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1. Namba R, Young LJ, Maglione JE, McGoldrick ET, Liu S, Wurz GT, DeGregorio MW, Borowsky AD, MacLeod CL, Cardiff RD, Gregg JP: Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ. Breast Cancer Res; 2005;7(6):R881-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Selective estrogen receptor modulators inhibit growth and progression of premalignant lesions in a mouse model of ductal carcinoma in situ.
  • INTRODUCTION: Ductal carcinoma in situ (DCIS) is a noninvasive premalignant lesion and is considered a precursor to invasive carcinoma.
  • DCIS accounts for nearly 20% of newly diagnosed breast cancer, but the lack of experimentally amenable in vivo DCIS models hinders the development of treatment strategies.
  • Here, we demonstrate the utility of a mouse transplantation model of DCIS for chemoprevention studies using selective estrogen receptor modulators (SERMs).
  • This model consists of a set of serially transplanted lines of genetically engineered mouse mammary intraepithelial neoplasia (MIN) outgrowth (MIN-O) tissue that have stable characteristics.
  • METHODS: The estrogen receptor (ER) status and ovarian-hormone-dependence of the mouse MIN outgrowth tissue were determined by immunohistochemistry and ovarian ablation.
  • The effects on ER status, cell proliferation, and apoptosis were studied with immunohistochemistry.
  • Likewise, tamoxifen and ospemifene treatments decreased the MIN growth and tumor incidence in comparison with the control (P < 0.01).
  • Both SERMs significantly decreased cell proliferation.
  • Between the two SERM treatment groups, there were no statistically significant differences in MIN-O size, tumor latency, or proliferation rate.
  • In contrast, the ospemifene treatment significantly increased ER levels while tamoxifen significantly decreased them.
  • CONCLUSION: Tamoxifen and ospemifene inhibit the growth of premalignant mammary lesions and the progression to invasive carcinoma in a transplantable mouse model of DCIS.
  • These data demonstrate the value of this model system for preclinical testing of antiestrogen or other therapies designed to prevent or delay the malignant transformation of premalignant mammary lesions in chemoprevention.

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  • (PMID = 16280035.001).
  • [ISSN] 1465-542X
  • [Journal-full-title] Breast cancer research : BCR
  • [ISO-abbreviation] Breast Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA89140-01; United States / NCI NIH HHS / CA / R01 CA089140; United States / NCRR NIH HHS / RR / U42 RR014905; United States / NCRR NIH HHS / RR / U42RR14905; United States / NCI NIH HHS / CA / R01CA81376
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Receptors, Estrogen; 0 / Selective Estrogen Receptor Modulators; 094ZI81Y45 / Tamoxifen; B0P231ILBK / Ospemifene
  • [Other-IDs] NLM/ PMC1410776
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2. Gandhi A, Holland PA, Knox WF, Potten CS, Bundred NJ: Effects of a pure antiestrogen on apoptosis and proliferation within human breast ductal carcinoma in situ. Cancer Res; 2000 Aug 1;60(15):4284-8
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  • [Title] Effects of a pure antiestrogen on apoptosis and proliferation within human breast ductal carcinoma in situ.
  • Adjuvant antiestrogen (AE) therapy has been proposed for all women with ductal carcinoma in situ (DCIS).
  • However, many cases of DCIS are of the high-grade, estrogen receptor (ER)-negative subtype that are unlikely to respond to AE treatment.
  • Hormonal agents work by increasing apoptosis and/or decreasing cell proliferation; therefore, we studied the effect of a pure AE on levels of apoptosis and proliferation in human DCIS xenografts using an in vivo model.
  • Women (n = 23) with mammographic microcalcification suggestive of DCIS were identified at the time of surgery (day 0), a sample of representative tissue was obtained, divided into multiple 2x2x1-mm xenografts, and implanted s.c. into female BALB/c nu/nu mice (eight xenografts/mouse).
  • Fourteen days after implantation, four xenografts were retrieved and mice were randomly divided into one of three treatment groups: (a) insertion of a slow release 2-mg 17beta-estradiol pellet;.
  • After 2 weeks of treatment, the remaining four xenografts were retrieved from each mouse.
