine is a first line agent for pancreatic cancer, but yields minimal survival benefit.
  • This study evaluated in vitro and in vivo effects of a monoclonal antibody (TRA-8) to human death receptor 5, combined with gemcitabine, using two human pancreatic cancer cell lines, S2VP10 and MIA PaCa-2.
  • A subcutaneous model of pancreatic cancer was employed to test in vivo efficacy.
  • MIA PaCa-2 subcutaneous xenografts in athymic nude mice were evaluated for response to treatment with 200 mug of TRA-8 (intraperitoneal on days 9, 13, 16, 20, 23, and 27 postimplant) and 120 mg/kg gemcitabine (I.P. on days 10, 17, and 24).
  • MIA PaCa-2 and S2VP10 cells receiving combination treatment with TRA-8 and gemcitabine demonstrated enhanced cytotoxicity, annexin V staining, and mitochondrial destabilization compared to either agent alone.
  • Combination treatment produced enhanced caspase-3 and -8 activation in both cell lines compared with either agent alone.
  • In vivo studies demonstrated mean subcutaneous tumor surface area (produce of two largest diameters) doubling times of 38 days untreated, 32 days gemcitabine, 49 days TRA-8, and 64 days combination treatment.
  • These findings, with substantial inhibition of tumor growth in a mouse pancreatic cancer xenograft model receiving combination therapy, are encouraging for anti-death receptor therapy in the treatment of pancreatic cancer.
  • [MeSH-major] Antibodies, Monoclonal / pharmacology. Antimetabolites, Antineoplastic / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Deoxycytidine / analogs & derivatives. Pancreatic Neoplasms / drug therapy. Receptors, TNF-Related Apoptosis-Inducing Ligand / immunology
  • [MeSH-minor] Animals. Annexin A5 / metabolism. Apoptosis. Caspases / metabolism. Cell Line, Tumor. Drug Synergism. Female. Flow Cytometry. Humans. Mice. Mice, Nude. Xenograft Model Antitumor Assays

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  • [CommentIn] Gastroenterology. 2007 Jun;132(7):2607-8; discussion 2608-9 [17570234.001]
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  • (PMID = 17114015.001).
  • [ISSN] 1091-255X
  • [Journal-full-title] Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
  • [ISO-abbreviation] J. Gastrointest. Surg.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / T32 CA091078; United States / NCI NIH HHS / CA / 1 P20 CA10195-01; United States / NCI NIH HHS / CA / T32 CA91078
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Annexin A5; 0 / Antibodies, Monoclonal; 0 / Antimetabolites, Antineoplastic; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10B protein, human; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 3.4.22.- / Caspases
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11. Corvaro M, Fuoco C, Wagner M, Cecconi F: Analysis of apoptosome dysregulation in pancreatic cancer and of its role in chemoresistance. Cancer Biol Ther; 2007 Feb;6(2):209-17
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  • [Title] Analysis of apoptosome dysregulation in pancreatic cancer and of its role in chemoresistance.
  • Its importance during development has been clearly demonstrated by knocking out key genes in mouse.
  • APAF1 is the core protein of the apoptosome and its dosage is also critical in various cancer types, i.e., melanoma, germ line tumor, gastrointestinal cancer and B-type chronic lymphocytic leukemia.
  • We investigated the putative roles of the apoptosome in pancreatic ductal adenocarcinoma (PDAC).
  • The response to cell death induction and its biochemical features were assessed by treatment of each line with commonly used chemotherapeutic agents.
  • [MeSH-major] Apoptosomes / metabolism. Apoptotic Protease-Activating Factor 1 / metabolism. Carcinoma, Pancreatic Ductal / metabolism. Caspase 9 / metabolism. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Death. Cell Line, Tumor. Drug Resistance, Neoplasm / physiology. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Mice

