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1. Matsuzaki T, Yashiro M, Kaizaki R, Yasuda K, Doi Y, Sawada T, Ohira M, Hirakawa K: Synergistic antiproliferative effect of mTOR inhibitors in combination with 5-fluorouracil in scirrhous gastric cancer. Cancer Sci; 2009 Dec;100(12):2402-10
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  • [Title] Synergistic antiproliferative effect of mTOR inhibitors in combination with 5-fluorouracil in scirrhous gastric cancer.
  • The aim of this study is to clarify the benefit of combination chemotherapy in gastric cancer based on a cell-signal inhibitor and an anticancer drug.
  • Two scirrhous gastric cancer cell lines and two non-scirrhous gastric cancer cell lines were used.
  • Five anticancer drugs (5-fluorouracil [5FU], paclitaxel, oxaliplatin, irinotecan, and gemcitabine) and four cell-signal inhibitors, mammalian target of rapamycin (mTOR) inhibitor, glycogen synthase kinase 3beta, p38alphabetaMAPK, and cyclin-dependent kinase, were used.
  • The apoptosis of cancer cells and the expression of apoptosis-related molecules were examined by flow cytometry, real-time PCR, and immunostaining. mTOR inhibitors with 5FU showed a synergistic antiproliferative effect in scirrhous gastric cancer, whereas the other signal inhibitors showed no synergistic effect with any anticancer drugs. mTOR inhibitor decreased the IC(50) of 5FU and increased the apoptosis rate in scirrhous gastric cancer cells, but not in non-scirrhous gastric cancer cells.
  • The pan-caspase inhibitor, zVAD-fmk, inhibits apoptosis induced in combination with 5FU and mTOR inhibitor. mTOR inhibitor decreased dihydropyrimidine dehydrogenase, thymidylatesynthase, and bcl-2 expression, and increased caspase-3 and p21 expression of scirrhous gastric cancer cells, but did not affect those of non-scirrhous gastric cancer cells.
  • In an in vivo study, mTOR inhibitor significantly enhanced the therapeutic efficacy of S1, an analog of 5FU.
  • These findings suggest that mTOR inhibitor interacts with 5FU in a synergistic manner in scirrhous gastric cancer cells by the activation of the apoptosis signal.
  • Therefore, mTOR inhibitor is a promising therapeutic agent in combination with 5FU in scirrhous gastric cancer.
  • [MeSH-major] Adenocarcinoma, Scirrhous / drug therapy. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fluorouracil / administration & dosage. Intracellular Signaling Peptides and Proteins / antagonists & inhibitors. Protein-Serine-Threonine Kinases / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Amino Acid Chloromethyl Ketones / pharmacology. Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Synergism. Humans. Mice. Mice, Inbred BALB C. TOR Serine-Threonine Kinases. Xenograft Model Antitumor Assays

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  • (PMID = 19764996.001).
  • [ISSN] 1349-7006
  • [Journal-full-title] Cancer science
  • [ISO-abbreviation] Cancer Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Amino Acid Chloromethyl Ketones; 0 / Intracellular Signaling Peptides and Proteins; 0 / benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone; 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; U3P01618RT / Fluorouracil
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2. Loo D, Pryer N, Young P, Liang T, Coberly S, King KL, Kang K, Roberts P, Tsao M, Xu X, Potts B, Mather JP: The glycotope-specific RAV12 monoclonal antibody induces oncosis in vitro and has antitumor activity against gastrointestinal adenocarcinoma tumor xenografts in vivo. Mol Cancer Ther; 2007 Mar;6(3):856-65
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  • [Title] The glycotope-specific RAV12 monoclonal antibody induces oncosis in vitro and has antitumor activity against gastrointestinal adenocarcinoma tumor xenografts in vivo.
  • More than 90% of tumors of colorectal, gastric, and pancreatic origin express RAAG12, and a majority of these tumors exhibit uniform RAAG12 expression.
  • In the case of SNU-16 tumor cells, twice weekly treatment of established s.c. tumors with 10 mg/kg RAV12 caused a approximately 70% suppression of tumor growth at the end of the study.
  • This preclinical data has led to the initiation of a phase I/IIA clinical study of RAV12 in patients with metastatic or recurrent adenocarcinoma.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antibodies, Monoclonal / therapeutic use. Antigens, Tumor-Associated, Carbohydrate / immunology. Gastrointestinal Neoplasms / drug therapy
  • [MeSH-minor] Animals. CHO Cells. Cricetinae. Cricetulus. DNA-Binding Proteins / immunology. DNA-Binding Proteins / metabolism. Enzyme-Linked Immunosorbent Assay. Epitopes / immunology. Female. Fetus. Glycosylation. Humans. Immunization. Kidney / metabolism. Kidney / pathology. Male. Mice. Mice, Inbred BALB C. Polymerase Chain Reaction. Repressor Proteins / immunology. Repressor Proteins / metabolism. Tissue Array Analysis. Tumor Cells, Cultured. Xenograft Model Antitumor Assays. Zinc Fingers

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  • (PMID = 17363480.001).
  • [ISSN] 1535-7163
  • [Journal-full-title] Molecular cancer therapeutics
  • [ISO-abbreviation] Mol. Cancer Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antigens, Tumor-Associated, Carbohydrate; 0 / DNA-Binding Proteins; 0 / Epitopes; 0 / Repressor Proteins; 0 / ZNF354C protein, human; 0 / Zfp354c protein, mouse
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3. Yashiro M, Shinto O, Nakamura K, Tendo M, Matsuoka T, Matsuzaki T, Kaizaki R, Miwa A, Hirakawa K: Synergistic antitumor effects of FGFR2 inhibitor with 5-fluorouracil on scirrhous gastric carcinoma. Int J Cancer; 2010 Feb 15;126(4):1004-16
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  • [Title] Synergistic antitumor effects of FGFR2 inhibitor with 5-fluorouracil on scirrhous gastric carcinoma.
  • Scirrhous gastric carcinoma (SGC) carries the highest mortality because of a frequent metastasis to lymph node (LN).
  • S1, a 5-fluorouracil (5-FU) analog, is clinically available for gastric cancer at an advanced stage.
  • The objective of this study is to clarify the benefit of a combination of S1 and kinase inhibitors including FGFR2 inhibitor Ki23057 in gastric cancer.
  • These findings suggested that the combined treatment with 5-FU and Ki23057 produced synergistic antitumor effects and is therapeutically promising for SGC treatment.
  • [MeSH-major] Adenocarcinoma, Scirrhous / drug therapy. Antineoplastic Agents / therapeutic use. Fluorouracil / therapeutic use. Indoles / therapeutic use. Pyrroles / therapeutic use. Receptor, Fibroblast Growth Factor, Type 2 / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / therapeutic use. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Apoptosis / drug effects. Cell Division / drug effects. Flow Cytometry. Mice. Pyridines / therapeutic use. RNA, Messenger / drug effects. RNA, Messenger / genetics. Receptor Protein-Tyrosine Kinases / antagonists & inhibitors. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 19621385.001).
  • [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 / Antimetabolites, Antineoplastic; 0 / Antineoplastic Agents; 0 / Indoles; 0 / Pyridines; 0 / Pyrroles; 0 / RNA, Messenger; 0 / sunitinib; EC 2.7.10.1 / Fgfr2 protein, mouse; EC 2.7.10.1 / Receptor Protein-Tyrosine Kinases; EC 2.7.10.1 / Receptor, Fibroblast Growth Factor, Type 2; U3P01618RT / Fluorouracil; UA8SE1325T / gimeracil
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4. Nakahara C, Nakamura K, Yamanaka N, Baba E, Wada M, Matsunaga H, Noshiro H, Tanaka M, Morisaki T, Katano M: Cyclosporin-A enhances docetaxel-induced apoptosis through inhibition of nuclear factor-kappaB activation in human gastric carcinoma cells. Clin Cancer Res; 2003 Nov 1;9(14):5409-16
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  • [Title] Cyclosporin-A enhances docetaxel-induced apoptosis through inhibition of nuclear factor-kappaB activation in human gastric carcinoma cells.
  • PURPOSE: We sought to determine whether cyclosporin-A (CsA) enhances docetaxel [Taxotere (TXT)]- induced apoptosis in human gastric carcinoma cells, and, if so, to determine the relation between this apoptosis and nuclear factor-kappaB (NF-kappaB) activation.
  • EXPERIMENTAL DESIGN: Two human gastric carcinoma cell lines (GCTM-1 and MK-1), a human embryonic pulmonary fibroblast cell line, and human umbilical vein endothelial cells were used as drug targets.
  • The therapeutic effects of a combination of TXT and CsA were assessed in a mouse peritoneal dissemination model.
  • RESULTS: A combination of CsA (5 micro M) and TXT (10 nM) significantly enhanced apoptotic cell death in both carcinoma cell lines but not in nonmalignant cell lines in comparison with the single-agent treatment alone.
  • This effect was not related to drug uptake, efflux, or MDR1 expression.
  • These effects were also observed in freshly obtained TXT-resistant gastric carcinoma cells isolated from a patient with malignant ascites.
  • TXT alone induced NF-kappaB activation in both carcinoma cell types, and this activation was suppressed by CsA.
  • CONCLUSIONS: Treatment with CsA and TXT in combination may be an effective therapeutic strategy for patients with gastric carcinoma.
  • [MeSH-major] Apoptosis / drug effects. Colonic Neoplasms / drug therapy. Cyclosporine / pharmacology. NF-kappa B / antagonists & inhibitors. Stomach Neoplasms / drug therapy. Taxoids / pharmacology
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / pathology. Animals. Antineoplastic Agents, Phytogenic / pharmacology. Blotting, Western. Caspase Inhibitors. Caspases / metabolism. Chromatography, High Pressure Liquid. Drug Combinations. Enzyme Inhibitors / pharmacology. Female. Humans. Mice. Mice, Inbred BALB C. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / prevention & control. Peritoneal Neoplasms / secondary. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Tumor Cells, Cultured