  • Retrieved xenografts containing DCIS were assessed for morphological evidence of apoptotic cell death [apoptotic index (AI)] and cell proliferation (by immunohistochemical detection of the Ki67 proliferation antigen LI).
  • AI and LI values within ER- DCIS did not differ between xenografts exposed to 17beta-estradiol or AE treatment compared with the controls or pretreatment values (mean AI and LI in estradiol-treated, antiestrogen-treated, and control groups 1.04% versus 0.98% versus 1.29% and 17.2% versus 20.5% versus 17.7% respectively).
  • In contrast, treatment of mice bearing ER+ DCIS xenografts with 17beta-estradiol raised both the AI (1.03% versus 0.40%, P = 0.03) and LI (11.0% versus 5.1%, P = 0.007) compared with controls.
  • AE therapy of ER+ DCIS xenografts did not affect proliferation but resulted in higher apoptosis than in controls (0.9% versus 0.4% respectively, P = 0.04).
  • AE therapy should be reserved for patients with estrogen receptor positive DCIS.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Breast Neoplasms / pathology. Carcinoma in Situ / pathology. Estradiol / analogs & derivatives. Estrogen Receptor Modulators / pharmacology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Animals. Cell Division / drug effects. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Neoplasm Transplantation. Receptors, Estrogen / physiology. Transplantation, Heterologous

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  • (PMID = 10945643.001).
  • [ISSN] 0008-5472
  • [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 / Antineoplastic Agents; 0 / Estrogen Receptor Modulators; 0 / Receptors, Estrogen; 22X328QOC4 / fulvestrant; 4TI98Z838E / Estradiol
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3. 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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4. 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.
  • In vivo, the twice weekly i.p. administration of FG-3019 decreased tumor growth and metastasis and attenuated tumor angiogenesis and cancer cell proliferation.
  • 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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5. Feldmann G, Habbe N, Dhara S, Bisht S, Alvarez H, Fendrich V, Beaty R, Mullendore M, Karikari C, Bardeesy N, Ouellette MM, Yu W, Maitra A: Hedgehog inhibition prolongs survival in a genetically engineered mouse model of pancreatic cancer. Gut; 2008 Oct;57(10):1420-30
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  • [Title] Hedgehog inhibition prolongs survival in a genetically engineered mouse model of pancreatic cancer.
  • Current therapeutic strategies are virtually ineffective in controlling advanced, metastatic disease.
  • METHODS: Here it is shown that the Hedgehog pathway is activated in the Pdx1-Cre;LsL-Kras(G12D);Ink4a/Arf(lox/lox) transgenic mouse model of pancreatic cancer.
  • Microarray analysis was performed on non-malignant human pancreatic ductal cells overexpressing Gli1 in order to screen for downstream Hedgehog target genes likely to be involved in pancreatic cancer progression.
  • RESULTS: Hedgehog inhibition with cyclopamine significantly prolonged median survival in the transgenic mouse model used here (67 vs 61 days; p = 0.026).
  • CONCLUSION: This study provides another line of evidence that Hedgehog signalling is a valid target for the development of novel therapeutics for pancreatic cancer that might be worth evaluating soon in a clinical setting.

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  • (PMID = 18515410.001).
  • [ISSN] 1468-3288
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R01 CA113669-02; United States / NCI NIH HHS / CA / P50CA62924; United States / NCI NIH HHS / CA / R01 CA113669-01; United States / NCI NIH HHS / CA / CA113669-02; United States / NCI NIH HHS / CA / CA113669-04; United States / NCI NIH HHS / CA / P50 CA062924; United States / NCI NIH HHS / CA / R01CA113669; United States / NCI NIH HHS / CA / CA113669-03; United States / NCI NIH HHS / CA / R01 CA113669-05; United States / NCI NIH HHS / CA / R01 CA113669-03; United States / NCI NIH HHS / CA / R01 CA113669; United States / NCI NIH HHS / CA / R01 CA113669-04; United States / NCI NIH HHS / CA / CA113669-05; United States / NCI NIH HHS / CA / CA113669-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hedgehog Proteins; 0 / Neoplasm Proteins; 0 / Veratrum Alkaloids; ZH658AJ192 / cyclopamine
  • [Other-IDs] NLM/ NIHMS97875; NLM/ PMC2707354
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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.
