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Items 1 to 36 of about 36
1. 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.
  • A combination of TXT and NF-kappaB decoy, a well-known NF-kappaB inhibitor, also enhanced apoptotic cell death in the carcinoma cells.
  • 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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2. 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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3. Kim R, Emi M, Tanabe K, Toge T: Preclinical evaluation of antisense bcl-2 as a chemosensitizer for patients with gastric carcinoma. Cancer; 2004 Nov 15;101(10):2177-86
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  • [Title] Preclinical evaluation of antisense bcl-2 as a chemosensitizer for patients with gastric carcinoma.
  • BACKGROUND: Because bcl-2 is a critical factor for anticancer drug-induced apoptosis, the authors conducted a preclinical evaluation of antisense (AS) bcl-2 as an enhancer of the chemotherapeutic effect in the treatment of patietns with gastric carcinoma.
  • METHODS: AS bcl-2 was used with 18-mer phosphorothiated oligonucleotides in the MKN-45 gastric carcinoma cell line.
  • Drug sensitivity in vitro was evaluated using the methyl-thiazoldiphenyl tetrazolium assay, and antitumor effects in vivo were evaluated using the nude mouse xenograft.
  • Anticancer drugs were administered intraperitoneally four times per week.
  • RESULTS: bcl-2 was down-regulated to 60% of its initial value after treatment with 1.0 muM AS bcl-2 compared with the controls of random and mismatched oligonucleotides.
  • Drug sensitivity to doxorubicin, cisplatin, and paclitaxel (TXL) was increased 3-4-fold when used in combination with AS bcl-2, which was determined with 50% inhibitory concentration values, compared with the control group.
  • Increased drug sensitivity was associated with apoptosis, which increased in Bax and poly-adenosine diphosphate (ADP-ribose) polymerase and decreased in phosphorylated Akt (pAkt).
  • Down-regulation of bcl-2 was observed on Day 4 after the treatment with AS bcl-2.
  • CONCLUSIONS: Combination treatment with AS bcl-2 and anticancer drugs, including cisplatin and TXL, may be a new strategy for enhancing chemotherapeutic effects in the treatment of gastric carcinoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. DNA, Antisense / pharmacology. Drug Resistance, Neoplasm. Proto-Oncogene Proteins c-bcl-2 / genetics. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Apoptosis / physiology. Blotting, Western. Cell Line, Tumor. Humans. In Situ Nick-End Labeling. Mice. Mice, Nude. Poly(ADP-ribose) Polymerases / drug effects. Poly(ADP-ribose) Polymerases / metabolism. Protein-Serine-Threonine Kinases / drug effects. Protein-Serine-Threonine Kinases / metabolism. Proto-Oncogene Proteins / drug effects. Proto-Oncogene Proteins / metabolism. Proto-Oncogene Proteins c-akt. bcl-2-Associated X Protein

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  • [Copyright] (c) 2004 American Cancer Society
  • (PMID = 15476281.001).
  • [ISSN] 0008-543X
  • [Journal-full-title] Cancer
  • [ISO-abbreviation] Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / BAX protein, human; 0 / Bax protein, mouse; 0 / DNA, Antisense; 0 / Proto-Oncogene Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / bcl-2-Associated X Protein; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 2.7.11.1 / AKT1 protein, human; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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4. Dong ZP, Hu ZQ, Peng W, Shu ZJ, Cao YM, Lu L: [Effects of Baihe Recipe on expressions of vascular endothelial growth factor and p53 proteins in tumor tissues of nude mice bearing orthotopically transplanted gastric carcinoma BGC-823]. Zhong Xi Yi Jie He Xue Bao; 2009 May;7(5):458-62
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  • [Title] [Effects of Baihe Recipe on expressions of vascular endothelial growth factor and p53 proteins in tumor tissues of nude mice bearing orthotopically transplanted gastric carcinoma BGC-823].
  • OBJECTIVE: To investigate the effects of Baihe Recipe, a compound traditional Chinese herbal medicine, on growth and metastasis of orthotopically transplanted gastric carcinoma and the expressions of vascular endothelial growth factor (VEGF) and p53 proteins in the tumor tissues in nude mice.
  • METHODS: Forty-five nude mice orthotopically transplanted with BGC-823 human gastric cancer cells were randomly divided into three groups: Baihe Recipe group, 5-fluorouracil (5-FU) group and untreated group.
  • The mice in the Baihe Recipe group received intragastric administration of 0.5 mL Baihe Recipe (crude drug content was 0.2 g/mL) for 6 weeks, and the mice in the untreated group received 0.5 mL normal saline.
  • All mice were sacrificed after 6-week treatment.
  • The metastasis rates in Baihe Recipe group, 5-FU group and untreated group were 33.33%, 35.71% and 80.00% respectively, with significant difference (P<0.05), and the expressions of VEGF and p53 proteins in tumor tissues in the Baihe Recipe group were lower than those in the untreated group and the 5-FU group (P<0.01, P<0.05).
  • CONCLUSION: Baihe Recipe has inhibitory effects on tumor growth and metastasis of gastric cancer orthotopically transplanted in nude mice by down-regulating the expressions of VEGF and p53 proteins.
  • [MeSH-major] Drugs, Chinese Herbal / therapeutic use. Phytotherapy. Stomach Neoplasms / drug therapy. Tumor Suppressor Protein p53 / metabolism. Vascular Endothelial Growth Factor A / metabolism
  • [MeSH-minor] Animals. Antineoplastic Agents, Phytogenic / therapeutic use. Male. Mice. Mice, Inbred BALB C. Mice, Nude. Neoplasm Transplantation. Random Allocation

