[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 16 of about 16
1. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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


2. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • Genetic Alliance. consumer health - Diphtheria.
  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Am J Pathol. 2004 Mar;164(3):903-14 [14982844.001]
  • [Cites] Cancer Biol Ther. 2008 Jul;7(7):986-94 [18443433.001]
  • [Cites] Am J Pathol. 2004 Aug;165(2):651-7 [15277238.001]
  • [Cites] J Exp Med. 2004 Aug 2;200(3):297-306 [15289501.001]
  • [Cites] Bacteriol Rev. 1975 Mar;39(1):54-85 [164179.001]
  • [Cites] Cancer Res. 1986 Sep;46(9):4660-4 [3460697.001]
  • [Cites] Int J Cancer. 1994 Apr 1;57(1):90-7 [8150545.001]
  • [Cites] Nature. 1996 Jul 4;382(6586):88-90 [8657311.001]
  • [Cites] Trends Biochem Sci. 1997 Mar;22(3):77-80 [9066256.001]
  • [Cites] J Am Coll Surg. 1999 Jul;189(1):1-7 [10401733.001]
  • [Cites] Proc Natl Acad Sci U S A. 1999 Sep 28;96(20):11531-6 [10500211.001]
  • [Cites] Biotechniques. 2004 Oct;37(4):598, 600, 602 [15517972.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Nov 9;101(45):16028-33 [15520369.001]
  • [Cites] Gene Ther. 2005 Jan;12(2):187-93 [15526007.001]
  • [Cites] Pancreas. 2005 May;30(4):349-54 [15841046.001]
  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
  • [Cites] Clin Cancer Res. 2005 Aug 15;11(16):5840-6 [16115924.001]
  • [Cites] Gene Ther. 2005 Nov;12(21):1573-80 [16034457.001]
  • [Cites] Am J Clin Pathol. 2005 Dec;124(6):838-45 [16416732.001]
  • [Cites] Gastroenterology. 2006 Jun;130(7):2145-54 [16762635.001]
  • [Cites] Cancer Res. 2006 Oct 1;66(19):9369-73 [17018589.001]
  • [Cites] Prostate. 2007 Jun 1;67(8):855-62 [17427200.001]
  • [Cites] Mol Ther. 2007 Jul;15(7):1306-12 [17375071.001]
  • [Cites] Ann Surg. 2007 Aug;246(2):173-80 [17667493.001]
  • [Cites] Eur J Surg Oncol. 2007 Sep;33(7):817-23 [17331695.001]
  • [Cites] J Immunother. 2000 Jul-Aug;23(4):473-9 [10916757.001]
  • [Cites] Cancer Res. 2001 Jun 1;61(11):4320-4 [11389052.001]
  • [Cites] Cancer J. 2001 Jul-Aug;7(4):251-8 [11561601.001]
  • [Cites] Clin Cancer Res. 2001 Dec;7(12):3862-8 [11751476.001]
  • [Cites] Cancer Res. 2002 Feb 1;62(3):819-26 [11830538.001]
  • [Cites] Oncogene. 2002 May 2;21(19):2961-70 [12082526.001]
  • [Cites] Mol Ther. 2002 Oct;6(4):537-45 [12377196.001]
  • [Cites] Cell Cycle. 2003 May-Jun;2(3):181-4 [12734418.001]
  • [Cites] EMBO J. 2003 May 15;22(10):2422-32 [12743036.001]
  • [Cites] Cancer Res. 2003 Jul 15;63(14):4158-66 [12874021.001]
  • [Cites] Mod Pathol. 2003 Sep;16(9):902-12 [13679454.001]
  • [Cites] Cancer Res. 2003 Dec 15;63(24):8614-22 [14695172.001]
  • [Cites] Clin Cancer Res. 2007 Sep 1;13(17):5144-9 [17785569.001]
  • [Cites] Cancer Res. 2007 Oct 1;67(19):9055-65 [17909009.001]
  • [Cites] Mod Pathol. 2007 Dec;20(12):1238-44 [17906614.001]
  • [Cites] Mol Cancer Ther. 2008 Feb;7(2):286-96 [18281514.001]
  • [Cites] BMC Cancer. 2008;8:43 [18254976.001]
  • [Cites] Mol Cell Biol. 2004 Apr;24(7):2986-97 [15024086.001]
  • (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
  •  go-up   go-down


3. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


Advertisement
4. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


5. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


6. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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.