  • Dasatinib inhibited the migration and invasion of PDAC cell lines, although no effects on proliferation were seen at concentrations that inhibited Src kinase activity.
  • 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. 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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  • [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.
  • 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.
  • 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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8. Ninomiya K, Ohi S, Tabei I, Jin S, Tachibana T, Yamashita S, Yanaga K, Hashimoto H: Establishment and characterization of a cell line (BTIC) including HER-2-positive cells derived from pleural effusion of recurrent breast invasive ductal carcinoma, scirrhous type. Hum Cell; 2007 Aug;20(3):85-90
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  • [Title] Establishment and characterization of a cell line (BTIC) including HER-2-positive cells derived from pleural effusion of recurrent breast invasive ductal carcinoma, scirrhous type.
  • Adjuvant chemotherapy with trastuzumab has improved the prognosis of patients with HER-2 positive high-grade breast cancer.
  • However, patients often experience appearance and proliferation of recurrent tumor cells after trastuzumab treatment.
  • In this study, we report the successful establishment and characterization of a cell line (BTIC) derived from a patient with recurrent breast cancer after adjuvant chemotherapy with trastuzumab.
  • Characteristics of the BTIC cell line were investigated by phase contrast or electron microscopic observations, chromosome analysis, xenotransplantation, immunohistochemistry and radioimmunoassay for tumor markers.
  • We confirmed that the BTIC cell line grown as multilayered culture in culture dishes, has a poorly developed endoplasmic reticulum in the cytoplasm and some desmosomes.
  • The population doubling time was approximately 44 hr.
  • A graft in nude mouse after xenotransplantation was diagnosed as scirrhous carcinoma.
  • [MeSH-major] Breast Neoplasms / pathology. Carcinoma, Ductal, Breast / pathology. Cell Line, Tumor. Pleural Effusion / pathology
  • [MeSH-minor] Adult. Animals. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Humanized. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / analysis. Chemotherapy, Adjuvant. Female. Genes, erbB-2. Humans. Immunohistochemistry. Karyotyping. Mice. Mice, Nude. Microscopy, Electron. Neoplasm Recurrence, Local. Neoplasm Transplantation. Transplantation, Heterologous. Trastuzumab


9. 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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  • The apoptosome is a multiprotein complex mediating the mitochondrial pathway of cell death.
  • 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).
  • Similarly, several PDAC cell lines exhibited variable levels of both APAF1 protein and mRNA.
  • The response to cell death induction and its biochemical features were assessed by treatment of each line with commonly used chemotherapeutic agents.
  • We found that the apoptosome pathway was not functional in most cell lines upon cytochrome c release from mitochondria.
  • [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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10. 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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  • [Title] Claudin-4: a new target for pancreatic cancer treatment using Clostridium perfringens enterotoxin.
  • 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.
  • In vivo, intratumoral injections of CPE in Panc-1 xenografts led to large areas of tumor cell necrosis and significant reduction of tumor growth.
  • 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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11. Hoffmann K, Mehrle S, Schmidt J, Büchler MW, Märten A: Interferon-alpha restitutes the chemosensitivity in pancreatic cancer. Anticancer Res; 2008 May-Jun;28(3A):1499-507
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  • BACKGROUND: Multidrug resistance is a major obstacle in the treatment of pancreatic cancer.
  • MATERIALS AND METHODS: Pancreatic cancer was induced in an orthotopic mouse model.
  • Animals received standard chemotherapy or combinative treatment with interferon-alpha.
  • Expression and function of drug-resistance proteins were analyzed.
  • Immunological phenotyping, cytotoxic activity assays and analysis of T-cell activation status were performed.
  • RESULTS: Addition of interferon-alpha to chemotherapeutic regimes significantly reduced chemotherapy-induced expression of multidrug resistance proteins and drug efflux activity of cancer cells.
  • Tumor size and metastatic seeding decreased significantly upon combination therapy and survival was prolonged.
  • A significantly higher proportion of activated and cytotoxic active CD8+ tumor infiltrating lymphocytes was detectable after induction of drug resistance.
  • CONCLUSION: Restitution of chemosensitivity by the addition of interferon alpha to chemotherapy was demonstrated in experimental pancreatic cancer for the first time.