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  • (PMID = 17224646.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] Italy / Telethon / / TCR04004
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / APAF1 protein, human; 0 / Antineoplastic Agents; 0 / Apoptosomes; 0 / Apoptotic Protease-Activating Factor 1; EC 3.4.22.- / Caspase 9
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12. Ito D, Fujimoto K, Mori T, Kami K, Koizumi M, Toyoda E, Kawaguchi Y, Doi R: In vivo antitumor effect of the mTOR inhibitor CCI-779 and gemcitabine in xenograft models of human pancreatic cancer. Int J Cancer; 2006 May 1;118(9):2337-43
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  • [Title] In vivo antitumor effect of the mTOR inhibitor CCI-779 and gemcitabine in xenograft models of human pancreatic cancer.
  • We investigated the expression of the phosphatidylinositol 3'-kinase (PI3K)/mTOR signaling pathway in human pancreatic cancer cells and tissues, and the in vivo antitumor effects of the mTOR inhibitor CCI-779 with/without gemcitabine in xenograft models of human pancreatic cancer.
  • We found that the Akt, mTOR and p70 S6 kinase (S6K1) from the PI3K/mTOR signaling pathway were activated in all of the pancreatic cancer cell lines examined.
  • When surgically resected tissue specimens of pancreatic ductal adenocarcinoma were examined, phosphorylation of Akt, mTOR and S6K1 was detected in 50, 55 and 65% of the specimens, respectively.
  • Furthermore, in the Suit-2 peritoneal dissemination xenograft model, the combination of these 2 drugs achieved significantly better survival when compared with CCI-779 or gemcitabine alone.
  • These results demonstrate promising activity of the mTOR inhibitor CCI-779 against human pancreatic cancer, and suggest that the inhibition of mTOR signaling can be exploited as a potentially tumor-selective therapeutic strategy.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antimetabolites, Antineoplastic / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Deoxycytidine / analogs & derivatives. Pancreatic Neoplasms / drug therapy. Sirolimus / analogs & derivatives

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  • [Copyright] 2005 Wiley-Liss, Inc.
  • (PMID = 16331623.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; 624KN6GM2T / temsirolimus; B76N6SBZ8R / gemcitabine; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; W36ZG6FT64 / Sirolimus
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13. Showalter SL, Huang YH, Witkiewicz A, Costantino CL, Yeo CJ, Green JJ, Langer R, Anderson DG, Sawicki JA, Brody JR: Nanoparticulate delivery of diphtheria toxin DNA effectively kills Mesothelin expressing pancreatic cancer cells. Cancer Biol Ther; 2008 Oct;7(10):1584-90
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  • [Title] Nanoparticulate delivery of diphtheria toxin DNA effectively kills Mesothelin expressing pancreatic cancer cells.
  • Pancreatic cancer is the fourth leading cause of cancer-related deaths in this country, and there is currently no effective targeted treatment for this deadly disease.
  • A dire need exists to rapidly translate our molecular understanding of this devastating disease into effective, novel therapeutic options.
  • Mesothelin is a candidate target protein shown by a number of laboratories to be specifically overexpressed in pancreatic cancers and not in the adjacent normal tissue.
  • Translational investigations have shown promising results using this molecule as a therapeutic target (e.g., vaccine strategies).
  • Using a novel, proven, biodegradable nanoparticulate system, we sought to target mesothelin-expressing pancreatic cancer cells with a potent suicide gene, diphtheria toxin-A (DT-A).
  • We first confirmed reports that a majority of pancreatic cancer cell lines and resected pancreatic ductal adenocarcinoma specimens overexpressed mesothelin at the mRNA and protein levels.
  • High mesothelin-expressing pancreatic cancer cell lines produced more luciferase than cell lines with undetectable mesothelin expression when transfected with a luciferase sequence under the regulation of the mesothelin promoter.
  • We achieved dramatic inhibition of protein translation (>95%) in mesothelin-expressing pancreatic cancer cell lines when DT-A DNA, driven by the mesothelin promoter, was delivered to pancreatic cancer cells.
  • We show that this inhibition effectively targets the death of pancreatic cancer cells that overexpress mesothelin.
  • The work presented here provides evidence that this strategy will work in pre-clinical mouse pancreatic cancer models, and suggests that such a strategy will work in the clinical setting against the majority of pancreatic tumors, most of which overexpress mesothelin.