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  • (PMID = 14614027.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Caspase Inhibitors; 0 / Drug Combinations; 0 / Enzyme Inhibitors; 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / Taxoids; 15H5577CQD / docetaxel; 83HN0GTJ6D / Cyclosporine; EC 3.4.22.- / Caspases
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5. Xi S, Zhang Q, Xie H, Liu L, Liu C, Gao X, Zhang J, Wu L, Qian L, Deng X: [Effects of hydroxy safflor yellow A on blood vessel and mRNA expression with VEGF and bFGF of transplantation tumor with gastric adenocarcinoma cell line BGC-823 in nude mice]. Zhongguo Zhong Yao Za Zhi; 2009 Mar;34(5):605-10
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  • [Title] [Effects of hydroxy safflor yellow A on blood vessel and mRNA expression with VEGF and bFGF of transplantation tumor with gastric adenocarcinoma cell line BGC-823 in nude mice].
  • OBJECTIVE: To investigate the effects of Hydroxy Safflor yellow A (HSYA) on the growth of blood vessel of transplantation tumor of gastric adenocarcinoma cell line BGC-823 in nude mice and its underlying mechanism of antagonizing tumor angiogenesis.
  • The model group were treated with normal sodium by intraperitoneal injection, HSYA groups were treated with HSYA at concentration of 0.056 g x L(-1) and 0.028 g x L(-1) by intraperitoneal injection, and in these groups each mouse was injected 2 times everyday with 0.2 mL by 4-6 hours interval.
  • The control group were injected in enterocoelia 1 times every 2 days starting from the third day with cytoxan at 2 g x L(-1).
  • The pathological change of tumor tissue was observed under optical microscope.
  • The mRNA expression of VEGF and bFGF of transplantation tumor were detected by real time quantitative PCR.
  • RESULT: The volume (607.42 +/- 252.96) mm3, weight (0.88 +/- 0.14) g of transplantation tumor, the mRNA expression level of VEGF 0.49 +/- 0.13 and bFGF 0.60 +/- 0.48 are reduced significantly after treatment with HSYA at the concentration of 0.028 g x L(-1) compared with physiologic saline-treated group (P < 0.05 or P < 0.01).
  • [MeSH-major] Adenocarcinoma / drug therapy. Angiogenesis Inhibitors / administration & dosage. Chalcone / analogs & derivatives. Fibroblast Growth Factors / genetics. Gene Expression Regulation, Neoplastic / drug effects. Quinones / administration & dosage. Stomach Neoplasms / drug therapy. Vascular Endothelial Growth Factor A / genetics
  • [MeSH-minor] Animals. Blood Vessels / drug effects. Cell Line, Tumor. Drugs, Chinese Herbal / administration & dosage. Female. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Random Allocation

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  • (PMID = 19526794.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Drugs, Chinese Herbal; 0 / Quinones; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 146087-19-6 / hydroxysafflor yellow A; 5S5A2Q39HX / Chalcone; 62031-54-3 / Fibroblast Growth Factors
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6. Bae JS, Jang KH, Jin HK: Effects of natural polysaccharides on the growth and peritoneal carcinomatosis of human gastric adenocarcinoma in a nude mouse model. Cancer Lett; 2006 Apr 8;235(1):60-8
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  • [Title] Effects of natural polysaccharides on the growth and peritoneal carcinomatosis of human gastric adenocarcinoma in a nude mouse model.
  • We have examined the effects of natural polysaccharides isolated from Phellinus gilvus (PG) in vitro and in vivo against gastric cancer.
  • These data showed that polysaccharides isolated from PG significantly inhibited tumor growth and metastasis in an orthotopic model of human gastric adenocarcinoma, without detectable problematic adverse effects.
  • [MeSH-major] Adenocarcinoma / drug therapy. Basidiomycota / chemistry. Disease Models, Animal. Peritoneal Neoplasms / drug therapy. Polysaccharides / pharmacology. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Body Weight / drug effects. Cell Proliferation / drug effects. Dose-Response Relationship, Drug. Female. Mice. Mice, Nude. Tumor Cells, Cultured

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  • (PMID = 15899545.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Polysaccharides
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7. Saukkonen K, Rintahaka J, Sivula A, Buskens CJ, Van Rees BP, Rio MC, Haglund C, Van Lanschot JJ, Offerhaus GJ, Ristimaki A: Cyclooxygenase-2 and gastric carcinogenesis. APMIS; 2003 Oct;111(10):915-25
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  • [Title] Cyclooxygenase-2 and gastric carcinogenesis.
  • Epidemiological studies have shown that the use of nonsteroid anti-inflammatory drugs (NSAIDs) is associated with reduced risk of gastric cancer.
  • Two Cox genes have been cloned, of which Cox-2 has been connected with gastric carcinogenesis.
  • Expression of Cox-2 is elevated in gastric adenocarcinomas, which correlates with several clinicopathological parameters, including depth of invasion and lymph node metastasis.
  • Cox-2 expression is especially prominent in intestinal-type gastric carcinoma and it is already present in dysplastic precursor lesions of this disease, which suggests that Cox-2 contributes to gastric carcinogenesis already at the preinvasive stage.
  • Our most recent data show that Cox-2 is expressed in gastric adenomas of trefoil factor 1 deficient mice.
  • Treatment of these mice with a Cox-2 selective inhibitor, celecoxib, reduced the size of the adenomas.
  • Taken together these data support efforts to initiate clinical studies to investigate the effect of Cox-2 inhibitors as chemotherapeutic agents and as adjuvant treatment modalities against gastric neoplasias.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Adenocarcinoma / pathology. Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Cyclooxygenase Inhibitors / therapeutic use. Gene Expression. Humans. Membrane Proteins. Mice. Mice, Knockout. Models, Biological. Peptides / deficiency. Peptides / genetics

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  • (PMID = 14616542.001).
  • [ISSN] 0903-4641
  • [Journal-full-title] APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
  • [ISO-abbreviation] APMIS
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 0 / Peptides; 0 / Tff1 protein, mouse; EC 1.14.99.1 / Cyclooxygenase 2; EC 1.14.99.1 / PTGS2 protein, human; EC 1.14.99.1 / Prostaglandin-Endoperoxide Synthases
  • [Number-of-references] 76
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8. Lang SA, Gaumann A, Koehl GE, Seidel U, Bataille F, Klein D, Ellis LM, Bolder U, Hofstaedter F, Schlitt HJ, Geissler EK, Stoeltzing O: Mammalian target of rapamycin is activated in human gastric cancer and serves as a target for therapy in an experimental model. Int J Cancer; 2007 Apr 15;120(8):1803-10
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  • [Title] Mammalian target of rapamycin is activated in human gastric cancer and serves as a target for therapy in an experimental model.
  • The mammalian target of rapamycin (mTOR) has become an interesting target for cancer therapy through its influence on oncogenic signals, which involve phosphatidylinositol-3-kinase and hypoxia-inducible factor-1alpha (HIF-1alpha).
  • Since mTOR is an upstream regulator of HIF-1alpha, a key mediator of gastric cancer growth and angiogenesis, we investigated mTOR activation in human gastric adenocarcinoma specimens and determined whether rapamycin could inhibit gastric cancer growth in mice.
  • Expression of phospho-mTOR was assessed by immunohistochemical analyses of human tissues.
  • For in vitro studies, human gastric cancer cell lines were used to determine S6K1, 4E-BP-1 and HIF-1alpha activation and cancer cell motility upon rapamycin treatment.
  • Immunohistochemical analyses showed strong expression of phospho-mTOR in 60% of intestinal- and 64% of diffuse-type human gastric adenocarcinomas.
  • In vitro, rapamycin-treatment effectively blocked S6K1, 4E-BP-1 and HIF-1alpha activation, and significantly impaired tumor cell migration.
  • In vivo, rapamycin-treatment led to significant inhibition of subcutaneous tumor growth, decreased CD31-positive vessel area and reduced tumor cell proliferation.
  • Similar significant results were obtained in an orthotopic model of gastric cancer.
  • In the dorsal-skin-fold chamber model, rapamycin-treatment significantly inhibited tumor vascularization in vivo.
  • In conclusion, mTOR is frequently activated in human gastric cancer and represents a promising new molecular target for therapy.
  • [MeSH-major] Antibiotics, Antineoplastic / therapeutic use. Disease Models, Animal. Neovascularization, Pathologic / prevention & control. Protein Kinases / metabolism. Sirolimus / therapeutic use. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Animals. Cell Hypoxia. Cell Line, Tumor. Cell Movement / drug effects. Cell Proliferation / drug effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / metabolism. Intestinal Neoplasms / drug therapy. Intestinal Neoplasms / metabolism. Intestinal Neoplasms / pathology. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Phosphatidylinositol 3-Kinases / metabolism. Phosphorylation / drug effects. Ribosomal Protein S6 Kinases, 70-kDa / metabolism. Signal Transduction. Survival Rate. TOR Serine-Threonine Kinases. Vascular Endothelial Growth Factor A / metabolism