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  • (PMID = 19435561.001).
  • [ISSN] 1672-1977
  • [Journal-full-title] Zhong xi yi jie he xue bao = Journal of Chinese integrative medicine
  • [ISO-abbreviation] Zhong Xi Yi Jie He Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Drugs, Chinese Herbal; 0 / Tumor Suppressor Protein p53; 0 / Vascular Endothelial Growth Factor A; 0 / vascular endothelial growth factor A, mouse
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5. 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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6. Yashiro M, Shinto O, Nakamura K, Tendo M, Matsuoka T, Matsuzaki T, Kaizaki R, Ohira M, Miwa A, Hirakawa K: Effects of VEGFR-3 phosphorylation inhibitor on lymph node metastasis in an orthotopic diffuse-type gastric carcinoma model. Br J Cancer; 2009 Oct 6;101(7):1100-6
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  • [Title] Effects of VEGFR-3 phosphorylation inhibitor on lymph node metastasis in an orthotopic diffuse-type gastric carcinoma model.
  • METHODS: Ki23057 was administered orally to gastric cancer models created by orthotopic inoculation of diffuse-type gastric cancer cells, OCUM-2MLN.
  • Murine gastric cancer models created by the orthotopic inoculation of OCUM-2MLN cells showed the diffusely infiltrating growth and frequently developed LN metastasis.
  • The oral administration of Ki23057 significantly (P<0.01) reduced the size of orthotopic tumours and the number of the metastatic LN in gastric cancer models.
  • The degree of lymphatic invasion and lymphangiogenesis was significantly (P<0.05) lower in the gastric tumours treated by Ki23057.
  • Ki23057 inhibited the phosphorylation of VEGFR-3 of lymphatic endothelial cells in gastric tumours.
  • CONCLUSION: The inhibition of lymphangiogenesis targeting VEGFR-3 phosphorylation is a therapeutic strategy for inhibiting LN metastasis of diffuse-type gastric cancer.
  • [MeSH-major] Lymphatic Metastasis / prevention & control. Quinolines / therapeutic use. Stomach Neoplasms / drug therapy. Vascular Endothelial Growth Factor Receptor-3 / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Glycoproteins / analysis. Humans. Lymphangiogenesis / drug effects. Mice. Mice, Inbred BALB C. Phosphorylation. Vascular Endothelial Growth Factor C / analysis

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  • (PMID = 19738610.001).
  • [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 / Glycoproteins; 0 / Ki23057; 0 / Quinolines; 0 / Vascular Endothelial Growth Factor C; 0 / Xlkd1 protein, mouse; 0 / vascular endothelial growth factor C, mouse; EC 2.7.10.1 / Vascular Endothelial Growth Factor Receptor-3
  • [Other-IDs] NLM/ PMC2768106
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7. Ichihara H, Matsuoka Y, Matsumoto Y, Ueoka R: Therapeutic effects of hybrid liposomes on gastric carcinoma involve apoptosis. Anticancer Res; 2010 Jun;30(6):2011-6
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  • [Title] Therapeutic effects of hybrid liposomes on gastric carcinoma involve apoptosis.
  • The inhibitory effects of HLs on the growth of gastric carcinoma (CoRa 622 G6) cells in vitro were investigated.
  • Remarkable inhibitory effects on the metastasis of gastric carcinoma along with apoptosis and prolonged survival were obtained for mouse models of gastric carcinoma with peritoneal dissemination after the treatment with HLs in vivo.
  • [MeSH-major] Apoptosis / drug effects. Dimyristoylphosphatidylcholine / administration & dosage. Polyethylene Glycols / administration & dosage. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Caspases / physiology. Cell Line, Tumor. Cell Proliferation / drug effects. Female. Humans. Liposomes. Mice. Mice, Inbred BALB C. Survival Rate

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  • (PMID = 20651345.001).
  • [ISSN] 1791-7530
  • [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 / Brij 35; 0 / Liposomes; 30IQX730WE / Polyethylene Glycols; EC 3.4.22.- / Caspases; U86ZGC74V5 / Dimyristoylphosphatidylcholine
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8. 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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9. Minagawa A, Otani Y, Kubota T, Wada N, Furukawa T, Kumai K, Kameyama K, Okada Y, Fujii M, Yano M, Sato T, Ito A, Kitajima M: The citrus flavonoid, nobiletin, inhibits peritoneal dissemination of human gastric carcinoma in SCID mice. Jpn J Cancer Res; 2001 Dec;92(12):1322-8
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  • [Title] The citrus flavonoid, nobiletin, inhibits peritoneal dissemination of human gastric carcinoma in SCID mice.
  • In the SCID mouse model, we found that nobiletin inhibited the formation of peritoneal dissemination nodules from TMK-1.
  • The enzymatic activity of MMP-9 expressed in culture medium obtained from a co-culture of TMK-1 and mouse fibroblastic cells was inhibited by nobiletin in a concentration-dependent manner.
  • In the SCID mouse model, total weight of dissemination nodules was significantly lower in the treated group compared with the vehicle control group (0.07 g vs. 0.78 g, P = 0.0059).
  • These results suggest that nobiletin may be a candidate anti-metastatic drug for prevention of peritoneal dissemination of gastric cancer.
  • [MeSH-major] Citrus / chemistry. Flavones. Flavonoids / therapeutic use. Peritoneal Neoplasms / drug therapy. Peritoneal Neoplasms / secondary. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology
  • [MeSH-minor] Animals. Body Weight / drug effects. Cell Division / drug effects. Dose-Response Relationship, Drug. Humans. Matrix Metalloproteinases / metabolism. Mice. Mice, SCID. Neoplasm Transplantation. Organ Size / drug effects. Organ Specificity. Tumor Cells, Cultured