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  • (PMID = 19039293.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] ENG
  • [Grant] United States / NIBIB NIH HHS / EB / R01 EB000244; United States / NCI NIH HHS / CA / R01 CA132091; United States / NCI NIH HHS / CA / R01 CA132091-01; United States / NIBIB NIH HHS / EB / R37 EB000244; United States / NCI NIH HHS / CA / CA132091-01; United States / NIBIB NIH HHS / EB / EB00244
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Diphtheria Toxin; 0 / GPI-Linked Proteins; 0 / Membrane Glycoproteins; 0 / RNA, Messenger; 0 / mesothelin
  • [Other-IDs] NLM/ NIHMS334791; NLM/ PMC3218426
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14. Egberts JH, Schniewind B, Pätzold M, Kettler B, Tepel J, Kalthoff H, Trauzold A: Dexamethasone reduces tumor recurrence and metastasis after pancreatic tumor resection in SCID mice. Cancer Biol Ther; 2008 Jul;7(7):1044-50
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  • [Title] Dexamethasone reduces tumor recurrence and metastasis after pancreatic tumor resection in SCID mice.
  • Inflammation accompanies most solid cancers including pancreatic ductal adenocarcinoma (PDAC), one of the most fatal cancers with surgery being the only potential curative therapeutic.
  • In the present work we investigated the influence of glucocorticoids on PDAC cells in vitro as well as in vivo in a pancreatic carcinoma resection mouse model.
  • METHODS: The influence of dexamethasone (DEX), a synthetic glucocorticoid, on proliferation and IL8 secretion in pancreatic cells (BxPC3, Colo357, PancTuI) was analyzed by cell counting and ELISA.
  • In the mouse resection model subtotal pancreatectomy was performed after orthotopic inoculation of human PDAC cells.
  • DEX was administered after resection as an adjuvant treatment regime and 4 weeks later, local recurrent tumor sizes as well as number of liver and spleen metastases were analyzed.
  • Therefore, DEX-treatment appears to be an interesting therapeutical option in an adjuvant setting after pancreatic cancer resection.
  • [MeSH-major] Dexamethasone / pharmacology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / surgery
  • [MeSH-minor] Animals. Antineoplastic Agents, Hormonal / pharmacology. Cell Line, Tumor. Cell Proliferation. Female. Humans. Mice. Mice, SCID. Neoplasm Metastasis. Neoplasm Transplantation. Recurrence. Signal Transduction. Treatment Outcome

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  • [CommentIn] Cancer Biol Ther. 2008 Jul;7(7):1051-2 [18698168.001]
  • (PMID = 18431088.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Hormonal; 7S5I7G3JQL / Dexamethasone
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15. Vogler M, Walczak H, Stadel D, Haas TL, Genze F, Jovanovic M, Bhanot U, Hasel C, Möller P, Gschwend JE, Simmet T, Debatin KM, Fulda S: Small molecule XIAP inhibitors enhance TRAIL-induced apoptosis and antitumor activity in preclinical models of pancreatic carcinoma. Cancer Res; 2009 Mar 15;69(6):2425-34
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  • [Title] Small molecule XIAP inhibitors enhance TRAIL-induced apoptosis and antitumor activity in preclinical models of pancreatic carcinoma.
  • Evasion of apoptosis is a characteristic feature of pancreatic cancer, a prototypic cancer that is refractory to current treatment approaches.
  • To explore X-linked inhibitor of apoptosis (XIAP) as a therapeutic target in pancreatic cancer, we analyzed the expression of XIAP in pancreatic tumor samples and evaluated the effect of small molecule XIAP inhibitors alone and in combination with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) against pancreatic carcinoma in vitro and in vivo.
  • Here, we report that XIAP is highly expressed in pancreatic adenocarcinoma samples compared with normal pancreatic ducts.
  • Small molecule XIAP inhibitors synergize with TRAIL to induce apoptosis and to inhibit long-term clonogenic survival of pancreatic carcinoma cells.
  • In contrast, they do not reverse the lack of toxicity of TRAIL on nonmalignant cells in vitro or normal tissues in vivo, pointing to a therapeutic index.
  • Most importantly, XIAP inhibitors cooperate with TRAIL to trigger apoptosis and suppress pancreatic carcinoma growth in vivo in two preclinical models, i.e., the chorioallantoic membrane model and a mouse xenograft model.
  • Parallel immunohistochemical analysis of tumor tissue under therapy reveals that the XIAP inhibitor acts in concert with TRAIL to cause caspase-3 activation and apoptosis.
  • In conclusion, our findings provide, for the first time, evidence in vivo that XIAP inhibitors prime pancreatic carcinoma cells for TRAIL-induced apoptosis and potentiate the antitumor activity of TRAIL against established pancreatic carcinoma.
  • These findings build the rationale for further (pre)clinical development of XIAP inhibitors and TRAIL against pancreatic cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Apoptosis / drug effects. Carcinoma, Pancreatic Ductal / drug therapy. Pancreatic Neoplasms / drug therapy. TNF-Related Apoptosis-Inducing Ligand / pharmacology. X-Linked Inhibitor of Apoptosis Protein / antagonists & inhibitors
  • [MeSH-minor] Animals. Caspase 3 / metabolism. Drug Synergism. Enzyme Activation. Female. HCT116 Cells. Humans. Mice. Mice, Nude. Mitochondria / drug effects. Mitochondria / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 19258513.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / X-Linked Inhibitor of Apoptosis Protein; 0 / XIAP protein, human; EC 3.4.22.- / Caspase 3
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16. Harikumar KB, Kunnumakkara AB, Sethi G, Diagaradjane P, Anand P, Pandey MK, Gelovani J, Krishnan S, Guha S, Aggarwal BB: Resveratrol, a multitargeted agent, can enhance antitumor activity of gemcitabine in vitro and in orthotopic mouse model of human pancreatic cancer. Int J Cancer; 2010 Jul 15;127(2):257-68
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Resveratrol, a multitargeted agent, can enhance antitumor activity of gemcitabine in vitro and in orthotopic mouse model of human pancreatic cancer.
  • Gemcitabine, while a standard treatment of advanced pancreatic cancer (PaCa), alone is not very effective.
  • Both the markers of proliferation index Ki-67 and the micro vessel density CD31 were significantly downregulated in tumor tissue by the combination of gemcitabine and resveratrol (p < 0.001 vs. control; p < 0.01 vs. gemcitabine).