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  • [Copyright] (c) 2007 Wiley-Liss, Inc.
  • (PMID = 17230506.001).
  • [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 / Antibiotics, Antineoplastic; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Vascular Endothelial Growth Factor A; EC 2.7.- / Protein Kinases; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.1 / MTOR protein, human; EC 2.7.1.1 / TOR Serine-Threonine Kinases; EC 2.7.1.1 / mTOR protein, mouse; EC 2.7.11.1 / Ribosomal Protein S6 Kinases, 70-kDa; W36ZG6FT64 / Sirolimus
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9. Hao Z, Li X, Qiao T, Li S, Lv Y, Fan D: Downregulated expression of CIAPIN1 may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression. Cancer Biol Ther; 2009 Jun;8(11):1064-70
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  • [Title] Downregulated expression of CIAPIN1 may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression.
  • Our previous studies revealed that cytokine induced apoptosis inhibitor 1 (CIAPIN1), which was reported to be essential in mouse definitive hematopoiesis, was related to multidrug resistance in gastric cancer cells and that the distribution of CIAPIN1 in normal human tissues was similar to the distribution of Ras.
  • This study aimed to explore whether CIAPIN1 plays a role in gastric carcinogenesis.
  • Expression of CIAPIN1 in normal, inflammatory gastric mucosa, gastric precancerous lesions and gastric adenocarcinoma was detected by immunohistochemistry and western blotting and, influence of CIAPIN1 on the proliferation of gastric cancer cells was investigated by ectopic expression of CIAPIN1 and RNA interference (RNAi).
  • Our immunohistochemical results demonstrated that the expression of CIAPIN1 in gastric antral mucosa was progressively reduced along the sequence of normal/inflammatory gastric mucosa-atrophy-intestinal metaplasia-dysplasia-adenocarcinoma.
  • The downregulation of CIAPIN1 in cancerous tissues was further confirmed by western blotting.
  • No relationship between the expression level of CIAPIN1 and the clinicopathological parameters such as age, gender, differentiation, TNM stage and the existence of metastasis was found in gastric cancer patients.
  • In in vitro cellular experiments, ectopic expression of CIAPIN1 by cDNA transfection resulted in suppression of cell proliferation and inhibition of cell cycle progression while knockdown of CIAPIN1 with siRNA accelerated cell proliferation and promoted cell cycle progression in SGC7901 and MKN28 gastric cancer cells.
  • These results suggest that downregulated CIAPIN1 expression may contribute to gastric carcinogenesis by accelerating cell proliferation and promoting cell cycle progression.
  • [MeSH-minor] Adult. Aged. Blotting, Western. Cell Cycle / physiology. Cell Growth Processes / physiology. Cell Line, Tumor. Down-Regulation. Drug Resistance, Multiple. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Middle Aged. Transfection

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  • (PMID = 19471113.001).
  • [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 / CIAPIN1 protein, human; 0 / Intracellular Signaling Peptides and Proteins; 0 / RNA, Small Interfering
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10. Kishi K, Yano M, Inoue M, Miyashiro I, Motoori M, Tanaka K, Goto K, Eguchi H, Noura S, Yamada T, Ohue M, Ohigashi H, Ishikawa O: Talaporfin-mediated photodynamic therapy for peritoneal metastasis of gastric cancer in an in vivo mouse model: drug distribution and efficacy studies. Int J Oncol; 2010 Feb;36(2):313-20

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  • [Title] Talaporfin-mediated photodynamic therapy for peritoneal metastasis of gastric cancer in an in vivo mouse model: drug distribution and efficacy studies.
  • Photodynamic therapy (PDT) is a potential treatment for the peritoneal dissemination of gastric cancer, because its cytotoxicity is limited to superficial lesions.
  • We also evaluated the pathological response after therapy.
  • The fluorescent intensity of the peritoneal metastatic nodules gradually decreased dependent on the time interval between the laser treatment and talaporfin administration.
  • The pathological response rates by dose were 52.5% at 2 J/cm2, 43.2% at 5 J/cm2, and 64.4% at 10 J/cm2, respectively, when the laser treatment was used 2 h after talaporfin administration, whereas at 4 h, they were 20.8, 25.5, and 26.2%, respectively.
  • Finally, the recommended treatment conditions were considered to be a 2 J/cm2 laser dose and a 4-h interval in terms of toxicity.
  • Talaporfin-mediated PDT may be an effective treatment modality for patients with advanced gastric adenocarcinoma and metastatic peritoneal nodules.
  • [MeSH-major] Peritoneal Neoplasms / drug therapy. Photochemotherapy / methods. Photosensitizing Agents / pharmacology. Porphyrins / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Male. Mice. Mice, Nude. Stomach Neoplasms / secondary. Tissue Distribution

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  • (PMID = 20043064.001).
  • [ISSN] 1791-2423
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Photosensitizing Agents; 0 / Porphyrins; P4ROX5ELT2 / Talaporfin
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11. Azatian A, Yu H, Dai W, Schneiders FI, Botelho NK, Lord RV: Effectiveness of HSV-tk suicide gene therapy driven by the Grp78 stress-inducible promoter in esophagogastric junction and gastric adenocarcinomas. J Gastrointest Surg; 2009 Jun;13(6):1044-51
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  • [Title] Effectiveness of HSV-tk suicide gene therapy driven by the Grp78 stress-inducible promoter in esophagogastric junction and gastric adenocarcinomas.
  • This study investigated the effectiveness of HSV-tk activation as gene therapy for gastroesophageal junction and gastric adenocarcinomas using either the stress-inducible Grp78 promoter or the murine leukemia virus long-terminal repeat (LTR) promoter.
  • METHODS: The HSV-tk gene, controlled by either the Grp78 promoter or the LTR promoter, was transduced into the gastroesophageal junction adenocarcinoma cell line SK-GT-5 and the gastric adenocarcinoma cell line MKN-74.
  • The same cell lines were used to develop a nude mouse model for studies of the HSV-tk/GCV effect in vivo.
  • CONCLUSION: HSV-tk xwith ganciclovir suicide gene therapy results in significant cell killing in gastroesophageal junction and gastric adenocarcinoma cells both in vitro and in vivo, but complete tumor elimination only occurred with the gastric adenocarcinoma cell tumors.
  • [MeSH-major] Adenocarcinoma / therapy. Genes, Transgenic, Suicide / genetics. Genetic Therapy / methods. Heat-Shock Proteins / genetics. Stomach Neoplasms / therapy. Thymidine Kinase / genetics
  • [MeSH-minor] Animals. Antiviral Agents / pharmacology. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Ganciclovir / pharmacology. Gene Expression Regulation, Neoplastic. Genetic Vectors / genetics. Humans. Mice. Mice, Nude. Promoter Regions, Genetic. Reverse Transcriptase Polymerase Chain Reaction. Simplexvirus / enzymology. Simplexvirus / genetics. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 19277794.001).
  • [ISSN] 1873-4626
  • [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
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antiviral Agents; 0 / Heat-Shock Proteins; 0 / molecular chaperone GRP78; EC 2.7.1.21 / Thymidine Kinase; P9G3CKZ4P5 / Ganciclovir
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12. Shi Y, Hu W, Yin F, Sun L, Liu C, Lan M, Fan D: Regulation of drug sensitivity of gastric cancer cells by human calcyclin-binding protein (CacyBP). Gastric Cancer; 2004;7(3):160-6
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  • [Title] Regulation of drug sensitivity of gastric cancer cells by human calcyclin-binding protein (CacyBP).
  • BACKGROUND: Calcyclin-binding protein (CacyBP) was previously identified as an upregulated gene in a multidrug-resistant gastric cancer cell line, SGC7901/ADR, compared to its parental cells, SGC7901, by subtractive hybridization.
  • The aim of this study was to explore the role of CacyBP in multidrug resistance (MDR) in gastric cancer cells.
  • METHODS: The cDNA encoding CacyBP was generated by reverse-transcription-polymerase chain reaction (RT-PCR), and mouse antisera against CacyBP was raised using recombinant CacyBP as the immunogen.
  • The expression of CacyBP in gastric cancer cells was determined by Northern and Western blots.
  • The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay was performed to evaluate the drug sensitivity of gastric cancer cells.
  • Flow cytometry was employed to determine adriamycin accumulation and retention in gastric cancer cells.
  • Meanwhile, as compared with SGC7901/ADR, SGC7901/ADR-anCacyBP cells exhibited significantly decreased ( P < 0.01) IC(50) values for these three drugs.
  • CONCLUSIONS: Upregulation of CacyBP is associated with MDR in gastric cancer cells.
  • CacyBP could regulate the responses of gastric cancer cells to chemotherapy.
  • [MeSH-major] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Calcium-Binding Proteins / pharmacology. Drug Resistance, Multiple / genetics. Gene Expression Profiling. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology