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  • (PMID = 11749698.001).
  • [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 / Flavones; 0 / Flavonoids; D65ILJ7WLY / nobiletin; EC 3.4.24.- / Matrix Metalloproteinases
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10. Hashimoto I, Koizumi K, Tatematsu M, Minami T, Cho S, Takeno N, Nakashima A, Sakurai H, Saito S, Tsukada K, Saiki I: Blocking on the CXCR4/mTOR signalling pathway induces the anti-metastatic properties and autophagic cell death in peritoneal disseminated gastric cancer cells. Eur J Cancer; 2008 May;44(7):1022-9
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  • [Title] Blocking on the CXCR4/mTOR signalling pathway induces the anti-metastatic properties and autophagic cell death in peritoneal disseminated gastric cancer cells.
  • Patients with advanced gastric carcinoma, especially peritoneal dissemination, have a poor prognosis even after any treatment.
  • We recently reported that the chemokine CXCL12 plays an important role in the development of peritoneal carcinomatosis from gastric carcinoma.
  • CXCL12 also induced the activation of p70S6K (S6K) and eukaryotic initiation factor 4E binding protein 1 (4E-BP1) included in mammalian target of rapamycin (mTOR) pathways which are located downstream of Akt, resulting in enhancements of metastatic properties such as MMP production, cell migration and cell growth in peritoneal disseminated gastric cancer, NUGC4 cells.
  • Furthermore, mTOR inhibitor rapamycin not only drastically inhibited migration and MMP production, but also induced type II programmed cell death, autophagic cell death.
  • In the present study, we have shown for the first time that the mTOR pathway plays a central role in the development of peritoneal carcinomatosis, and blocking this pathway induces autophagic cell death in disseminated gastric cancer.
  • Therefore, blocking on the CXCR4/mTOR signalling pathway may be useful for the future development of a more effective therapeutic strategy for gastric cancer involved in peritoneal dissemination.
  • [MeSH-major] Autophagy / physiology. Peritoneal Neoplasms / secondary. Protein Kinases / metabolism. Receptors, CXCR4 / antagonists & inhibitors. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Blotting, Western. Cell Migration Assays. Cell Proliferation. Chemokine CXCL12 / pharmacology. Humans. Mice. Mice, Nude. Neoplasm Transplantation. Phosphorylation. Proto-Oncogene Proteins c-akt / metabolism. Reverse Transcriptase Polymerase Chain Reaction. Signal Transduction / drug effects. TOR Serine-Threonine Kinases. Tumor Cells, Cultured


11. Ding L, Chen XP, Zhang ZW, Guan J, Zhang WG, Wang HP, Wang ZH, Li CL: Synergistic effect of bromocriptine and tumor necrosis factor-alpha on reversing hepatocellular carcinoma multidrug resistance in nude mouse MDR1 model of liver neoplasm. World J Gastroenterol; 2005 Sep 28;11(36):5621-6
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  • [Title] Synergistic effect of bromocriptine and tumor necrosis factor-alpha on reversing hepatocellular carcinoma multidrug resistance in nude mouse MDR1 model of liver neoplasm.
  • AIM: To investigate the effect of bromocriptine (BCT) and tumor necrosis factor-alpha (TNF-alpha) on hepatocellular carcinoma (HCC) multidrug resistance (MDR) in nude mouse MDR model of liver neoplasm.
  • METHODS: Human hepatocarcinoma cell line HepG(2), drug resistant hepatocarcinoma cell line HepG(2)/adriamycin (ADM) and hepatocarcinoma cell line transfected with TNF-alpha gene HepG(2)/ADM/TNF were injected into the liver of nude mice via orthotopic implantation and MDR model of liver neoplasm in vivo was established (HepG(2), ADM, TNF, BCT groups).
  • Among these groups, BCT group and TNF group were treated with BCT through gastric canal.
  • Each group was divided into control group and chemotherapy group.
  • RESULTS: The nude mouse model of each cell line was inoculated successfully.
  • After chemotherapy, abdominal cavity tumor growth inhibition rate was higher in BCT group (67%) compared to ADM and TNF groups, and similar to HepG(2) group (54%).
  • CONCLUSION: BCT and TNF-alpha can reverse HCC MDR in nude mouse MDR1 model of liver neoplasm.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Bromocriptine / pharmacology. Drug Resistance, Neoplasm / drug effects. Liver Neoplasms / drug therapy. P-Glycoprotein / metabolism. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Drug Synergism. Female. Gene Expression Regulation, Neoplastic. Genes, MDR / genetics. Genes, MDR / physiology. Humans. Mice. Mice, Nude. Neoplasm Transplantation. RNA, Messenger / metabolism

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  • (PMID = 16237754.001).
  • [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 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 3A64E3G5ZO / Bromocriptine
  • [Other-IDs] NLM/ PMC4481477
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12. Toyoda T, Tsukamoto T, Takasu S, Hirano N, Ban H, Shi L, Kumagai T, Tanaka T, Tatematsu M: Pitavastatin fails to lower serum lipid levels or inhibit gastric carcinogenesis in helicobacter pylori-infected rodent models. Cancer Prev Res (Phila); 2009 Aug;2(8):751-8
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  • [Title] Pitavastatin fails to lower serum lipid levels or inhibit gastric carcinogenesis in helicobacter pylori-infected rodent models.
  • Statins are commonly used lipid-lowering drugs that reduce the risk of cardiovascular morbidity and mortality.
  • Although recent studies have pointed to chemopreventive effects of statins against various cancers, their efficacy for gastric cancer is unclear.
  • Here, we examined the effects of pitavastatin, a lipophilic statin, on Helicobacter pylori (H. pylori)-associated stomach carcinogenesis and gastritis using Mongolian gerbil and mouse models.
  • The incidences of H. pylori-associated gastric adenocarcinomas and degrees of chronic gastritis were not decreased by pitavastatin compared with those of control values.
  • Furthermore, in the H. pylori-infected groups, serum total cholesterol, triglyceride, and low-density lipoprotein levels were significantly increased by pitavastatin treatment, contrary to expectation.
  • These findings indicate pitavastatin to be ineffective for suppressing gastritis and chemoprevention of gastric carcinogenesis in H. pylori-infected gerbils.
  • [MeSH-major] Carcinoma / prevention & control. Helicobacter Infections / drug therapy. Lipids / blood. Quinolines / therapeutic use. Stomach Neoplasms / prevention & control
  • [MeSH-minor] Animals. Disease Models, Animal. Down-Regulation / drug effects. Enzyme Inhibitors / pharmacology. Enzyme Inhibitors / therapeutic use. Gerbillinae. Helicobacter pylori. Male. Mice. Mice, Inbred C57BL. Models, Biological. Rodentia. Treatment Failure