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  • (PMID = 19908231.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL004137-06; United States / NHLBI NIH HHS / HL / K30 HL004137-06
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / Stilbenes; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; Q369O8926L / resveratrol
  • [Other-IDs] NLM/ NIHMS279630; NLM/ PMC3090706
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17. Singh M, Lima A, Molina R, Hamilton P, Clermont AC, Devasthali V, Thompson JD, Cheng JH, Bou Reslan H, Ho CC, Cao TC, Lee CV, Nannini MA, Fuh G, Carano RA, Koeppen H, Yu RX, Forrest WF, Plowman GD, Johnson L: Assessing therapeutic responses in Kras mutant cancers using genetically engineered mouse models. Nat Biotechnol; 2010 Jun;28(6):585-93
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Assessing therapeutic responses in Kras mutant cancers using genetically engineered mouse models.
  • The low rate of approval of novel anti-cancer agents underscores the need for better preclinical models of therapeutic response as neither xenografts nor early-generation genetically engineered mouse models (GEMMs) reliably predict human clinical outcomes.
  • Whereas recent, sporadic GEMMs emulate many aspects of their human disease counterpart more closely, their ability to predict clinical therapeutic responses has never been tested systematically.
  • We evaluated the utility of two state-of-the-art, mutant Kras-driven GEMMs--one of non-small-cell lung carcinoma and another of pancreatic adenocarcinoma--by assessing responses to existing standard-of-care chemotherapeutics, and subsequently in combination with EGFR and VEGF inhibitors.
  • Comparisons with corresponding clinical trials indicate that these GEMMs model human responses well, and lay the foundation for the use of validated GEMMs in predicting outcome and interrogating mechanisms of therapeutic response and resistance.
  • [MeSH-major] Disease Models, Animal. Genetic Engineering. Mutation / genetics. Neoplasms / genetics. Neoplasms / therapy. Proto-Oncogene Proteins p21(ras) / genetics
  • [MeSH-minor] Animals. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Carcinoma, Non-Small-Cell Lung / pathology. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / pathology. Deoxycytidine / analogs & derivatives. Deoxycytidine / therapeutic use. Erlotinib Hydrochloride. Humans. Lung Neoplasms / drug therapy. Lung Neoplasms / pathology. Mice. Quinazolines / therapeutic use. Survival Analysis. Vascular Endothelial Growth Factor A / immunology