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  • (PMID = 15449204.001).
  • [ISSN] 1436-3291
  • [Journal-full-title] Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association
  • [ISO-abbreviation] Gastric Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CACYBP protein, human; 0 / Calcium-Binding Proteins; 0 / DNA, Complementary
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13. Saikawa Y, Kubota T, Maeda S, Otani Y, Kumai K, Kitajima M: Inhibition of DNA methyltransferase by antisense oligodeoxynucleotide modifies cell characteristics in gastric cancer cell lines. Oncol Rep; 2004 Sep;12(3):527-31
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  • [Title] Inhibition of DNA methyltransferase by antisense oligodeoxynucleotide modifies cell characteristics in gastric cancer cell lines.
  • In the present study, we designed an antisense oligodeoxynucleotide of DNMT1 (AS/MT: 5'-CGGTAC GCGCCGGCATCT-3') and demonstrated successful inhibition of DNMT1 expression by AS/MT at the protein level, using gastric cancer cell lines in vitro.
  • E-cadherin protein expression was increased, and both cyclin D1 and PCNA were decreased by AS/MT treatment.
  • An in vivo model of peritoneal dissemination using the nude mouse system showed an increased malignant potential of AS/MT treated TMK-1 cells as demonstrated by a greater number of peritoneal tumor nodules in the AS/MT as compared to the NS/MT treated group, 34.8+/-4.3 vs. 22.4+/-3.0 nodules, respectively (p=0.0039).
  • In conclusion, the inhibition of DNA methylation by DNMT1 by an antisense oligodeoxynucleotide influences cell morphology and adhesion, as well as cell growth in gastric cancer cells in vitro.
  • Moreover, these alterations in the characteristics of cancer cells resulted in an increased ability to attach onto the peritoneum in the nude mouse system in vivo, suggesting that strict clinical guidelines will be necessary to utilize such a DNA methylation inhibitor, since it does not always mean a therapeutic antitumor strategy.
  • [MeSH-major] DNA (Cytosine-5-)-Methyltransferase / antagonists & inhibitors. Oligonucleotides, Antisense / pharmacology. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Animals. Base Sequence. Blotting, Western. Bromodeoxyuridine / pharmacology. Cadherins / metabolism. Cell Adhesion. Cell Division. Cell Line, Tumor. Cyclin D1 / metabolism. DNA Methylation. Dose-Response Relationship, Drug. Fibroblasts / metabolism. Humans. Immunohistochemistry. Mice. Mice, Nude. Molecular Sequence Data. Neoplasm Invasiveness. Proliferating Cell Nuclear Antigen / metabolism. Signal Transduction. Time Factors


14. Zhi M, Wu KC, Dong L, Hao ZM, Deng TZ, Hong L, Liang SH, Zhao PT, Qiao TD, Wang Y, Xu X, Fan DM: Characterization of a specific phage-displayed Peptide binding to vasculature of human gastric cancer. Cancer Biol Ther; 2004 Dec;3(12):1232-5
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  • [Title] Characterization of a specific phage-displayed Peptide binding to vasculature of human gastric cancer.
  • Antivascular therapy provides a promising method for anticancer therapy.
  • But targeting to gastric cancer vessels is nonselective due in part to the lack of specific cell-surface receptors identified on target vascular cells.
  • Herein we used in vivo screening of phage displayed peptide library to identify some peptides that bind selectively to endothelial cells of human gastric cancer rather than nonendothelial cells.
  • After four rounds of selection, one phage was obtained with a cyclic 7-mer peptide CGNSNPKSC homing to human gastric adenocarcinoma .
  • There was a 4.6 approximately 137.26-fold increase in the number of the selected phage in gastric cancer xenograft in comparision with control organs brain, heart, liver, spleen and kidney.
  • Immunohistochemistry in mouse and human tissue showed that this phage peptide only bind to the endothelial cells of human gastric cancer.
  • This peptide may be a possible candidate for targeted drug delivery in antivascular therapy.
  • [MeSH-minor] Animals. Humans. Mice. Mice, Inbred BALB C. Mice, SCID. Peptide Library. Protein Binding. Tissue Distribution

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  • (PMID = 15492500.001).
  • [ISSN] 1538-4047
  • [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 / Angiogenesis Inhibitors; 0 / Peptide Fragments; 0 / Peptide Library
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15. Zhao AG, Yang JK, You SF, Li T, Zhao HL, Gu Y, Tang LD: [Difference of gene expression profile in human gastric cancer grafted onto nude mice treated with WCA]. Zhongguo Zhong Yao Za Zhi; 2007 Oct;32(19):2028-36
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  • [Title] [Difference of gene expression profile in human gastric cancer grafted onto nude mice treated with WCA].
  • OBJECTIVE: Chinese jianpi herbal recipe Weichangan (WCA) could increase the survival rate of advanced gastric cancer.
  • This study was designed to investigate the molecular mechanism of WCA in treatment of gastric cancer by cDNA array, real-time quantitative PCR and immunohistochemical technique.
  • METHOD: A human gastric adenocarcinoma cell line SGC-7901 grafted onto nude mouse was used as the animal model.
  • To assess the effect of therapy tumor weight was determined by a electron balance immediately after the animals killed.
  • For detection of apoptotic cells, apoptotic indices (AI) were examined by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate fluorescence nick end labeling (TUNEL) method.
  • The expression profiles in paired WCA treated gastric cancer samples and the N. S. control samples were studied by using a cDNA array representing 14, 181 cDNA clusters.
  • The alterations in gene expression levels were confirmed by real-time quantitative PCR.
  • RESULT: When compared with controls, tumor growth was significantly inhibited by treatment with the WCA or 5-FU (P < 0.01, respectively).
  • AI of human gastric cancer xenografts in nude mice was significantly increased to (9.72 +/- 4.51)% using TUNEL method in WCA group compared with the controls (2.45 +/- 1.37)%.
  • By using Real-time Quantitative PCR, the expression level of Stat3 (2(-deltadeltaCT) = 0.16) , RIPX (2(-deltadeltaCT) = 0.18), ROD1 (2(-deltadeltaCT) = 0.23) and bcl-2 (2 (-deltadeltaCT) = 0.10) was lower in WCA group than that in control group respectively.
  • CONCLUSION: Chinese jianpi herbal recipe WCA could inhibit gastric cancer cell SGC-7901 growth in vivo.
  • WCA could induce gastric cancer cell apoptosis and suppress proliferation.
  • [MeSH-major] Adenocarcinoma / drug therapy. Drugs, Chinese Herbal / pharmacology. Gene Expression Profiling. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antimetabolites, Antineoplastic / pharmacology. Antimetabolites, Antineoplastic / therapeutic use. Apoptosis / drug effects. Caspase 3 / metabolism. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Combinations. Expressed Sequence Tags. Fluorouracil / pharmacology. Fluorouracil / therapeutic use. Humans. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Nerve Tissue Proteins / metabolism. Plants, Medicinal / chemistry. Polypyrimidine Tract-Binding Protein. Proliferating Cell Nuclear Antigen / metabolism. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA-Binding Proteins / metabolism. STAT3 Transcription Factor / metabolism. Xenograft Model Antitumor Assays / methods

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  • (PMID = 18161298.001).
  • [ISSN] 1001-5302
  • [Journal-full-title] Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica
  • [ISO-abbreviation] Zhongguo Zhong Yao Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / Drug Combinations; 0 / Drugs, Chinese Herbal; 0 / Nerve Tissue Proteins; 0 / PTBP3 protein, human; 0 / Proliferating Cell Nuclear Antigen; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA-Binding Proteins; 0 / STAT3 Transcription Factor; 0 / Singar1 protein, rat; 139076-35-0 / Polypyrimidine Tract-Binding Protein; EC 3.4.22.- / Caspase 3; U3P01618RT / Fluorouracil
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16. Xiao F, Crissey MA, Lynch JP, Kaestner KH, Silberg DG, Suh E: Intestinal metaplasia with a high salt diet induces epithelial proliferation and alters cell composition in the gastric mucosa of mice. Cancer Biol Ther; 2005 Jun;4(6):669-75
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  • [Title] Intestinal metaplasia with a high salt diet induces epithelial proliferation and alters cell composition in the gastric mucosa of mice.
  • Intestinal metaplasia of the gastric mucosa is an important component in the pathway to adenocarcinoma.
  • High dietary salt has been known as one of the risk factors for gastric cancer development in humans.
  • Therefore, we investigated the role of high salt diet on gastric epithelial cell proliferation and differentiation, using our mouse model that ectopically expressed Cdx2 homeodomain transcription factor and induced an intestinal metaplastic phenotype in the gastric epithelia.
  • Sixty Cdx2 transgenic and sixty age-matched wild-type littermates were studied.
  • Fifty-percent Cdx2 transgenic and wild type mice were administered a high-salt diet and the other fifty-percent was fed a standard diet starting at 12 weeks after birth.
  • Cell types and cell kinetics were assessed by immunohistochemistry.
  • At 52 weeks, significant alterations in pathology were observed in the Cdx2 transgenic mice fed a high-salt diet, including elongation of gastric pits, reduction of the glandular zone in the gastric corpus, and deepening of glands in the antrum.
  • In the Cdx2 transgenic mice fed a high salt diet, the parietal and chief cells were significantly decreased in the gastric corpus.
  • A significant increase in cell proliferation and apoptosis in the corpus and antrum were observed in Cdx2 transgenic mice fed a high-salt diet as compared to wild-type littermates.
  • Taken together, these data implicate that intestinal metaplasia in concert with a high-salt diet induces epithelial proliferation, apoptosis, and alters cellular types in the gastric mucosa of mice.
  • Alteration in the composition of the gastric epithelium may play a role in influencing the microenvironment to engender susceptibility to carcinogens.
  • [MeSH-major] Gastric Mucosa / pathology. Intestine, Small / pathology. Sodium Chloride, Dietary / administration & dosage
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cell Differentiation / drug effects. Cell Lineage. Cell Proliferation / drug effects. Homeodomain Proteins / physiology. Immunohistochemistry. Metaplasia. Mice. Mice, Transgenic. Reverse Transcriptase Polymerase Chain Reaction. Transcription Factors / physiology