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  • (PMID = 19622613.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Lipids; 0 / Quinolines; M5681Q5F9P / pitavastatin
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13. Yang J, Li ZH, Zhou JJ, Chen RF, Cheng LZ, Zhou QB, Yang LQ: Preparation and antitumor effects of nanovaccines with MAGE-3 peptides in transplanted gastric cancer in mice. Chin J Cancer; 2010 Apr;29(4):359-64
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  • [Title] Preparation and antitumor effects of nanovaccines with MAGE-3 peptides in transplanted gastric cancer in mice.
  • This study prepared nanovaccines with MAGE-3-derived CD4+-CD8+T cell epitope peptides, and investigated its character and antitumor effects on transplanted gastric cancer in mice.
  • These nanoparticles presented a delayed release pattern in phosphate buffered saline (PBS) at pH 7.4, and the full release time was about 48 h.
  • In 2 mg/mL lysozyme, the nanoparticles showed a sudden release, and the full release time was about 24 h.
  • CONCLUSIONS: MAGE-3 peptide/chitosan-deoxycholic acidvaccine-loaded nanoparticles can stimulate antitumor immune response in vivo and can regress the growth of mouse forestomach carcinoma cell line MFC.
  • [MeSH-major] Antigens, Neoplasm / immunology. Cancer Vaccines / administration & dosage. Dendritic Cells / immunology. Neoplasm Proteins / immunology. Stomach Neoplasms / therapy. T-Lymphocytes, Cytotoxic / immunology
  • [MeSH-minor] Animals. Cell Line, Tumor. Chitosan / chemistry. Deoxycholic Acid / chemistry. Drug Carriers / chemistry. Epitopes, T-Lymphocyte / immunology. Male. Mice. Nanoparticles. Neoplasm Transplantation. Tumor Burden

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  • (PMID = 20346208.001).
  • [ISSN] 1000-467X
  • [Journal-full-title] Chinese journal of cancer
  • [ISO-abbreviation] Chin J Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Cancer Vaccines; 0 / Drug Carriers; 0 / Epitopes, T-Lymphocyte; 0 / MAGEA3 protein, human; 0 / Neoplasm Proteins; 005990WHZZ / Deoxycholic Acid; 9012-76-4 / Chitosan
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14. Kamata S, Kishimoto T, Kobayashi S, Miyazaki M, Ishikura H: Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells. Cancer Biol Ther; 2007 Jul;6(7):1036-43
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  • [Title] Possible involvement of persistent activity of the mammalian target of rapamycin pathway in the cisplatin resistance of AFP-producing gastric cancer cells.
  • AFP-producing gastric carcinoma (AFPGC) is a highly malignant variant of gastric cancer.
  • An effective chemotherapy is needed to improve on the poor outcome of this disease.
  • We investigated the role of a pivotal kinase pathway, the mammalian target of rapamycin complex 1 (mTORC1) pathway, in the effectiveness of chemotherapeutic agents in three AFPGC cell lines (GCIY, FU97 and Takigawa) as well as in four cell lines of conventional-type gastric carcinoma (CGC).
  • Finally, combined treatment of rapamycin and cisplatin significantly suppressed the subcutaneously implanted GCIY cells.
  • In conclusion rapamycin may be a potential supplemental agent for the treatment of AFPGC when used in combination with cisplatin.
  • [MeSH-major] Antineoplastic Agents / pharmacology. Cisplatin / pharmacology. Protein Kinases / physiology. Signal Transduction / physiology. Stomach Neoplasms / drug therapy. alpha-Fetoproteins / biosynthesis
  • [MeSH-minor] Animals. Cell Line, Tumor. Drug Resistance, Neoplasm. Humans. Male. Mice. Mice, Inbred BALB C. Sirolimus / pharmacology. TOR Serine-Threonine Kinases. Transcription Factors / physiology. Xenograft Model Antitumor Assays. bcl-2-Associated X Protein / analysis

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  • (PMID = 17568186.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / CRTC1 protein, human; 0 / Transcription Factors; 0 / alpha-Fetoproteins; 0 / bcl-2-Associated X Protein; EC 2.7.- / Protein 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; Q20Q21Q62J / Cisplatin; W36ZG6FT64 / Sirolimus
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15. Chen JL, Zhu JS, Hong J, Chen MX, Lu JL, Chen WX, Shen B, Zhu ZM, Chen NW: Effect of 2-(8-hydroxy-6-methoxy-1-oxo-1H-2-benzopyran-3-yl) propionic acid in combination with carboplatin on gastric carcinoma growth in vivo. World J Gastroenterol; 2007 Jan 28;13(4):509-14
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of 2-(8-hydroxy-6-methoxy-1-oxo-1H-2-benzopyran-3-yl) propionic acid in combination with carboplatin on gastric carcinoma growth in vivo.
  • AIM: To investigate the effects of 2-(8-hydroxy-6-methoxy-1-oxo-1H-2-benzopyran-3-yl) propionic acid (NM-3) alone and in combination with carboplatin on tumor growth and apoptosis in mouse models of human gastric cancer constructed by subcutaneous implantation of histologically intact tumor tissue.
  • METHODS: Human gastric cancer SGC-7901 tissues were implanted into the dorsal subcutis of nude mice.
  • As controls of combined treatment, another 4 groups of mice were injected with either NM-3 at 10 mg/kg, 20 mg/kg or 40 mg/kg, or with carboplatin alone (5 mg/kg).
  • Apoptosis of human gastric cancer was detected by TUNEL method and flow cytometry analysis, respectively.
  • RESULTS: The mean tumor volume (692.40 +/- 58.43 mm(3), 548.30 +/- 66.02 mm(3), 382.13 +/- 43.52 mm(3)) after treatment with carboplatin combined NM-3 at the dose of 10 mg/kg, 20 mg/kg or 40 mg/kg was lower than that after treatment with either NM-3 at the dose of 10 mg/kg, 20 mg/kg or 40 mg/kg or with carboplatin alone.
  • NM-3 significantly reduced the neo-microvascular formation of gastric cancer.
  • CONCLUSION: The results suggest that the inhibitory effect of NM-3 on gastric cancer growth is mediated through decreased angiogenesis and the increased induction of apoptosis.
  • Furthermore, NM-3 alone at the dose of 10 mg/kg or in combination with carboplatin has no obvious effects on body changes, indicating that NM-3 in combination with carboplatin may be effective in the treatment of gastric cancer.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carboplatin / administration & dosage. Isocoumarins / administration & dosage. Neovascularization, Pathologic / drug therapy. Stomach Neoplasms / drug therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Humans. Male. Mice. Mice, Inbred BALB C. Neoplasm Transplantation. Transplantation, Heterologous