18. Olive KP, Tuveson DA: The use of targeted mouse models for preclinical testing of novel cancer therapeutics. Clin Cancer Res; 2006 Sep 15;12(18):5277-87
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of targeted mouse models for preclinical testing of novel cancer therapeutics.
  • Despite the generally disappointing findings using tumor xenografts and certain early transgenic cancer models to predict therapeutic efficacy in patients, the dramatic progress of mouse models in recent years engenders optimism that the newest generation of mouse models will provide a higher standard of predictive utility in the process of drug development.
  • [MeSH-major] Disease Models, Animal. Drug Evaluation, Preclinical / methods. Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Animals. Antineoplastic Agents / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / radiography. Carcinoma, Pancreatic Ductal / radionuclide imaging. Carcinoma, Pancreatic Ductal / ultrasonography. Drug Design. Humans. Mice. Mice, Transgenic. Models, Biological

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  • (PMID = 17000660.001).
  • [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 / CA084291; United States / NCI NIH HHS / CA / CA101973; United States / NCI NIH HHS / CA / CA105490; United States / NCI NIH HHS / CA / CA111292
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Number-of-references] 47
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19. Michl P, Buchholz M, Rolke M, Kunsch S, Löhr M, McClane B, Tsukita S, Leder G, Adler G, Gress TM: Claudin-4: a new target for pancreatic cancer treatment using Clostridium perfringens enterotoxin. Gastroenterology; 2001 Sep;121(3):678-84
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Claudin-4: a new target for pancreatic cancer treatment using Clostridium perfringens enterotoxin.
  • Using expression profiling, we previously found claudin-4 to be overexpressed in pancreatic cancer.
  • Because claudin-4 has been described as a receptor for the cytotoxic Clostridium perfringens enterotoxin (CPE), we investigated the effect of CPE on pancreatic cancer cells.
  • The in vivo effect of CPE was studied in claudin-4-expressing nude mouse xenografts of the Panc-1 cell line.
  • RESULTS: Expression analyses showed that claudin-4 was overexpressed in most pancreatic cancer tissues and cell lines and several other gastrointestinal tumors.
  • CONCLUSIONS: Our findings suggest that targeting claudin-4-expressing tumors with CPE represents a promising new treatment modality for pancreatic cancer and other solid tumors.
  • [MeSH-major] Adenocarcinoma / drug therapy. Carcinoma, Pancreatic Ductal / drug therapy. Enterotoxins / pharmacology. Membrane Proteins / genetics. Pancreatic Neoplasms / drug therapy
  • [MeSH-minor] Animals. Claudin-4. Dose-Response Relationship, Drug. Gene Expression Regulation, Neoplastic. Humans. In Vitro Techniques. Mice. Mice, Nude. Neoplasm Transplantation. RNA, Messenger / analysis. Tight Junctions / physiology. Transforming Growth Factor beta / pharmacology. Transplantation, Heterologous. Tumor Cells, Cultured

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  • (PMID = 11522752.001).
  • [ISSN] 0016-5085
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United States / NIAID NIH HHS / AI / AI19844-17
  • [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 / CLDN4 protein, human; 0 / Claudin-4; 0 / Cldn4 protein, mouse; 0 / Enterotoxins; 0 / Membrane Proteins; 0 / RNA, Messenger; 0 / Transforming Growth Factor beta; 0 / enterotoxin, Clostridium
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20. Luo J, Guo P, Matsuda K, Truong N, Lee A, Chun C, Cheng SY, Korc M: Pancreatic cancer cell-derived vascular endothelial growth factor is biologically active in vitro and enhances tumorigenicity in vivo. Int J Cancer; 2001 May 1;92(3):361-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Pancreatic cancer cell-derived vascular endothelial growth factor is biologically active in vitro and enhances tumorigenicity in vivo.
  • Although both VEGF and its receptors are overexpressed in human pancreatic ductal adenocarcinoma (PDAC), this malignancy is not generally considered to be highly vascular.
  • To address this issue, we measured the angiogenic effects of pancreatic cancer cell-derived VEGF in an in vitro endothelial cell proliferation assay and characterized the consequences of suppressing VEGF expression on pancreatic tumor growth in an athymic nude mouse model.
  • We found that human pancreatic cancer cell lines secrete large quantities of biologically active VEGF into conditioned medium (CM).
  • Stable transfection of an anti-sense VEGF(189) (AS-VEGF(189)) expression construct into PANC-1 pancreatic cancer cells resulted in decreased VEGF expression and secretion, a decreased capacity of the resultant CM to enhance endothelial cell proliferation and a significant attenuation of tumor cell proliferation in vitro.
  • These results support the hypothesis that VEGF promotes pancreatic cancer growth in vivo and suggest that anti-VEGF therapy may be useful in the treatment of this disease.
  • [MeSH-major] Endothelial Growth Factors / antagonists & inhibitors. Endothelium, Vascular / drug effects. Lymphokines / antagonists & inhibitors. Oligonucleotides, Antisense / pharmacology. Pancreatic Neoplasms / metabolism
  • [MeSH-minor] Animals. Carcinogenicity Tests. Cell Division / drug effects. Disease Models, Animal. Gene Expression / drug effects. Genetic Vectors. Humans. Mice. Mice, Nude. RNA / biosynthesis. RNA / drug effects. Time Factors. Transfection. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors. Xenograft Model Antitumor Assays