  • Since drug-resistance proteins may function as tumor antigens, our data support immunochemotherapy as an encouraging new approach.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / pharmacology. Carcinoma, Pancreatic Ductal / therapy. Interferon-alpha / pharmacology. Pancreatic Neoplasms / therapy
  • [MeSH-minor] Cell Line, Tumor. Cisplatin / administration & dosage. Combined Modality Therapy. Deoxycytidine / administration & dosage. Deoxycytidine / analogs & derivatives. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Drug Synergism. Fluorouracil / administration & dosage. Humans. P-Glycoprotein / biosynthesis. P-Glycoprotein / metabolism

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  • (PMID = 18630504.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Interferon-alpha; 0 / P-Glycoprotein; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine; Q20Q21Q62J / Cisplatin; U3P01618RT / Fluorouracil
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12. Ziske C, Tiemann K, Schmidt T, Nagaraj S, Märten A, Schmitz V, Clarenbach R, Sauerbruch T, Schmidt-Wolf IG: Real-time high-resolution compound imaging allows percutaneous initiation and surveillance in an orthotopic murine pancreatic cancer model. Pancreas; 2008 Mar;36(2):146-52
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  • [Title] Real-time high-resolution compound imaging allows percutaneous initiation and surveillance in an orthotopic murine pancreatic cancer model.
  • METHODS: To assess time-related changes in orthotopic tumor volume, we applied transabdominal high-resolution compound imaging to the murine pancreas.
  • A 15-MHz ultrasound probe was used to determine the feasibility of real-time transabdominal high-resolution ultrasonography to initiate tumor growth by inoculation of pancreatic tumor cells into the pancreas and monitor tumor growth, as well as use as a tool for assessing response to chemotherapy.
  • CONCLUSIONS: High-resolution real-time compound imaging substitutes killing of mice during longitudinal studies and can be used for minimizing animal consumption because each mouse can be followed in an experimental group rather than having to resort to euthanasia for tissue harvesting.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / ultrasonography. Pancreatic Neoplasms / ultrasonography. Ultrasonography, Interventional
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacology. Antimetabolites, Antineoplastic / therapeutic use. Cell Line, Tumor. Deoxycytidine / analogs & derivatives. Deoxycytidine / pharmacology. Deoxycytidine / therapeutic use. Disease Progression. Female. Mice. Mice, Inbred C57BL. Neoplasm Transplantation. Neoplasms, Experimental / ultrasonography. Time Factors

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  • (PMID = 18376305.001).
  • [ISSN] 1536-4828
  • [Journal-full-title] Pancreas
  • [ISO-abbreviation] Pancreas
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine
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13. Toneff MJ, Du Z, Dong J, Huang J, Sinai P, Forman J, Hilsenbeck S, Schiff R, Huang S, Li Y: Somatic expression of PyMT or activated ErbB2 induces estrogen-independent mammary tumorigenesis. Neoplasia; 2010 Sep;12(9):718-26
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  • Here, we report that in a retrovirus-based somatic mouse model (replication-competent ALV-LTR splice acceptor/tumor virus A) that closely mimics the evolution of sporadic human breast cancers, mammary epithelial cells harboring PyMT or activated ErbB2 evolve into tumors independent of estrogen or other ovarian functions in contrast to previous observations of estrogen-dependent cancer formation in germ line mouse models of ErbB2 activation.
  • Therefore, aberrant activation of growth factor signaling contributes to estrogen-independent proliferation of both preneoplastic and cancerous mammary cells, and prophylactic therapy against both growth factor signaling and estrogen signaling may need to be considered in women with increased risk of breast cancer.

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  • (PMID = 20824048.001).
  • [ISSN] 1476-5586
  • [Journal-full-title] Neoplasia (New York, N.Y.)