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Nucl Med. 2005 Aug;46(8):1333-41 [16085591.001]
  • [Cites] Ann Surg. 2005 Aug;242(2):235-43 [16041214.001]
  • [Cites] J Oral Pathol Med. 2006 Jan;35(1):1-10 [16393247.001]
  • [Cites] Mol Pharm. 2006 Sep-Oct;3(5):472-87 [17009846.001]
  • [Cites] J Nucl Med. 2007 Jan;48 Suppl 1:4S-18S [17204716.001]
  • [Cites] J Nucl Med. 2007 Jan;48 Suppl 1:78S-88S [17204723.001]
  • [Cites] Radiology. 2007 Feb;242(2):360-85 [17255408.001]
  • [Cites] Cancer Res. 2007 Feb 1;67(3):1030-7 [17283135.001]
  • [Cites] J Pathol. 2007 Jul;212(3):316-24 [17503414.001]
  • [Cites] Cancer Res. 2007 Jun 15;67(12):5889-95 [17575158.001]
  • [Cites] Cancer Res. 2007 Aug 15;67(16):7833-40 [17699789.001]
  • [Cites] Cancer Invest. 2007 Oct;25(7):632-46 [18027153.001]
  • [Cites] Cancer Res. 2008 Jan 15;68(2):561-70 [18199553.001]
  • [Cites] Clin Oncol (R Coll Radiol). 2008 Feb;20(1):61-6 [17981018.001]
  • [Cites] Am J Pathol. 2008 May;172(5):1271-86 [18385522.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2008;15(4):429-35 [18670846.001]
  • [Cites] Clin Cancer Res. 2008 Oct 15;14(20):6351-3 [18927272.001]
  • [Cites] J Nucl Med. 2000 Mar;41(3):429-38 [10716315.001]
  • [Cites] Int J Cancer. 2001 Jun 1;92(5):641-50 [11340566.001]
  • [Cites] Adv Drug Deliv Rev. 2003 Feb 10;55(2):217-50 [12564978.001]
  • [Cites] Nat Rev Drug Discov. 2003 Mar;2(3):214-21 [12612647.001]
  • [Cites] Nat Rev Drug Discov. 2003 May;2(5):347-60 [12750738.001]
  • [Cites] Semin Nucl Med. 2004 Jan;34(1):56-69 [14735459.001]
  • [Cites] Histopathology. 2004 Sep;45(3):226-36 [15330800.001]
  • [Cites] J Biol Chem. 1990 Jul 15;265(20):11502-7 [2365683.001]
  • [Cites] Radiology. 1993 Dec;189(3):847-50 [8234714.001]
  • [Cites] J Histochem Cytochem. 1993 Oct;41(10):1521-7 [8245410.001]
  • [Cites] J Cell Sci. 1995 Jun;108 ( Pt 6):2241-51 [7673344.001]
  • [Cites] AJR Am J Roentgenol. 1998 Dec;171(6):1565-70 [9843289.001]
  • [Cites] Ann Surg. 1999 May;229(5):729-37; discussion 737-8 [10235532.001]
  • [Cites] J Clin Invest. 2005 Feb;115(2):339-47 [15668738.001]
  • [Cites] J Hepatobiliary Pancreat Surg. 2004;11(1):4-10 [15747028.001]
  • [Cites] Cancer Metastasis Rev. 2005 Sep;24(3):395-402 [16258727.001]
  • (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
  •  go-up   go-down