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  • [Copyright] Copyright 2001 Wiley-Liss, Inc.
  • (PMID = 11291072.001).
  • [ISSN] 0020-7136
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-40162
  • [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 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Oligonucleotides, Antisense; 0 / VEGFA protein, human; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 63231-63-0 / RNA
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21. Hausner SH, Abbey CK, Bold RJ, Gagnon MK, Marik J, Marshall JF, Stanecki CE, Sutcliffe JL: Targeted in vivo imaging of integrin alphavbeta6 with an improved radiotracer and its relevance in a pancreatic tumor model. Cancer Res; 2009 Jul 15;69(14):5843-50
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted in vivo imaging of integrin alphavbeta6 with an improved radiotracer and its relevance in a pancreatic tumor model.
  • The cell surface receptor alpha(v)beta(6) is epithelial specific, and its expression is tightly regulated; it is low or undetectable in adult tissues but has been shown to be increased in many different cancers, including pancreatic, cervical, lung, and colon cancers.
  • We have recently shown the feasibility of imaging alpha(v)beta(6) in vivo by positron emission tomography (PET) using the peptide [(18)F]FBA-A20FMDV2.
  • Here, we describe improved alpha(v)beta(6) imaging agents and test their efficacy in a mouse model with endogenous alpha(v)beta(6) expression.
  • In vivo studies using either a melanoma cell line (transduced alpha(v)beta(6) expression) or the BxPC-3 human pancreatic carcinoma cell line (endogenous alpha(v)beta(6) expression) revealed that the modified compounds showed significantly improved tumor retention.
  • Pancreatic ductal adenocarcinoma is highly metastatic and current preoperative evaluation of resectability using noninvasive imaging has limited success, with most patients having metastases at time of surgery.
  • The fact that these tumors express alpha(v)beta(6) suggests that this probe has significant potential for the in vivo detection of this malignancy, thus having important implications for patient care and therapy.

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  • (PMID = 19549907.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA107792-02; United States / NCI NIH HHS / CA / R21 CA107792; United States / NCI NIH HHS / CA / R21 CA107792-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Benzoates; 0 / Fluorine Radioisotopes; 0 / Integrins; 0 / Radiopharmaceuticals; 0 / Viral Proteins; 0 / integrin alphavbeta6; V5ROO2HOU4 / 4-fluorobenzoic acid
  • [Other-IDs] NLM/ NIHMS117292; NLM/ PMC2711989
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22. Liang J, Moore RE, Moher ED, Munroe JE, Al-awar RS, Hay DA, Varie DL, Zhang TY, Aikins JA, Martinelli MJ, Shih C, Ray JE, Gibson LL, Vasudevan V, Polin L, White K, Kushner J, Simpson C, Pugh S, Corbett TH: Cryptophycins-309, 249 and other cryptophycin analogs: preclinical efficacy studies with mouse and human tumors. Invest New Drugs; 2005 Jun;23(3):213-24
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cryptophycins-309, 249 and other cryptophycin analogs: preclinical efficacy studies with mouse and human tumors.
  • With no method to adequately stabilize the chlorohydrins at the time, Cryptophycin-52 (LY 355073) entered clinical trials, producing only marginal antitumor activity.
  • Since that time, glycinate esters of the hydroxyl group of the chlorohydrins have been synthesized and found to provide stability.
  • The following %T/C and Log Kill (LK) values were obtained from a single course of IV treatment (Q2d x 5) against early staged SC transplantable tumors of mouse and human origin: Mam 17/Adr [a pgp (+) MDR tumor]: 0%T/C, 3.2 LK; Mam 16/C/Adr [a pgp (-) MDR tumor]: 0%T/C, 3.3 LK; Mam 16/C: 0%T/C, 3.8 LK; Colon 26: 0%T/C, 2.2 LK; Colon 51: 0%T/C, 2.4 LK; Pancreatic Ductal Adenocarcinoma 02 (Panc 02): 0%T/C, 2.4 LK; Human Colon HCT15 [a pgp (+) MDR tumor]: 0%T/C, 3.3 LK; Human Colon HCT116: 0%T/C, 4.1 LK.
  • However, there was sufficient material for only a single C-249 trial in which a 4.0 LK was obtained against the multidrug resistant breast adenocarcinoma Mam-16/C/Adr.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Depsipeptides / pharmacology. Epoxy Compounds / pharmacology. Neoplasms, Experimental / drug therapy. Peptides, Cyclic / pharmacology
  • [MeSH-minor] Animals. Drug Screening Assays, Antitumor. Esters. Humans. Mice. Mice, Inbred BALB C. Mice, Inbred ICR. Mice, SCID. Neoplasm Transplantation. Structure-Activity Relationship