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  • (PMID = 15970710.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / P30-DK-50306; United States / NIDDK NIH HHS / DK / R01-DK46704; United States / NIDDK NIH HHS / DK / R01-DK59539
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cdx2 protein, mouse; 0 / Homeodomain Proteins; 0 / Sodium Chloride, Dietary; 0 / Transcription Factors
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17. Zhu JS, Song MQ, Chen GQ, Li Q, Sun Q, Zhang Q: Molecular mechanisms of paclitaxel and NM-3 on human gastric cancer in a severe combined immune deficiency mice orthotopic implantation model. World J Gastroenterol; 2007 Aug 14;13(30):4131-5
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  • [Title] Molecular mechanisms of paclitaxel and NM-3 on human gastric cancer in a severe combined immune deficiency mice orthotopic implantation model.
  • AIM: To explore the molecular mechanisms of action of paclitaxel and NM-3 on human gastric cancer in severe combined immune deficiency (SCID) mice.
  • METHODS: Human gastric cancer cells SGC-7901 were implanted into SCID mice and mice were treated with paclitaxel and NM-3.
  • The effects of paclitaxel and NM-3 on apoptosis of human gastric cancer cells were analyzed using flow cytometry, TUNEL assays, and DNA fragment analyses.
  • CONCLUSION: Paclitaxel in combination with NM-3 is able to induce apoptosis of the human gastric cancer cells in SCID mice effectively and synergistically.
  • [MeSH-major] Adenocarcinoma / drug therapy. Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Isocoumarins / pharmacology. Paclitaxel / pharmacology. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Antigens, Viral, Tumor / drug effects. Antigens, Viral, Tumor / genetics. Cell Line, Tumor. Disease Models, Animal. Drug Synergism. Drug Therapy, Combination. Humans. Male. Mice. Mice, Nude. Mice, SCID. Viral Core Proteins / drug effects. Viral Core Proteins / genetics. Xenograft Model Antitumor Assays

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  • (PMID = 17696236.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Viral, Tumor; 0 / Antineoplastic Agents; 0 / Isocoumarins; 0 / Viral Core Proteins; 0 / isocoumarin NM-3; 0 / p27 antigen, Mouse mammary tumor virus; P88XT4IS4D / Paclitaxel
  • [Other-IDs] NLM/ PMC4205319
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18. Chen L, Chen D, Gong M, Na M, Li L, Wu H, Jiang L, Qian Y, Fang G, Xue X: Concomitant use of Ad5/35 chimeric oncolytic adenovirus with TRAIL gene and taxol produces synergistic cytotoxicity in gastric cancer cells. Cancer Lett; 2009 Nov 1;284(2):141-8
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  • [Title] Concomitant use of Ad5/35 chimeric oncolytic adenovirus with TRAIL gene and taxol produces synergistic cytotoxicity in gastric cancer cells.
  • Chimeric adenoviral vectors possessing fiber derived from human adenovirus subgroup B (Ad35) have been developed for their high infection efficiency in cell types which are refractory to adenovirus serotype 5 (Subgroup C).
  • It was found that SG235-TRAIL preferentially replicated in gastric cancer cell lines, SGC-7901 and BGC-823 compared to in normal human fibroblast BJ cells.
  • In addition, SG235-TRAIL in combination with the chemotherapeutic drug, taxol, produced a synergistic cytotoxic effect in cancer cells in vitro without causing significant toxicity to normal cells.
  • In the gastric tumor xenograft mouse model, intratumoral SG235-TRAIL injection produced a significant antitumor effect 14 days after treatment.
  • [MeSH-major] Adenocarcinoma / therapy. Adenoviruses, Human / genetics. Antineoplastic Agents, Phytogenic / therapeutic use. Genetic Therapy. Genetic Vectors / therapeutic use. Paclitaxel / therapeutic use. Stomach Neoplasms / therapy. TNF-Related Apoptosis-Inducing Ligand / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor / drug effects. Cell Line, Tumor / virology. Combined Modality Therapy. Defective Viruses / physiology. Fibroblasts / virology. Genes, Synthetic. Humans. Mice. Recombinant Fusion Proteins / genetics. Recombinant Fusion Proteins / therapeutic use. Transgenes. Virus Replication. Xenograft Model Antitumor Assays

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  • [Copyright] 2009 Elsevier Ireland Ltd.
  • (PMID = 19447545.001).
  • [ISSN] 1872-7980
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Recombinant Fusion Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; P88XT4IS4D / Paclitaxel
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19. Xie YS, Zhang YH, Liu SP, Liu SQ, Peng CW, Wu L, Luo HS, Li Y: Synergistic gastric cancer inhibition by chemogenetherapy with recombinant human adenovirus p53 and epirubicin: an in vitro and in vivo study. Oncol Rep; 2010 Dec;24(6):1613-20
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  • [Title] Synergistic gastric cancer inhibition by chemogenetherapy with recombinant human adenovirus p53 and epirubicin: an in vitro and in vivo study.
  • This study was designed to investigate the in vitro and in vivo antitumor effect on SGC-7901 gastric cancer cells by chemogenetherapy.
  • SGC-7901 cells were treated by chemogenetherapy with Gendicine, a recombinant human Ad-p53 injection (rAd-p53), and epirubicin hydrochloride (EPI), a cytotoxic chemotherapy agent.
  • Compared with blank control, rAd-p53, EPI, and combined therapy achieved SGC-7901 growth inhibition by 32.26, 35.48, 43.44%, respectively on day 1 and 70.62, 78.82, 87.15%, respectively on day 2 (rAd-p53, EPI VS control, p<0.01; rAd-p53+EPI VS either alone, p<0.05).
  • Compared with the blank control, treatment with rAd-p53 at the dose of 10 ┬Ál of 10(12) vp/ml and EPI at the dose of 1.25 mg/kg, 7 times in 3 weeks, resulted in 80 and 60% of tumor growth inhibition, respectively.
  • No animal death was observed, although 2 nude mice in rAd-p53 group developed liver toxicity and 1 nude mouse in EPI group developed cardiac toxicity. rAd-p53 and EPI have synergistic tumor inhibition effect on gastric cancer cells.
  • [MeSH-major] Adenocarcinoma / therapy. Epirubicin / therapeutic use. Stomach Neoplasms / therapy. Tumor Suppressor Protein p53 / genetics
  • [MeSH-minor] Adenoviridae / genetics. Adenoviridae / physiology. Algorithms. Animals. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Combined Modality Therapy. Drug Synergism. Female. Genetic Therapy. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Models, Biological. Recombinant Proteins / genetics. Xenograft Model Antitumor Assays

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  • (PMID = 21042759.001).
  • [ISSN] 1791-2431
  • [Journal-full-title] Oncology reports
  • [ISO-abbreviation] Oncol. Rep.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 0 / Tumor Suppressor Protein p53; 3Z8479ZZ5X / Epirubicin
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20. Nakamura K, Yashiro M, Matsuoka T, Tendo M, Shimizu T, Miwa A, Hirakawa K: A novel molecular targeting compound as K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, for Scirrhous gastric cancer. Gastroenterology; 2006 Nov;131(5):1530-41
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  • [Title] A novel molecular targeting compound as K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, for Scirrhous gastric cancer.
  • BACKGROUND & AIMS: Scirrhous gastric carcinoma carries the highest mortality of all gastric cancers.
  • The poor prognosis is reported to be associated with K-samII amplification, which encodes fibroblast growth factor receptor type 2 (FGF-R2).
  • Ki23057, a newly developed small molecule-acting K-samII/FGF-R2 autophosphorylation inhibitor, is a tyrosine kinase inhibitor that competes with adenosine triphosphate for the binding site.
  • The aim of the current study is to clarify the possibility of molecular target therapy with Ki23057 for treating scirrhous gastric cancer.
  • METHODS: Five human gastric cancer cell lines were used.
  • The influences of Ki23057 on the mitogen-activated protein kinase and phosphatidylinositol 3 kinase signaling pathways and the apoptosis pathway in the gastric cancer cells were also examined.
  • For in vivo experiments, the Ki23057 was administered orally to mouse models of peritoneal dissemination.
  • Ki23057 significantly inhibited the proliferation of scirrhous cancer cells but not nonscirrhous gastric carcinoma cells.
  • CONCLUSIONS: A novel K-samII/FGF-R2 phosphorylation inhibitor, Ki23057, appears therapeutically promising in scirrhous gastric carcinoma with K-samII amplification.
  • [MeSH-major] Adenocarcinoma, Scirrhous / drug therapy. Protein Kinase Inhibitors / pharmacology. Quinolines / pharmacology. Receptor, Epidermal Growth Factor / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Peritoneal Neoplasms / pathology. Phosphorylation. Receptor, ErbB-2. Signal Transduction. Transplantation, Heterologous