7. Van Dyke T: Finding the tumor copycat: approximating a human cancer. Nat Med; 2010 Sep;16(9):976-7
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Drugs. 2006;66(8):1059-72 [16789792.001]
  • [Cites] Drug Discov Today. 2008 Jan;13(1-2):30-7 [18190861.001]
  • [Cites] Science. 2009 Jun 12;324(5933):1457-61 [19460966.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):5995-6004 [18829478.001]
  • [Cites] Genes Dev. 2009 Jan 1;23(1):24-36 [19136624.001]
  • [Cites] Proc Natl Acad Sci U S A. 2009 Mar 17;106(11):4254-9 [19246386.001]
  • [Cites] Nature. 2008 Sep 18;455(7211):406-10 [18754008.001]
  • (PMID = 20823881.001).
  • [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
  •  go-up   go-down


8. Müerköster SS, Werbing V, Koch D, Sipos B, Ammerpohl O, Kalthoff H, Tsao MS, Fölsch UR, Schäfer H: Role of myofibroblasts in innate chemoresistance of pancreatic carcinoma--epigenetic downregulation of caspases. Int J Cancer; 2008 Oct 15;123(8):1751-60
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of myofibroblasts in innate chemoresistance of pancreatic carcinoma--epigenetic downregulation of caspases.
  • We recently reported on continuous tumor-stroma interactions essentially contributing to chemoresistance of pancreatic ductal adenocarcinoma (PDAC) cells.
  • As demonstrated here, long-term coculture with pancreatic myofibroblasts representing the main stromal compartment of PDAC resulted in a chemoresistant phenotype in the pancreatic ductal epithelial cell line H6c7 as well as in the chemosensitive PDAC cell line T3M4.
  • In SCID mice, tumors arising from coinoculated T3M4 cells and myofibroblasts (co-tumors) responded less towards chemotherapy than mono-tumors, exhibiting decreased apoptosis, no remission and reduced expression of caspases and STAT1.
  • [MeSH-major] Caspases / biosynthesis. Fibroblasts / pathology. Pancreatic Neoplasms / drug therapy. Pancreatic Neoplasms / genetics
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / genetics. Azacitidine / analogs & derivatives. Azacitidine / pharmacology. Carcinoma, Pancreatic Ductal / drug therapy. Carcinoma, Pancreatic Ductal / enzymology. Carcinoma, Pancreatic Ductal / genetics. Carcinoma, Pancreatic Ductal / pathology. Cell Line, Tumor. Cell Nucleus / enzymology. Coculture Techniques. DNA (Cytosine-5-)-Methyltransferase / biosynthesis. DNA (Cytosine-5-)-Methyltransferase / metabolism. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Down-Regulation. Drug Resistance, Neoplasm. Epigenesis, Genetic. Etoposide / pharmacology. Female. Humans. Mice. Mice, SCID. STAT1 Transcription Factor / biosynthesis. STAT1 Transcription Factor / genetics. Transfection

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. AZACITIDINE .
  • Hazardous Substances Data Bank. ETOPOSIDE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18649362.001).
  • [ISSN] 1097-0215
  • [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 / STAT1 Transcription Factor; 0W860991D6 / Deoxycytidine; 6PLQ3CP4P3 / Etoposide; 776B62CQ27 / decitabine; B76N6SBZ8R / gemcitabine; EC 2.1.1.37 / DNA (Cytosine-5-)-Methyltransferase; EC 2.1.1.37 / DNA (cytosine-5-)-methyltransferase 1; EC 3.4.22.- / Caspases; M801H13NRU / Azacitidine
  •  go-up   go-down