  • [ISO-abbreviation] Neoplasia
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / AI45764; United States / NCI NIH HHS / CA / R01 CA113869; United States / NCI NIH HHS / CA / CA113869; United States / NIAID NIH HHS / AI / R01 AI045764; United States / NCI NIH HHS / CA / CA124820; United States / NCI NIH HHS / CA / R01 CA124820
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Estrogens; EC 2.7.10.1 / Erbb2 protein, mouse; EC 2.7.10.1 / Receptor, ErbB-2
  • [Other-IDs] NLM/ PMC2933692
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14. Trastour C, Benizri E, Ettore F, Ramaioli A, Chamorey E, Pouysségur J, Berra E: HIF-1alpha and CA IX staining in invasive breast carcinomas: prognosis and treatment outcome. Int J Cancer; 2007 Apr 1;120(7):1451-8
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  • [Title] HIF-1alpha and CA IX staining in invasive breast carcinomas: prognosis and treatment outcome.
  • Hypoxia stabilizes HIF-1alpha (Hypoxia Inducible Factor-1alpha), which then triggers the expression of several genes involved in many aspects of cancer progression, including metabolic adaptation, cell survival and angiogenesis.
  • The aim of our study was to evaluate the impact of HIF-1alpha and CA IX (carbonic anhydrase IX) (one of its target genes) expression on prognosis and treatment outcome of patients with breast cancer.
  • Afterwards, the immunohistochemical staining of HIF-1alpha and CA IX was evaluated in 132 invasive breast carcinomas with a 10-year follow-up, and correlated to classical clinicopathological parameters and response to adjuvant therapy.
  • Furthermore, overexpression of HIF-1alpha or CA IX correlates with a poor outcome after conventional adjuvant therapy.
  • CA IX is, however, a weaker prognostic and predictive factor than HIF-1alpha, and its association with HIF-1alpha does not modify the survival curve neither response to therapy, compared to HIF-1alpha alone.
  • [MeSH-major] Antigens, Neoplasm / metabolism. Breast Neoplasms / metabolism. Carbonic Anhydrases / metabolism. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Animals. Antineoplastic Agents / therapeutic use. Biomarkers, Tumor / metabolism. Carcinoma, Ductal, Breast / drug therapy. Carcinoma, Ductal, Breast / metabolism. Carcinoma, Ductal, Breast / pathology. Carcinoma, Lobular / drug therapy. Carcinoma, Lobular / metabolism. Carcinoma, Lobular / pathology. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / metabolism. Carcinoma, Medullary / pathology. Chemotherapy, Adjuvant. Female. Humans. Immunoenzyme Techniques. Male. Mice. Mice, Nude. Middle Aged. Neoplasm Invasiveness. Prognosis. Survival Rate. Treatment Outcome

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17245699.001).
  • [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 / Antigens, Neoplasm; 0 / Antineoplastic Agents; 0 / Biomarkers, Tumor; 0 / HIF1A protein, human; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; EC 4.2.1.1 / CA9 protein, human; EC 4.2.1.1 / Carbonic Anhydrases
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15. Rowland-Goldsmith MA, Maruyama H, Kusama T, Ralli S, Korc M: Soluble type II transforming growth factor-beta (TGF-beta) receptor inhibits TGF-beta signaling in COLO-357 pancreatic cancer cells in vitro and attenuates tumor formation. Clin Cancer Res; 2001 Sep;7(9):2931-40
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Soluble type II transforming growth factor-beta (TGF-beta) receptor inhibits TGF-beta signaling in COLO-357 pancreatic cancer cells in vitro and attenuates tumor formation.
  • Human pancreatic ductal adenocarcinomas overexpress transforming growth factor-betas (TGF-betas).
  • TGF-betas bind to a type II TGF-beta receptor (TbetaRII) dimer, which heterotetramerizes with a type I TGF-beta receptor (TbetaRI) dimer, thereby activating downstream signaling.
  • PURPOSE AND EXPERIMENTAL DESIGN: To determine whether blocking TGF-beta actions would suppress pancreatic cancer cell growth in vivo, we expressed a soluble TbetaRII, encoding amino acids 1-159 of the extracellular domain in COLO-357 human pancreatic cancer cells.
  • This cell line expresses all of the three mammalian TGF-beta isoforms and is growth inhibited by TGF-beta in vitro.
  • CONCLUSIONS: These results indicate that endogenous TGF-betas can confer a growth advantage in vivo to a pancreatic cancer cell line that is growth inhibited in vitro and suggest that a soluble receptor approach can be used to block these tumorigenic effects of TGF-betas.