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  • (PMID = 17278215.001).
  • [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 / Isocoumarins; 0 / isocoumarin NM-3; BG3F62OND5 / Carboplatin
  • [Other-IDs] NLM/ PMC4065971
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16. Lee CW, Rickman B, Rogers AB, Ge Z, Wang TC, Fox JG: Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice. Cancer Res; 2008 May 1;68(9):3540-8
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  • [Title] Helicobacter pylori eradication prevents progression of gastric cancer in hypergastrinemic INS-GAS mice.
  • Helicobacter pylori infection results in chronic gastritis, which may progress to gastric cancer.
  • In this study, we investigated the efficacy of H. pylori eradication in preventing the progression of gastritis to gastric cancer in H. pylori-infected transgenic INS-GAS mice. H. pylori infection induced severe dysplasia and gastric cancer classified as high-grade and low-grade gastrointestinal intraepithelial neoplasia (GIN) in INS-GAS mice at 28 weeks postinfection (WPI). H. pylori eradication therapy using omeprazole, metronidazole, and clarithromycin was administered p.o. at 8, 12, or 22 WPI.
  • Although not as effective as early antimicrobial treatment, prevention of progression to high-grade GIN was achieved by H. pylori eradication at 12 and 22 WPI (P < 0.05).
  • Consistent with reduced gastric pathology, H. pylori eradication at all time points significantly down-regulated gastric Interferon-gamma, tumor necrosis factor-alpha, inducible nitric oxide synthase, and Reg 1 mRNA levels (P < 0.05) and reduced epithelial proliferation in the corpus (P < 0.01) compared with untreated infected mice.
  • We concluded that H. pylori eradication prevented gastric cancer to the greatest extent when antibiotics are given at an early point of infection, but that eradication therapy given at a later time point delayed the development of severe dysplastic lesions.

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  • (PMID = 18441088.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NIAID NIH HHS / AI / R01 AI037750-12; United States / NIEHS NIH HHS / ES / P30ES02109; United States / NIEHS NIH HHS / ES / ES002109-299010; United States / NIAID NIH HHS / AI / AI037750-12; United States / NCI NIH HHS / CA / R01 CA093405; United States / NIAID NIH HHS / AI / R01 AI037750-13; United States / NIAID NIH HHS / AI / AI037750-13; United States / NIAID NIH HHS / AI / R01AI37750; United States / NCI NIH HHS / CA / R01 CA093405-07A1; United States / NCI NIH HHS / CA / CA093405-07A1; United States / NIAID NIH HHS / AI / R01 AI037750; United States / NIEHS NIH HHS / ES / P30 ES002109; United States / NCI NIH HHS / CA / P01 CA026731-299002; United States / NIEHS NIH HHS / ES / P30 ES002109-299010; United States / NCI NIH HHS / CA / P01 CA026731; United States / NCI NIH HHS / CA / P01CA26731; United States / NCI NIH HHS / CA / CA026731-299002
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Anti-Ulcer Agents; 0 / Lithostathine; 0 / Reg1 protein, mouse; 0 / Tumor Necrosis Factor-alpha; 82115-62-6 / Interferon-gamma; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, mouse; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole
  • [Other-IDs] NLM/ NIHMS95242; NLM/ PMC2653414
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17. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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


18. 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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19. Huang SG, Kong BH, Yang RF, Jiang S: [Primary study of arsenic trioxide inhibits abdomino-metastatic tumor formation of human ovarian carcinoma in nude mice and its mechanisms]. Ai Zheng; 2002 Apr;21(4):401-4
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  • [Title] [Primary study of arsenic trioxide inhibits abdomino-metastatic tumor formation of human ovarian carcinoma in nude mice and its mechanisms].
  • BACKGROUND AND OBJECTIVE: Arsenic trioxide (As2O3) has been successfully used to treat the patients with acute promyelocyutic leukemia in clinic, and for the experimental studies of liver cancer, colorectal cancer, gastric cancer, etc.
  • The objective of this study was to explore the inhibitory effect of As2O3 on the abdomino-metastasis of human ovarian carcinoma in nude mice and its mechanisms.
  • METHODS: Compared with cisplatin(cDDP), the growth inhibiting rates to human ovarian cancer cell line 3AO by treatment with various concentrations of As2O3 for 48 h were determined by methyl thiazolyl tetrazolium(MTT) method.
  • After treatment with As2O3, the changes of Fas, FasL, and nm23 gene expressions were estimated by flow cytometry (FCM).
  • CONCLUSION: As2O3 could inhibit the abdomino-plantation of human ovarian carcinoma in nude mice and its mechanism may be associated with Fas gene and nm23 gene over-expressions.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Arsenicals / therapeutic use. Neoplasms, Experimental / drug therapy. Nucleoside-Diphosphate Kinase. Ovarian Neoplasms / pathology. Oxides / therapeutic use
  • [MeSH-minor] Animals. Antigens, CD95 / biosynthesis. Disease Models, Animal. Fas Ligand Protein. Female. Humans. Membrane Glycoproteins / biosynthesis. Mice. Mice, Nude. Monomeric GTP-Binding Proteins / biosynthesis. NM23 Nucleoside Diphosphate Kinases. Neoplasm Metastasis. Neoplasm Transplantation. Transcription Factors / biosynthesis. Treatment Outcome. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12452020.001).
  • [Journal-full-title] Ai zheng = Aizheng = Chinese journal of cancer
  • [ISO-abbreviation] Ai Zheng
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Antineoplastic Agents; 0 / Arsenicals; 0 / FASLG protein, human; 0 / Fas Ligand Protein; 0 / Fasl protein, mouse; 0 / Membrane Glycoproteins; 0 / NM23 Nucleoside Diphosphate Kinases; 0 / Oxides; 0 / Transcription Factors; EC 2.7.4.6 / NME1 protein, human; EC 2.7.4.6 / Nme1 protein, mouse; EC 2.7.4.6 / Nucleoside-Diphosphate Kinase; EC 3.6.5.2 / Monomeric GTP-Binding Proteins; S7V92P67HO / arsenic trioxide
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20. Han Z, Hong Z, Chen C, Gao Q, Luo D, Fang Y, Cao Y, Zhu T, Jiang X, Ma Q, Li W, Han L, Wang D, Xu G, Wang S, Meng L, Zhou J, Ma D: A novel oncolytic adenovirus selectively silences the expression of tumor-associated STAT3 and exhibits potent antitumoral activity. Carcinogenesis; 2009 Dec;30(12):2014-22
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  • Consequently, the STAT3 protein is emerging as an ideal target for cancer therapy.
  • This paper reports the generation of an oncolytic adenovirus (M4), which selectively blocks STAT3 signaling in tumor cells as a novel therapeutic strategy.
  • Systemic administration of M4 significantly inhibited tumor growth in an orthotopic gastric carcinoma mouse model, eliminated abdominal cavity metastases and prolonged survival time.
  • In summary, M4 has low toxicity and great potential as a therapeutic agent for different types of cancers.
  • [MeSH-minor] Animals. Apoptosis. Cell Line, Tumor. Collagen / chemistry. Drug Combinations. Humans. Laminin / chemistry. Male. Mice. Mice, Inbred BALB C. Models, Genetic. Mutation. Neoplasm Metastasis. Neovascularization, Pathologic. Oligonucleotides, Antisense / genetics. Proteoglycans / chemistry. Signal Transduction