21. Zhao AG, Zhao HL, Jin XJ, Yang JK, Tang LD: Effects of Chinese Jianpi herbs on cell apoptosis and related gene expression in human gastric cancer grafted onto nude mice. World J Gastroenterol; 2002 Oct;8(5):792-6
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  • [Title] Effects of Chinese Jianpi herbs on cell apoptosis and related gene expression in human gastric cancer grafted onto nude mice.
  • AIM: To explore the mechanism of the Sijunzi decoction and another Chinese herbal recipe (SRRS) based mainly on the Sijunzi decoction in treatment of gastric cancer.
  • METHODS: A human gastric adenocarcinoma cell line SGC-7901 grafted onto nude mouse was used as the animal model.
  • The effect of therapy was assessed by two ways:.
  • For detection of apoptotic cells, apoptotic indices(AI) were examined by the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate fluorescence nick end labeling (TUNEL) method.
  • RESULTS: When compared with controls, tumor growth (size and weight) was significantly inhibited by treatment with the Sijunzi decoction (P<0.05) or SRRS (P<0.01).
  • AI of human gastric cancer xenografts in nude mice was significantly increased to 16.24+/-3.21 % using TUNEL method and 11.38+/-6.46 % by FACScan in the Sijunzi decoction group compared with the controls (TUNEL: 2.63+/-1.03 %, P<0.01; FACScan: 7.15+/- 1.32 %, P<0.05).
  • CONCLUSION: The inhibition of gastric cancer cell growth in vivo by Chinese Jianpi herbs and SRRS is related to induction of the cell apoptosis which may be involved in aberrant expression of p53 and bcl-2 genes.
  • [MeSH-major] Apoptosis / drug effects. Drugs, Chinese Herbal / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Division / drug effects. Female. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Proto-Oncogene Proteins c-bcl-2 / genetics. RNA, Messenger / analysis. Tumor Suppressor Protein p53 / genetics

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  • (PMID = 12378617.001).
  • [ISSN] 1007-9327
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Drugs, Chinese Herbal; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / Tumor Suppressor Protein p53
  • [Other-IDs] NLM/ PMC4656563
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22. Kinoshita J, Fushida S, Harada S, Yagi Y, Fujita H, Kinami S, Ninomiya I, Fujimura T, Kayahara M, Yashiro M, Hirakawa K, Ohta T: Local angiotensin II-generation in human gastric cancer: correlation with tumor progression through the activation of ERK1/2, NF-kappaB and survivin. Int J Oncol; 2009 Jun;34(6):1573-82
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  • [Title] Local angiotensin II-generation in human gastric cancer: correlation with tumor progression through the activation of ERK1/2, NF-kappaB and survivin.
  • Angiotensin II is a main effector peptide in renin-angiotensin system, acting as a growth promoter via angiotensin II type 1 (AT1) receptor.
  • The present study examined intrinsic angiotensin II generating system in gastric cancer and potential roles of angiotensin II in cellular proliferation and survival.
  • The expression of AT1 receptor was examined in gastric cancer cell lines and tissues.
  • In addition, we measured angiotensin II concentration in tissues from twenty gastric cancer and corresponding normal region using the florisil method.
  • In vitro, we investigated the potential roles of angiotensin II in cellular proliferation and cell survival in cultured human gastric cancer cell line.
  • The effects of AT1 receptor blocker candesartan were evaluated in a mouse model of peritoneal carcinomatosis.
  • AT1 receptor protein was expressed in gastric cancer cell lines and tissues.
  • Angiotensin II stimulates the cell proliferation in the AT1 receptor-positive OCUM2MD3 gastric cancer cell line and this proliferative effect of angiotensin II was inhibited by a specific AT1 receptor antagonist, candesartan.
  • Candesartan significantly prolonged survival time in a mouse model of peritoneal carcinomatosis compared with control group (p=0.0.197, log-rank test).
  • Our data provide in vivo evidence of intrinsic angiotensin II generating system in gastric cancer and indicate locally formed angiotensin II is involved in cellular proliferation and survival.
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / metabolism. Adenocarcinoma / secondary. Adenocarcinoma, Clear Cell / drug therapy. Adenocarcinoma, Clear Cell / metabolism. Adenocarcinoma, Clear Cell / secondary. Adenocarcinoma, Mucinous / drug therapy. Adenocarcinoma, Mucinous / metabolism. Adenocarcinoma, Mucinous / secondary. Adult. Aged. Angiotensin II Type 1 Receptor Blockers / pharmacology. Animals. Apoptosis / drug effects. Benzimidazoles / pharmacology. Blotting, Western. Carcinoma, Medullary / drug therapy. Carcinoma, Medullary / metabolism. Carcinoma, Medullary / secondary. Case-Control Studies. Cell Proliferation / drug effects. Disease Progression. Electrophoretic Mobility Shift Assay. Female. Humans. Immunoenzyme Techniques. Inhibitor of Apoptosis Proteins. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Middle Aged. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / metabolism. Peritoneal Neoplasms / pathology. Receptor, Angiotensin, Type 1 / chemistry. Receptor, Angiotensin, Type 1 / drug effects. Receptor, Angiotensin, Type 1 / metabolism. Stomach / metabolism. Stomach / pathology. Survival Rate. Tetrazoles / pharmacology. Tumor Cells, Cultured

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  • (PMID = 19424575.001).
  • [ISSN] 1019-6439
  • [Journal-full-title] International journal of oncology
  • [ISO-abbreviation] Int. J. Oncol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / BIRC5 protein, human; 0 / Benzimidazoles; 0 / Inhibitor of Apoptosis Proteins; 0 / Microtubule-Associated Proteins; 0 / NF-kappa B; 0 / Receptor, Angiotensin, Type 1; 0 / Tetrazoles; 11128-99-7 / Angiotensin II; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 1; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3; S8Q36MD2XX / candesartan
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23. Kawajiri H, Yashiro M, Shinto O, Nakamura K, Tendo M, Takemura S, Node M, Hamashima Y, Kajimoto T, Sawada T, Ohira M, Hirakawa K: A novel transforming growth factor beta receptor kinase inhibitor, A-77, prevents the peritoneal dissemination of scirrhous gastric carcinoma. Clin Cancer Res; 2008 May 1;14(9):2850-60
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  • [Title] A novel transforming growth factor beta receptor kinase inhibitor, A-77, prevents the peritoneal dissemination of scirrhous gastric carcinoma.
  • PURPOSE: Transforming growth factor beta receptor (TGFbeta-R) is reported to correlate with the malignant potential of scirrhous gastric carcinoma.
  • The aim of the current study is to clarify the possibility of molecular target therapy with a TGFbeta-R inhibitor, A-77, for the treatment of peritoneal dissemination of scirrhous gastric cancer.
  • EXPERIMENTAL DESIGN: Three scirrhous gastric cancer cell lines and two fibroblasts were used.
  • For in vivo experiments, the A-77 was administered i.p. to mouse models of peritoneal dissemination.
  • RESULTS: The A-77 administration resulted in a significantly (P < 0.01) better prognosis for the mice with peritoneal dissemination (median survival time, 51 days), compared with the control (median survival time, 25 days).
  • A-77 decreased the expression of alpha(2), alpha(3), and alpha(5) integrins in gastric cancer cells.
  • CONCLUSION: The TGFbeta-R inhibitor, A-77, decreased the expression of integrins in cancer cells and the proliferation of fibroblasts, which resulted in the decreased adhesive and invasive abilities of scirrhous gastric cancer cells to peritoneum.
  • A-77 is thus considered to be useful for the inhibition of peritoneal dissemination of scirrhous gastric carcinoma.
  • [MeSH-major] Adenocarcinoma, Scirrhous / drug therapy. Antineoplastic Agents / therapeutic use. Neoplasm Metastasis / prevention & control. Peritoneal Neoplasms / secondary. Pyrazoles / therapeutic use. Quinolines / therapeutic use. Receptors, Transforming Growth Factor beta / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Integrins / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Invasiveness. Phosphorylation. RNA, Small Interfering / metabolism. Smad2 Protein / metabolism

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  • (PMID = 18451253.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / A-77 compound; 0 / Antineoplastic Agents; 0 / Integrins; 0 / Pyrazoles; 0 / Quinolines; 0 / RNA, Small Interfering; 0 / Receptors, Transforming Growth Factor beta; 0 / Smad2 Protein
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24. Matsumoto K, Konno H, Tanaka T, Baba M, Kanai T, Kamiya K, Ohba K, Nakamura S: Combination therapy with vascular endothelial growth factor neutralizing antibody and mitomycin C on human gastric cancer xenograft. Jpn J Cancer Res; 2000 Jul;91(7):748-52
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  • [Title] Combination therapy with vascular endothelial growth factor neutralizing antibody and mitomycin C on human gastric cancer xenograft.
  • Antiangiogenic therapy has been proposed as a new strategy for the treatment of solid tumors.
  • To enhance the therapeutic effect of antiangiogenic agents, combination with conventional anticancer therapy should be investigated.
  • In the present study, we investigated the therapeutic effect of the combination of vascular endothelial growth factor neutralizing antibody (VEGF Ab) and mitomycin C (MMC) on MT-2, a human gastric cancer xenograft.
  • When small pieces of MT-2 were transplanted orthotopically into 62 nude mice, liver metastasis developed 6 weeks after transplantation.
  • The VEGF Ab (100 micro g / mouse) was administered i.p. in the VEGF Ab group (n = 14) and the combination group (n = 16) twice a week from day 10 after transplantation.
  • Compared with the control group, in which saline solution was administered i.p., all three treatments inhibited tumor growth significantly and the effects of MMC and combination therapy were potent.
  • Liver metastases were also inhibited significantly by the administration of VEGF Ab alone, MMC alone or combination therapy.
  • Liver metastasis developed in 9 mice of the control group, 3 of the VEGF Ab group, and 4 of the MMC group, but no mice had liver metastasis in the combination therapy group.
  • These results suggest that combination therapy with VEGF Ab and MMC may be a potent therapy for human gastric cancer.
  • [MeSH-major] Adenocarcinoma / therapy. Antibiotics, Antineoplastic / pharmacology. Antibodies, Monoclonal / pharmacology. Endothelial Growth Factors / immunology. Lymphokines / immunology. Mitomycin / pharmacology. Neovascularization, Pathologic / therapy. Stomach Neoplasms / therapy
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Division / drug effects. Cell Division / physiology. Combined Modality Therapy. Humans. Liver Neoplasms, Experimental / blood supply. Liver Neoplasms, Experimental / prevention & control. Liver Neoplasms, Experimental / secondary. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Organ Size / drug effects. Spleen / anatomy & histology. Spleen / drug effects. Transplantation, Heterologous. Tumor Cells, Cultured. Vascular Endothelial Growth Factor A. Vascular Endothelial Growth Factors