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  • (PMID = 15868377.001).
  • [ISSN] 0167-6997
  • [Journal-full-title] Investigational new drugs
  • [ISO-abbreviation] Invest New Drugs
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA12623; United States / NCI NIH HHS / CA / CA53001
  • [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 / Antineoplastic Agents; 0 / Depsipeptides; 0 / Epoxy Compounds; 0 / Esters; 0 / Peptides, Cyclic; 0 / cryptophycin 249; 0 / cryptophycin 309; 124689-65-2 / cryptophycin
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23. Rhim AD: A combined, rational approach towards inhibition of the MEK-ERK and mTOR pathways in pancreatic ductal adenocarcinoma: promise or deja vu? Cancer Biol Ther; 2009 Oct;8(20):1902-3
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A combined, rational approach towards inhibition of the MEK-ERK and mTOR pathways in pancreatic ductal adenocarcinoma: promise or deja vu?
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Pancreatic Ductal / drug therapy. Pancreatic Neoplasms / drug therapy. Signal Transduction / drug effects. Xenograft Model Antitumor Assays
  • [MeSH-minor] Animals. Apoptosis / drug effects. Benzimidazoles / administration & dosage. Benzimidazoles / pharmacology. Cell Line, Tumor. Cell Proliferation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Intracellular Signaling Peptides and Proteins / metabolism. Mice. Mice, Inbred NOD. Mice, SCID. Mitogen-Activated Protein Kinase Kinases / antagonists & inhibitors. Mitogen-Activated Protein Kinase Kinases / metabolism. Models, Biological. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Protein-Serine-Threonine Kinases / metabolism. Ribosomal Protein S6 / antagonists & inhibitors. Ribosomal Protein S6 / metabolism. Ribosomal Protein S6 Kinases / metabolism. Sirolimus / administration & dosage. Sirolimus / pharmacology. TOR Serine-Threonine Kinases

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  • (PMID = 19783905.001).
  • [ISSN] 1555-8576
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / K08 DK088945; United States / NCI NIH HHS / CA / L30 CA136450
  • [Publication-type] Comment; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AZD 6244; 0 / Benzimidazoles; 0 / Intracellular Signaling Peptides and Proteins; 0 / Ribosomal Protein S6; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Ribosomal Protein S6 Kinases; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.12.2 / Mitogen-Activated Protein Kinase Kinases; W36ZG6FT64 / Sirolimus
  • [Other-IDs] NLM/ NIHMS373407; NLM/ PMC3720128
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24. Van Dyke T: Finding the tumor copycat: approximating a human cancer. Nat Med; 2010 Sep;16(9):976-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [MeSH-minor] Adenocarcinoma / mortality. Adenocarcinoma / pathology. Animals. Antineoplastic Agents / administration & dosage. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / mortality. Carcinoma, Pancreatic Ductal / pathology. Cell Division. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacokinetics. Deoxycytidine / therapeutic use. Disease Models, Animal. Mice

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  • [ISSN] 1546-170X
  • [Journal-full-title] Nature medicine
  • [ISO-abbreviation] Nat. Med.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 CA999999
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
  • [Other-IDs] NLM/ NIHMS424156; NLM/ PMC3533444
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