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  • (PMID = 19843641.001).
  • [ISSN] 1460-2180
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Drug Combinations; 0 / Laminin; 0 / Oligonucleotides, Antisense; 0 / Proteoglycans; 0 / STAT3 Transcription Factor; 0 / STAT3 protein, human; 119978-18-6 / matrigel; 9007-34-5 / Collagen
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21. Kim YJ, Lee JS, Hong KS, Chung JW, Kim JH, Hahm KB: Novel application of proton pump inhibitor for the prevention of colitis-induced colorectal carcinogenesis beyond acid suppression. Cancer Prev Res (Phila); 2010 Aug;3(8):963-74
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  • Colitis-associated cancers arise in the setting of chronic inflammation wherein an "inflammation-dysplasia-carcinoma" sequence prevails.
  • Based on our previous findings in which the proton pump inhibitor could impose significant levels of anti-inflammatory, antiangiogenic, and selective apoptosis induction beyond gastric acid suppression, we investigated whether omeprazole could prevent the development of colitis-associated cancer in a mouse model induced by repeated bouts of colitis.
  • Nine of 12 (75.0%) mice in the control group developed multiple colorectal tumors, whereas tumors were noted in only 3 of 12 (25.0%) mice treated with daily injections of omeprazole.
  • The cancer-preventive results of omeprazole treatment was based on significant decreases in the levels of nitric oxide, thiobarbituric acid-reactive substance, and interleukin-6 accompanied with attenuated expressions of tumor necrosis factor-alpha, inducible nitric oxide synthase, and cyclooxygenase-2.
  • A significant induction of apoptosis was observed in tumor tissue treated with omeprazole.
  • The significant anti-inflammatory, antioxidative, and antimutagenic activities of omeprazole played a cancer-preventive role against colitis-induced carcinogenesis, and our novel in vivo evidence is suggestive of chemopreventive action independent of gastric acid suppression.
  • [MeSH-major] Carcinoma / prevention & control. Colitis / drug therapy. Colorectal Neoplasms / prevention & control. Gastric Acid / metabolism. Omeprazole / therapeutic use. Proton Pump Inhibitors / therapeutic use
  • [MeSH-minor] Animals. Cell Transformation, Neoplastic / drug effects. Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Down-Regulation / drug effects. Drug Evaluation, Preclinical. Female. HT29 Cells. Humans. Mice. Mice, Inbred C57BL

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  • [Copyright] 2010 AACR.
  • (PMID = 20628001.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Proton Pump Inhibitors; KG60484QX9 / Omeprazole
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22. 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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23. 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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24. Hao ZM, Luo JY, Cheng J, Li L, He D, Wang QY, Yang GX: Intensive inhibition of hTERT expression by a ribozyme induces rapid apoptosis of cancer cells through a telomere length-independent pathway. Cancer Biol Ther; 2005 Oct;4(10):1098-103
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  • A recombinant retrovirus was constructed to transduce the ribozyme to telomerase positive colon carcinoma cell line SW480 and gastric carcinoma cell line SGC7901.
  • Anti-hTERT ribozyme might be a potential means in the therapy of telomerase-positive malignancies.
  • [MeSH-major] Apoptosis / drug effects. DNA-Binding Proteins / antagonists & inhibitors. DNA-Binding Proteins / metabolism. RNA, Catalytic / pharmacology. Telomerase / antagonists & inhibitors. Telomerase / metabolism. Telomere / metabolism
  • [MeSH-minor] Animals. Carcinoma / pathology. Cell Line, Tumor. Colonic Neoplasms / enzymology. Colonic Neoplasms / genetics. Colonic Neoplasms / pathology. DNA, Recombinant / genetics. Humans. Mice. NIH 3T3 Cells. Retroviridae / genetics. Stomach Neoplasms / enzymology. Stomach Neoplasms / genetics. Stomach Neoplasms / pathology