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  • (PMID = 10920283.001).
  • [ISSN] 0910-5050
  • [Journal-full-title] Japanese journal of cancer research : Gann
  • [ISO-abbreviation] Jpn. J. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Antibodies, Monoclonal; 0 / Endothelial Growth Factors; 0 / Lymphokines; 0 / Vascular Endothelial Growth Factor A; 0 / Vascular Endothelial Growth Factors; 50SG953SK6 / Mitomycin
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25. Ninomiya S, Inomata M, Tajima M, Ali AT, Ueda Y, Shiraishi N, Kitano S: Effect of bevacizumab, a humanized monoclonal antibody to vascular endothelial growth factor, on peritoneal metastasis of MNK-45P human gastric cancer in mice. J Surg Res; 2009 Jun 15;154(2):196-202
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  • [Title] Effect of bevacizumab, a humanized monoclonal antibody to vascular endothelial growth factor, on peritoneal metastasis of MNK-45P human gastric cancer in mice.
  • BACKGROUND: The aim of this study was to clarify the effect of bevacizumab on gastric cancer with peritoneal metastasis in nude mice.
  • MATERIALS AND METHODS: The expression of vascular endothelial growth factor mRNA (VEGF mRNA) in four gastric cancer cell lines, NCI-N87, MKN-45, MKN-45P, and Kato-III, was examined by polymerase chain reaction.
  • We created a model of peritoneal metastasis by injecting mice with the human gastric cancer cell line MKN-45P.
  • Mice were injected intraperitoneally with bevacizumab (0.1 mg/100 microL) on days 5-14, after inoculation (n = 10) or with phosphate-buffered saline (PBS) over the same time period (n = 10).
  • [MeSH-major] Adenocarcinoma / secondary. Angiogenesis Inhibitors / pharmacology. Antibodies, Monoclonal / pharmacology. Peritoneal Neoplasms / secondary. Stomach Neoplasms / pathology. Vascular Endothelial Growth Factor A / immunology
  • [MeSH-minor] Animals. Antibodies, Monoclonal, Humanized. Bevacizumab. Cell Line, Tumor. Disease Models, Animal. Female. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / drug therapy

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  • (PMID = 19329124.001).
  • [ISSN] 1095-8673
  • [Journal-full-title] The Journal of surgical research
  • [ISO-abbreviation] J. Surg. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Angiogenesis Inhibitors; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse; 2S9ZZM9Q9V / Bevacizumab
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26. Otto C, Kaemmerer U, Illert B, Muehling B, Pfetzer N, Wittig R, Voelker HU, Thiede A, Coy JF: Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides. BMC Cancer; 2008;8:122
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  • [Title] Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides.
  • This phenomenon, known as aerobic glycolysis or the Warburg effect, may provide a rationale for therapeutic strategies that inhibit tumour growth by administration of a ketogenic diet with average protein but low in carbohydrates and high in fat enriched with omega-3 fatty acids and medium-chain triglycerides (MCT).
  • METHODS: Twenty-four female NMRI nude mice were injected subcutaneously with tumour cells of the gastric adenocarcinoma cell line 23132/87.
  • The two diets were compared based on tumour growth and survival time (interval between tumour cell injection and attainment of target tumour volume).
  • CONCLUSION: Application of an unrestricted ketogenic diet enriched with omega-3 fatty acids and MCT delayed tumour growth in a mouse xenograft model.
  • [MeSH-major] Adenocarcinoma / diet therapy. Diet, Carbohydrate-Restricted. Fatty Acids, Omega-3 / administration & dosage. Stomach Neoplasms / diet therapy. Triglycerides / administration & dosage
  • [MeSH-minor] 3-Hydroxybutyric Acid. Animals. Biomarkers, Tumor / biosynthesis. Cell Line, Tumor. Female. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Neovascularization, Pathologic / diet therapy. Tumor Burden / drug effects

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  • (PMID = 18447912.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Fatty Acids, Omega-3; 0 / Triglycerides; TZP1275679 / 3-Hydroxybutyric Acid
  • [Other-IDs] NLM/ PMC2408928
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27. Hahm KB, Kim DH, Lee KM, Lee JS, Surh YJ, Kim YB, Yoo BM, Kim JH, Joo HJ, Cho YK, Nam KT, Cho SW: Effect of long-term administration of rebamipide on Helicobacter pylori infection in mice. Aliment Pharmacol Ther; 2003 Jul;18 Suppl 1:24-38
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  • One of the potential clinical applications of rebamipide is the inhibition of the immunoinflammatory response in gastric mucosa imposed by Helicobacter pylori.
  • AIM: To determine the implications of long-term rebamipide treatment in H. pylori infection, we studied the underlying moleculo-pathological changes in gastric lesions in mice infected with H. pylori (SS1 strain), following this treatment.
  • Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels of IL-1beta, TNF-alpha, IFN-gamma and IL-10, mRNA transcripts of various mouse cytokines and chemokines, and NF-kappaB binding activities, and finally the presence of gastric adenocarcinoma were compared between an H. pylori infected group (HP), and an H. pylori infected group administered with long-term rebamipide-containing pellet diets (HPR).
  • RESULTS: Serum levels of IL-1beta, IFN-gamma and TNF-alpha, the gastric mucosal expression of ICAM-1, HCAM and MMP, and transcriptional regulation of NF-kappaB-DNA binding were all significantly decreased in the HPR group compared with the HP group.
  • In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not different in either group.
  • CONCLUSION: The long-term administration of rebamipide should be considered in the treatment of H. pylori since it demonstrated molecular and biological advantages like a lessening of gastric inflammation and a possible chemopreventive effect.
  • [MeSH-major] Alanine / analogs & derivatives. Alanine / therapeutic use. Anti-Ulcer Agents / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. Quinolones / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Blotting, Western. Cytokines / metabolism. Gastric Mucosa / microbiology. Gastric Mucosa / pathology. Gastritis / microbiology. Gastritis / pathology. Immunohistochemistry. Matrix Metalloproteinases / metabolism. Mice. Mice, Inbred C57BL. NF-kappa B / metabolism. Protein Binding. Proteins / metabolism. RNA, Messenger / metabolism

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  • (PMID = 12925138.001).
  • [ISSN] 0269-2813
  • [Journal-full-title] Alimentary pharmacology & therapeutics
  • [ISO-abbreviation] Aliment. Pharmacol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Cytokines; 0 / NF-kappa B; 0 / Proteins; 0 / Quinolones; 0 / RNA, Messenger; 111911-87-6 / rebamipide; EC 3.4.24.- / Matrix Metalloproteinases; OF5P57N2ZX / Alanine
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28. Yasui H, Inanami O, Asanuma T, Iizuka D, Nakajima T, Kon Y, Matsuda A, Kuwabara M: Treatment combining X-irradiation and a ribonucleoside anticancer drug, TAS106, effectively suppresses the growth of tumor cells transplanted in mice. Int J Radiat Oncol Biol Phys; 2007 May 1;68(1):218-28
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  • [Title] Treatment combining X-irradiation and a ribonucleoside anticancer drug, TAS106, effectively suppresses the growth of tumor cells transplanted in mice.
  • PURPOSE: To examine the in vivo antitumor efficacy of X-irradiation combined with administration of a ribonucleoside anticancer drug, 1-(3-C-ethynyl-beta-D-ribo-pentofuranosyl)cytosine (TAS106, ECyd), to tumor cell-transplanted mice.
  • METHODS AND MATERIALS: Colon26 murine rectum adenocarcinoma cells and MKN45 human gastric adenocarcinoma cells were inoculated into the footpad in BALB/c mice and severe combined immunodeficient mice, respectively.
  • They were treated with a relatively low dose of X-irradiation (2 Gy) and low amounts of TAS106 (0.1 mg/kg and 0.5 mg/kg).
  • RESULTS: When X-irradiation and TAS106 treatment were combined, significant inhibition of tumor growth was observed in both types of tumors compared with mice treated with X-irradiation or TAS106 alone.
  • Marked inhibition of tumor growth was observed in half of the mice that received the combined treatment three times at 2-day intervals.
  • [MeSH-major] Adenocarcinoma. Antineoplastic Agents / therapeutic use. Colonic Neoplasms. Cytidine / analogs & derivatives. Stomach Neoplasms
  • [MeSH-minor] Animals. Combined Modality Therapy. Drug Evaluation, Preclinical. Female. Inhibitor of Apoptosis Proteins. Ki-67 Antigen / metabolism. Mice. Mice, Inbred BALB C. Mice, Inbred ICR. Microtubule-Associated Proteins / metabolism. Neoplasm Proteins / metabolism. Neoplasm Transplantation. Repressor Proteins