  • [MeSH-major] Pancreatic Neoplasms / therapy. Receptors, Transforming Growth Factor beta / metabolism. Transforming Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Cell Division / drug effects. Cell Division / genetics. Cell Movement / drug effects. Female. Gene Expression. Genetic Vectors / genetics. Humans. Mice. Mice, Nude. Neoplasm Invasiveness. Neoplasm Transplantation. Signal Transduction. Solubility. Transfection. Transforming Growth Factor beta1. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism. Xenograft Model Antitumor Assays

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  • (PMID = 11555612.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-75059
  • [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 / Receptors, Transforming Growth Factor beta; 0 / TGFB1 protein, human; 0 / Tgfb1 protein, mouse; 0 / Transforming Growth Factor beta; 0 / Transforming Growth Factor beta1
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16. 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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  • 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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17. 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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  • 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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18. 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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  • 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.
  • The modified compounds maintained high affinity for alpha(v)beta(6) and >1,000-fold selectivity over related integrins (by ELISA) and showed significantly improved alpha(v)beta(6)-dependent binding in cell-based assays (>60% binding versus <10% for [(18)F]FBA-A20FMDV2).
  • 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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19. Molteni A, Ward WF, Ts'ao CH, Taylor J, Small W Jr, Brizio-Molteni L, Veno PA: Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists. Curr Pharm Des; 2003;9(9):751-61
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytostatic properties of some angiotensin I converting enzyme inhibitors and of angiotensin II type I receptor antagonists.
  • Angiotensin converting enzyme (ACE) inhibitors and angiotensin II (AII) type 1 receptor antagonists have strong cytostatic properties on in vitro cultures of many normal and neoplastic cells.
  • They are effective, in particular, in reducing the growth of human lung fibroblasts, renal canine epithelial cells, bovine adrenal endothelial cells, simian T lymphocytes, and of neoplastic cell lines derived from human neuroblastomas, a ductal pancreatic carcinoma of the Syrian hamsters, human salivary glands adenocarcinomas, and two lines of human breast adenocarcinomas.
  • ACE inhibitors and AII type 1 receptor antagonists are also effective in reducing excessive vascular neoformation in a model of injury to the cornea of rats and rabbits, and in controlling the excessive angiogenesis observed in the Solt-Farber model of experimentally induced hepatoma, in methylcholantrene or radiation-induced fibrosarcomas, in radiation-induced squamous cell carcinomas and in the MA-16 viral-induced mammary carcinoma of the mouse.
  • The mitogenic effect of AII is well established and a reduction of AII synthesis may well explain cell and neoplasm delayed growth.
  • Moreover, AII regulates and enhances the activity of several growth factors including transforming growth factor B (TGFB) and smooth muscle actin (SMA); and many of these factors are reduced in tissues of animals treated with ACE inhibitors and AII type 1 receptor antagonists.
  • The ACE inhibitors containing a sulphydril (SH) or thiol radical in their moiety (Captopril and CL242817) seemed to be more effective in controlling fibrosis and the growth of some neoplastic cells than those ACE inhibitors without this thiol radical in their structure, even if the second group of these drugs show in vitro a stronger inhibitory effect on converting enzyme activity.
  • However, although these additional properties are pharmacologically relevant, the blockade of AII synthesis plays an essential role in the cytostatic activity of these two categories of drugs.
  • These observations underline that in addition to the beneficial effect of these drugs on the cardiovascular system, new potential applications are opening for their wider deployment.
  • [MeSH-minor] Animals. Humans. Neoplasms / drug therapy. Neoplasms / metabolism. Receptors, Angiotensin / physiology

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  • (PMID = 12570792.001).
  • [ISSN] 1381-6128
  • [Journal-full-title] Current pharmaceutical design
  • [ISO-abbreviation] Curr. Pharm. Des.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA 24652; United States / NCI NIH HHS / CA / CA 52750; United States / NCI NIH HHS / CA / CA 64239; United States / NIDDK NIH HHS / DK / DK 15612; United States / NHLBI NIH HHS / HL / HL 25106
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Angiotensin Receptor Antagonists; 0 / Angiotensin-Converting Enzyme Inhibitors; 0 / Antineoplastic Agents; 0 / Receptors, Angiotensin
  • [Number-of-references] 70
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