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  • (PMID = 16205109.001).
  • [ISSN] 1538-4047
  • [Journal-full-title] Cancer biology & therapy
  • [ISO-abbreviation] Cancer Biol. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA, Recombinant; 0 / DNA-Binding Proteins; 0 / RNA, Catalytic; 0 / hammerhead ribozyme; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 2.7.7.49 / Tert protein, mouse
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25. Lane HA, Motoyama AB, Beuvink I, Hynes NE: Modulation of p27/Cdk2 complex formation through 4D5-mediated inhibition of HER2 receptor signaling. Ann Oncol; 2001;12 Suppl 1:S21-2
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  • The molecular mechanisms mediating the anti-proliferative effects of the murine anti-HER2 monoclonal antibody (4D5) were investigated in HER2-overexpressing human carcinoma cell lines.
  • Treatment with 4D5 resulted in a dramatic accumulation of BT-474 breast carcinoma cells in G1; concomitant with reduced expression of proteins involved in sequestration of the cyclin E/Cdk2 inhibitor protein p27, increased association of p27 with Cdk2 complexes and Cdk2 inactivation.
  • No equivalent effects were observed in BT-474 cells treated with a control, non-inhibitory HER2 monoclonal antibody (FRP5) or in a HER2-overexpressing cell line insensitive to 4D5 treatment (MKN7 gastric carcinoma cells), confirming the relationship between these molecular changes and 4D5-mediated inhibition of proliferation.
  • HER2-overexpressing breast tumor line (SKBR3), and suggests that the dependency of a given tumor cell on elevated HER2-receptor signaling for the maintenance of p27 sequestration proteins may determine the clinical response to treatment with the humanized anti-HER2 monoclonal antibody Herceptin (trastuzumab).

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  • (PMID = 11521716.001).
  • [ISSN] 0923-7534
  • [Journal-full-title] Annals of oncology : official journal of the European Society for Medical Oncology
  • [ISO-abbreviation] Ann. Oncol.
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Humanized; 0 / Antineoplastic Agents; 0 / Cdkn1b protein, mouse; 0 / Cell Cycle Proteins; 0 / Enzyme Inhibitors; 0 / Tumor Suppressor Proteins; 147604-94-2 / Cyclin-Dependent Kinase Inhibitor p27; EC 2.7.10.1 / Receptor, ErbB-2; EC 2.7.11.22 / Cyclin-Dependent Kinases; P188ANX8CK / Trastuzumab
  • [Number-of-references] 5
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26. Abe H, Kuroki M, Tachibana K, Li T, Awasthi A, Ueno A, Matsumoto H, Imakiire T, Yamauchi Y, Yamada H, Ariyoshi A, Kuroki M: Targeted sonodynamic therapy of cancer using a photosensitizer conjugated with antibody against carcinoembryonic antigen. Anticancer Res; 2002 May-Jun;22(3):1575-80

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeted sonodynamic therapy of cancer using a photosensitizer conjugated with antibody against carcinoembryonic antigen.
  • To this end, a photoimmunoconjugate (PIC) was prepared between ATX-70, a photosensitizer of a gallium-porphyrin analogue, and F11-39, a high affinity monoclonal antibody (MAb) against carcinoembryonic antigen (CEA), which is often overexpressed in various carcinoma cells.
  • The cytotoxicity of F39/ATX-70 against CEA-expressing human gastric carcinoma cells in vitro was found to be greater than that of ATX-70 when applied in combination with ultrasound irradiation.
  • When in vivo anti-tumor effects in a mouse xenograft model were assessed, intravenous administration of F39/ATX-70 followed by ultrasonic irradiation produced a marked growth inhibition of tumor compared with irradiation alone or irradiation after administration of ATX-70.
  • These results suggest that the PIC between anti-CEA MAb and ATX-70 may have applications in sonodynamic therapy where destruction of CEA-expressing tumor is required.
  • [MeSH-major] Carcinoembryonic Antigen / immunology. Immunoconjugates / pharmacology. Photosensitizing Agents / pharmacology. Porphyrins / pharmacology. Ultrasonic Therapy / methods
  • [MeSH-minor] Animals. Antibodies, Monoclonal / immunology. Antibodies, Monoclonal / metabolism. Antibodies, Monoclonal / pharmacology. Antibodies, Monoclonal / toxicity. Antibody Specificity. Mice. Mice, Inbred BALB C. Mice, Nude. Stomach Neoplasms / drug therapy. Stomach Neoplasms / immunology. Stomach Neoplasms / metabolism. Tumor Cells, Cultured. Xenograft Model Antitumor Assays

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  • (PMID = 12168839.001).
  • [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 / Antibodies, Monoclonal; 0 / Carcinoembryonic Antigen; 0 / Immunoconjugates; 0 / Photosensitizing Agents; 0 / Porphyrins; 135099-39-7 / ATX 70
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27. Kirikoshi H, Katoh M: Expression and regulation of WNT10B in human cancer: up-regulation of WNT10B in MCF-7 cells by beta-estradiol and down-regulation of WNT10B in NT2 cells by retinoic acid. Int J Mol Med; 2002 Oct;10(4):507-11
Hazardous Substances Data Bank. ESTRADIOL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have previously cloned and characterized the human orthologue of mouse proto-oncogene Wnt-10b using bioinformatics and cDNA-PCR.
  • Human WNT10B is moderately expressed in MKN45 and MKN74 cells derived from human gastric cancer, and is up-regulated by tumor necrosis factor alpha (TNFalpha) in MKN45 cells.
  • Here, expression and regulation of WNT10B in human cancer other than gastric cancer were investigated using cDNA-PCR.
  • WNT10B mRNA was expressed in the majority of squamous cell carcinoma cell lines derived from esophageal cancer and cervical cancer.
  • [MeSH-major] Estradiol / pharmacology. Gene Expression Regulation, Neoplastic / drug effects. Proto-Oncogene Proteins / genetics. Tretinoin / pharmacology
  • [MeSH-minor] Breast Neoplasms / drug therapy. Cell Line. Down-Regulation. Humans. Neoplasms, Germ Cell and Embryonal / drug therapy. Up-Regulation. Wnt Proteins