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  • (PMID = 17448876.001).
  • [ISSN] 0360-3016
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 1-(3-C-ethynylribopentofuranosyl)cytosine; 0 / Antineoplastic Agents; 0 / Birc5 protein, mouse; 0 / Inhibitor of Apoptosis Proteins; 0 / Ki-67 Antigen; 0 / Microtubule-Associated Proteins; 0 / Mki67 protein, mouse; 0 / Neoplasm Proteins; 0 / Repressor Proteins; 5CSZ8459RP / Cytidine
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29. Wang Y, Adachi Y, Imsumran A, Yamamoto H, Piao W, Li H, Ii M, Arimura Y, Park MY, Kim D, Lee CT, Carbone DP, Imai K, Shinomura Y: Targeting for insulin-like growth factor-I receptor with short hairpin RNA for human digestive/gastrointestinal cancers. J Gastroenterol; 2010 Feb;45(2):159-70
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  • METHODS: We constructed a recombinant adenovirus expressing short hairpin RNA targeting IGF-IR (shIGF-IR) and assessed its effect on signal transduction, proliferation, and survival in digestive/gastrointestinal cancer cell lines representing colorectal, gastric, and pancreatic adenocarcinoma, esophageal squamous cell carcinoma, and hepatoma.
  • We analyzed the effects of shIGF-IR alone and with chemotherapy in vitro and in nude mouse xenografts, as well as on insulin signaling and hybrid receptor formation between IGF-IR and insulin receptor.
  • RESULTS: shIGF-IR blocked expression and autophosphorylation of IGF-IR and downstream signaling by the IGFs, but not by insulin. shIGF-IR suppressed proliferation and carcinogenicity in vitro and up-regulated apoptosis in a dose-dependent fashion. shIGF-IR augmented the effects of chemotherapy on in vitro growth and apoptosis induction.
  • Moreover, the combination of shIGF-IR and chemotherapy was highly effective against tumors in mice. shIGF-IR reduced hybrid receptor formation without effect on expression of insulin receptor.
  • CONCLUSIONS: shIGF-IR may have therapeutic utility in human digestive/gastrointestinal cancers, both alone and in combination with chemotherapy.
  • [MeSH-major] Gastrointestinal Neoplasms / therapy. RNA, Small Interfering / administration & dosage. Receptor, IGF Type 1 / antagonists & inhibitors. Receptor, Insulin / metabolism
  • [MeSH-minor] Adenoviridae / genetics. Animals. Antineoplastic Agents / pharmacology. Apoptosis. Cell Line, Tumor. Cell Proliferation. Combined Modality Therapy. Dose-Response Relationship, Drug. Female. Gene Targeting / methods. Genetic Vectors. Humans. Insulin / metabolism. Mice. Mice, Inbred BALB C. Mice, Nude. Signal Transduction. Xenograft Model Antitumor Assays

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  • (PMID = 19902140.001).
  • [ISSN] 1435-5922
  • [Journal-full-title] Journal of gastroenterology
  • [ISO-abbreviation] J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Insulin; 0 / RNA, Small Interfering; EC 2.7.10.1 / Receptor, IGF Type 1; EC 2.7.10.1 / Receptor, Insulin
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30. Subramaniam D, May R, Sureban SM, Lee KB, George R, Kuppusamy P, Ramanujam RP, Hideg K, Dieckgraefe BK, Houchen CW, Anant S: Diphenyl difluoroketone: a curcumin derivative with potent in vivo anticancer activity. Cancer Res; 2008 Mar 15;68(6):1962-9
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  • Here, we assessed the in vivo therapeutic effects of EF24 on colon cancer cells.
  • Using hexosaminidase assay, we determined that EF24 inhibits proliferation of HCT-116 and HT-29 colon and AGS gastric adenocarcinoma cells but not of mouse embryo fibroblasts.
  • At the same time, cell cycle analysis showed that there was an increased number of cells in the G(2)-M phase.
  • Taken together, these data suggest that the novel curcumin-related compound EF24 is a potent antitumor agent that induces caspase-mediated apoptosis during mitosis and has significant therapeutic potential for gastrointestinal cancers.
  • [MeSH-major] Adenocarcinoma / drug therapy. Benzylidene Compounds / pharmacology. Colonic Neoplasms / drug therapy. Piperidones / pharmacology. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Cell Cycle / drug effects. Cell Growth Processes / drug effects. Cell Line, Tumor. Cyclooxygenase 2 / biosynthesis. Cyclooxygenase 2 / genetics. HCT116 Cells. HT29 Cells. Humans. Interleukin-8 / biosynthesis. Interleukin-8 / genetics. MAP Kinase Signaling System / drug effects. Male. Mice. Mice, Nude. Neovascularization, Pathologic / drug therapy. Neovascularization, Pathologic / pathology. Vascular Endothelial Growth Factor A / biosynthesis. Vascular Endothelial Growth Factor A / genetics. Xenograft Model Antitumor Assays

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  • (PMID = 18339878.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCCIH NIH HHS / AT / AT004118; United States / NCI NIH HHS / CA / CA109269; United States / NIDDK NIH HHS / DK / DK62265
  • [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 / 3,5-bis(2-fluorobenzylidene)piperidin-4-one; 0 / Benzylidene Compounds; 0 / Interleukin-8; 0 / Piperidones; 0 / Vascular Endothelial Growth Factor A; EC 1.14.99.1 / Cyclooxygenase 2
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31. Yasui H, Ogura A, Asanuma T, Matsuda A, Kashiwakura I, Kuwabara M, Inanami O: Inhibition of HIF-1alpha by the anticancer drug TAS106 enhances X-ray-induced apoptosis in vitro and in vivo. Br J Cancer; 2008 Nov 4;99(9):1442-52

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  • [Title] Inhibition of HIF-1alpha by the anticancer drug TAS106 enhances X-ray-induced apoptosis in vitro and in vivo.
  • In a previous study, we showed that a novel anticancer drug, 1-(3-C-ethynyl-beta-D-ribo-pentofuranosyl)cytosine (TAS106, ECyd) increased the antitumour efficacy of X-irradiation.
  • Here, we show that TAS106 enhances the induction of apoptosis in X-irradiated human gastric adenocarcinoma MKN45 and MKN28 cells under hypoxia in vitro.
  • At the same time, the accumulation of HIF-1alpha observed under hypoxia was shown to be decreased to the level of normoxia in the presence of 0.1 microM TAS106.
  • In in vivo experiments in which MKN45 cells were transplanted into severe combined immunodeficient (SCID) mice, TAS106 (0.5 mg kg(-1)) suppressed HIF-1alpha expression and subsequently reduced the area of the hypoxic region in the tumour and enhanced the induction of apoptosis in the hypoxic region when combined with 2 Gy of X-irradiation.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Apoptosis / drug effects. Hypoxia-Inducible Factor 1, alpha Subunit / antagonists & inhibitors. Radiation-Sensitizing Agents / pharmacology
  • [MeSH-minor] Animals. Cell Cycle. Cell Line, Tumor. Cell Survival / drug effects. Humans. Mice. Mice, SCID. Neoplasms, Experimental / pathology. Neoplasms, Experimental / therapy. Oligonucleotides, Antisense / pharmacology. Transcription, Genetic / drug effects. Uridine Kinase / genetics. Uridine Kinase / physiology. Vascular Endothelial Growth Factor A / genetics. X-Ray Therapy

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  • (PMID = 18854835.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / HIF1A protein, human; 0 / Hif1a protein, mouse; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Oligonucleotides, Antisense; 0 / Radiation-Sensitizing Agents; 0 / Vascular Endothelial Growth Factor A; EC 2.7.1.48 / UCK2 protein, human; EC 2.7.1.48 / Uridine Kinase
  • [Other-IDs] NLM/ PMC2579694
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32. Sorenson JR, Wangila GW: Co-treatment with copper compounds dramatically decreases toxicities observed with cisplatin cancer therapy and the anticancer efficacy of some copper chelates supports the conclusion that copper chelate therapy may be markedly more effective and less toxic than cisplatin therapy. Curr Med Chem; 2007;14(14):1499-503
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  • [Title] Co-treatment with copper compounds dramatically decreases toxicities observed with cisplatin cancer therapy and the anticancer efficacy of some copper chelates supports the conclusion that copper chelate therapy may be markedly more effective and less toxic than cisplatin therapy.
  • Initially it was found that copper sulfate treatment completely prevented lethality as well as gastric and nephrotoxicity without compromising Pt(II) (NH3)2(CL) 2 antineoplastic activity, which led to suggestions that prior Cu(II)-treatment be used clinically to prevent serious side effects of Pt(II) (NH3)2(CL)2-treatment.
  • In the course of these studies it was discovered that Cu(II)-treatments alone inhibited neoplastic growth and increased survival of rat and mouse models of cancer.
  • Subsequently it was discovered that a stable non-toxic and non-polar lipophilic chelate, Copper(II)2(3,5-diisopropylsalicylate)4, caused redifferentiation of cultured neuroblastoma and mouse muscle-implanted mammary adenocarcinoma without neoplastic cell killing.
  • Further, approaches to treating neoplastic diseases by removal of Cu from tissues with ammonium tetrathiomolybdate in an anticopper approach to therapy are not well founded based upon existing scientific literature.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Chelating Agents / therapeutic use. Cisplatin / adverse effects. Copper / therapeutic use. Neoplasms / drug therapy. Organometallic Compounds / adverse effects. Organometallic Compounds / therapeutic use
  • [MeSH-minor] Animals. Apoptosis / drug effects. Humans. Molybdenum / therapeutic use

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  • (PMID = 17584059.001).
  • [ISSN] 0929-8673
  • [Journal-full-title] Current medicinal chemistry
  • [ISO-abbreviation] Curr. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / Organometallic Compounds; 789U1901C5 / Copper; 81AH48963U / Molybdenum; 91U3TGV99T / tetrathiomolybdate; Q20Q21Q62J / Cisplatin
  • [Number-of-references] 49
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