9. 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
PDF icon [Fulltext service] Get downloadable fulltext PDFs of articles closely matching to this article, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [CommentIn] Gastroenterology. 2007 Jun;132(7):2607-8; discussion 2608-9 [17570234.001]
  • [Cites] Nat Med. 2001 Apr;7(4):383-5 [11283636.001]
  • [Cites] Science. 1997 Apr 4;276(5309):111-3 [9082980.001]
  • [Cites] J Clin Oncol. 2004 Sep 15;22(18):3776-83 [15365074.001]
  • [Cites] Int J Oncol. 1999 Oct;15(4):793-802 [10493964.001]
  • [Cites] Science. 1997 Aug 8;277(5327):818-21 [9242611.001]
  • [Cites] J Clin Oncol. 2002 Aug 1;20(15):3270-5 [12149301.001]
  • [Cites] Surgery. 2005 Jul;138(1):71-7 [16003319.001]
  • [Cites] J Immunol Methods. 1993 Mar 15;160(1):81-8 [7680699.001]
  • [Cites] J Biolumin Chemilumin. 1995 Jan-Feb;10 (1):29-34 [7762413.001]
  • [Cites] Br J Cancer. 2005 Apr 25;92(8):1430-41 [15846298.001]
  • [Cites] J Biol Chem. 2005 Dec 23;280(51):41940-52 [16234248.001]
  • [Cites] Biochem Biophys Res Commun. 1993 Nov 30;197(1):40-5 [8250945.001]
  • [Cites] J Biol Chem. 1996 May 31;271(22):12687-90 [8663110.001]
  • [Cites] J Transl Med. 2005 May 19;3(1):22 [15943879.001]
  • [Cites] Cancer Gene Ther. 2005 Feb;12 (2):109-15 [15486557.001]
  • [Cites] Cytokine Growth Factor Rev. 2003 Jun-Aug;14(3-4):337-48 [12787570.001]
  • [Cites] Gynecol Oncol. 2006 Apr;101(1):46-54 [16271751.001]
  • [Cites] Cancer Gene Ther. 2006 Feb;13(2):203-14 [16082379.001]
  • [Cites] Ann Oncol. 2003 Mar;14 (3):388-94 [12598343.001]
  • [Cites] J Biol Chem. 1998 Jun 5;273(23 ):14363-7 [9603945.001]
  • [Cites] Cancer Lett. 2001 Feb 10;163(1):71-81 [11163110.001]
  • [Cites] Proc Natl Acad Sci U S A. 1991 May 1;88(9):3671-5 [2023917.001]
  • [Cites] J Biol Chem. 1997 Sep 26;272(39):24198-202 [9305871.001]
  • [Cites] Ann Oncol. 2004 Feb;15(2):224-9 [14760113.001]
  • [Cites] Nat Med. 2001 Aug;7(8):954-60 [11479629.001]
  • [Cites] Curr Biol. 1997 Dec 1;7(12):1003-6 [9382840.001]
  • [Cites] J Clin Oncol. 2005 Nov 1;23(31):8033-40 [16258101.001]
  • [Cites] Br J Cancer. 2005 Jul 25;93(2):185-9 [15986036.001]
  • [Cites] J Clin Oncol. 2005 Dec 20;23(36):9394-407 [16361639.001]
  • [Cites] Pancreas. 2001 Jul;23 (1):72-9 [11451151.001]
  • [Cites] Immunity. 1995 Dec;3(6):673-82 [8777713.001]
  • [Cites] Oncogene. 2005 Jan 6;24(1):130-40 [15531922.001]
  • [Cites] J Clin Oncol. 2005 May 20;23(15):3509-16 [15908661.001]
  • [Cites] Science. 1997 Aug 8;277(5327):815-8 [9242610.001]
  • [Cites] J Biol Chem. 1998 Oct 16;273(42):27084-90 [9765224.001]
  • [Cites] J Biol Chem. 1997 Oct 10;272(41):25417-20 [9325248.001]
  • [Cites] Ann Oncol. 2001 Jan;12(1):101-3 [11249034.001]
  • [Cites] Nat Med. 2000 May;6(5):564-7 [10802713.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2403-13 [9196156.001]
  • [Cites] Anticancer Res. 2003 Jan-Feb;23(1A):251-8 [12680221.001]
  • (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
  •  go-up   go-down


10. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • Pharmacogenomics Knowledge Base. meta-databases - Pharmacogenomic Annotation 827855919 for PMID:19460966 [PharmGKB] .
  • Faculty of 1000. commentaries/discussion - See the articles recommended by F1000Prime's Faculty of more than 8,000 leading experts in Biology and Medicine. (subscription/membership/fee required).
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 2007 Oct 15;67(20):9903-12 [17942922.001]
  • [Cites] Ultrasound Med Biol. 2008 Apr;34(4):525-32 [18045768.001]
  • [Cites] Methods Enzymol. 2008;439:73-85 [18374157.001]
  • [Cites] Clin Cancer Res. 2008 Apr 15;14(8):2476-83 [18413840.001]
  • [Cites] Mol Cancer Ther. 2008 Apr;7(4):829-40 [18413796.001]
  • [Cites] J Med Chem. 2008 Apr 24;51(8):2412-20 [18257544.001]
  • [Cites] Nature. 2008 Sep 18;455(7211):406-10 [18754008.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):5995-6004 [18829478.001]
  • [Cites] Genes Dev. 2009 Jan 1;23(1):24-36 [19136624.001]
  • [Cites] Br J Cancer. 2001 May 18;84(10):1424-31 [11355958.001]
  • [Cites] Nat Med. 2001 Jun;7(6):706-11 [11385508.001]
  • [Cites] Nucleic Acids Res. 2002 Jul 15;30(14):3067-77 [12136089.001]
  • [Cites] Int J Cancer. 2002 Nov 10;102(2):101-8 [12385004.001]
  • [Cites] J Clin Oncol. 2003 Sep 15;21(18):3402-8 [12885837.001]
  • [Cites] Nature. 2003 Oct 23;425(6960):851-6 [14520413.001]
  • [Cites] Lancet. 2004 Mar 27;363(9414):1049-57 [15051286.001]
  • [Cites] Cancer Res. 1974 Sep;34(9):2243-5 [4843531.001]
  • [Cites] J Clin Oncol. 1991 Mar;9(3):491-8 [1999720.001]
  • [Cites] Oncol Res. 1993;5(6-7):223-8 [8123942.001]
  • [Cites] J Clin Oncol. 1997 Jun;15(6):2403-13 [9196156.001]
  • [Cites] Cancer Cell. 2005 May;7(5):469-83 [15894267.001]
  • [Cites] J Gastroenterol. 2005 May;40(5):518-25 [15942718.001]
  • [Cites] Cancer Res. 2006 Jan 1;66(1):95-106 [16397221.001]
  • [Cites] Nat Rev Cancer. 2006 Aug;6(8):583-92 [16862189.001]
  • [Cites] J Natl Cancer Inst. 2007 Oct 3;99(19):1441-54 [17895480.001]
  • [CommentIn] Science. 2009 Jun 12;324(5933):1400-1 [19520948.001]
  • (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
  •  go-up   go-down


11. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


12. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


13. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [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
  •  go-up   go-down


14. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down


15. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [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

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • Hazardous Substances Data Bank. SIROLIMUS .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cell. 1988 May 20;53(4):549-54 [2453289.001]
  • [Cites] Nature. 1976 Oct 28;263(5580):771-2 [995188.001]
  • [Cites] Cancer Biol Ther. 2009 Oct;8(20):1893-901 [20009539.001]
  • [Cites] Science. 2009 Jun 12;324(5933):1457-61 [19460966.001]
  • [Cites] Cancer Res. 1999 Aug 1;59(15):3581-7 [10446965.001]
  • [Cites] Nucleic Acids Res. 1988 Aug 25;16(16):7773-82 [3047672.001]
  • [CommentOn] Cancer Biol Ther. 2009 Oct;8(20):1893-901
  • (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
  •  go-up   go-down


16. 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
PDF icon [Fulltext service] Download fulltext PDF of this article and others, as many as you want.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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

  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • The Lens. Cited by Patents in .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (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
  •  go-up   go-down






Advertisement