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  • (PMID = 12239602.001).
  • [ISSN] 1107-3756
  • [Journal-full-title] International journal of molecular medicine
  • [ISO-abbreviation] Int. J. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins; 0 / WNT10B protein, human; 0 / Wnt Proteins; 4TI98Z838E / Estradiol; 5688UTC01R / Tretinoin
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28. Yamada N, Ohira M, Hirakawa K: [COX and study of cancer therapy]. Gan To Kagaku Ryoho; 2004 Aug;31(8):1147-51

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [COX and study of cancer therapy].
  • The increased expression of COX-2 in carcinoma tissue is found in gastric cancer, lung cancer and breast cancer as well as colon cancer.
  • It was shown that COX-2 played an important role in carcinogenesis by an experiment using a cultured cell and an animal experiment using a knockout mouse.
  • Food and Drug Administration (FDA) approved administration of a COX-2 inhibitor to FAP patients.
  • [MeSH-major] Cyclooxygenase Inhibitors / therapeutic use. Isoenzymes / biosynthesis. Neoplasms / enzymology. Prostaglandin-Endoperoxide Synthases / biosynthesis
  • [MeSH-minor] Adenomatous Polyposis Coli / drug therapy. Animals. Anti-Inflammatory Agents, Non-Steroidal / therapeutic use. Breast Neoplasms / enzymology. Colonic Neoplasms / enzymology. Cyclooxygenase 2. Cyclooxygenase 2 Inhibitors. Female. Humans. Lung Neoplasms / enzymology. Male. Membrane Proteins. Mice. Mice, Knockout. Neoplastic Cells, Circulating / drug effects. Stomach Neoplasms / enzymology

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  • (PMID = 15332534.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cyclooxygenase 2 Inhibitors; 0 / Cyclooxygenase Inhibitors; 0 / Isoenzymes; 0 / Membrane Proteins; 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] 27
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29. Lu Y, Lin P, Lu B, Wang J, Zhang J, Huang X: [Studies on release characteristics and cytotoxicity of 5-fluorouracil loaded polylactide microspheres on lung cancer cell lines]. Zhongguo Fei Ai Za Zhi; 2000 Dec 20;3(6):432-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The antitumor activities of 5-FU-PLA microspheres against human and mouse lung, gastric and hepatocellular carcinoma cell lines were detected byMTT colorimetric assay.
  • The lung and gastric cancer cell lines were more sensitive than hepatocellular cancer cell line to 5-FU-PLA microspheres.
  • The antitumor activity significantly correlated with the time of drug action and the dose of 5-FU released from the microspheres.
  • It can keep the antitumor activities for a relatively long time.
  • The current study provides an experimental basis for interventional therapy of tumors.

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  • (PMID = 21029576.001).
  • [ISSN] 1009-3419
  • [Journal-full-title] Zhongguo fei ai za zhi = Chinese journal of lung cancer
  • [ISO-abbreviation] Zhongguo Fei Ai Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
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30. Koshikawa N, Mizushima H, Minegishi T, Iwamoto R, Mekada E, Seiki M: Membrane type 1-matrix metalloproteinase cleaves off the NH2-terminal portion of heparin-binding epidermal growth factor and converts it into a heparin-independent growth factor. Cancer Res; 2010 Jul 15;70(14):6093-103
NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Membrane type 1-matrix metalloproteinase cleaves off the NH2-terminal portion of heparin-binding epidermal growth factor and converts it into a heparin-independent growth factor.
  • Epidermal growth factor (EGF) receptors (ErbB) and EGF family members represent promising targets for cancer therapy.
  • Heparin-binding EGF (HB-EGF) is a member of the EGF family and is an important target for therapy in some types of human cancers.
  • Here, we show that membrane type 1-matrix metalloproteinase (MT1-MMP; MMP14), a potent invasion-promoting protease, markedly enhances HB-EGF-dependent tumor formation in mice.
  • The ErbB family of receptors expressed in human gastric carcinoma cells play a role in mediating enhanced HB-EGF activity by MT1-MMP during invasive cell growth in collagen.
  • Thus, we shed light on a new mechanism whereby HB-EGF activity is regulated that should be considered when designing HB-EGF-targeted cancer therapy.
  • [MeSH-minor] Amino Acid Sequence. Animals. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line. Cell Line, Tumor. Dogs. Fibroblasts / cytology. Fibroblasts / drug effects. Gene Knockdown Techniques. Heparin-binding EGF-like Growth Factor. Humans. Mice. Molecular Sequence Data. Neoplasm Invasiveness. RNA, Messenger / biosynthesis. RNA, Messenger / genetics. RNA, Small Interfering / genetics. Rats. Rats, Inbred BUF. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Transfection

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  • [Copyright] (c)2010 AACR.
  • (PMID = 20587521.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / HBEGF protein, human; 0 / Hbegf protein, mouse; 0 / Hbegf protein, rat; 0 / Heparin-binding EGF-like Growth Factor; 0 / Intercellular Signaling Peptides and Proteins; 0 / RNA, Messenger; 0 / RNA, Small Interfering; EC 3.4.24.80 / Matrix Metalloproteinase 14
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31. Ahn CM, Tak JA, Choi SJ: Synthesis and in vitro antitumor activity of 2-alkyl, 2-aryl, and 2-piperazinyl benzimidazole-4,7-dione derivatives. Arch Pharm Res; 2000 Aug;23(4):288-301
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • A series of 2-alkyl, 2-aryl, and 2-piperazinyl benzimidazole-4,7-dione derivatives (7a-h) and 16m-o) were prepared, and their cytotoxicities were tested against three cancer cell lines (mouse lymphocytic leukemia cell line P388, and human gastric carcinoma cell lines SNU-1 and SNU-16).
  • [MeSH-minor] Animals. Humans. Leukemia P388 / drug therapy. Leukemia P388 / pathology. Mice. Stomach Neoplasms / drug therapy. Stomach Neoplasms / pathology. Structure-Activity Relationship. Tumor Cells, Cultured

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  • (PMID = 10976573.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] KOREA (SOUTH)
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzimidazoles
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32. Li HY, Li Y, Liu ZH, Wu HJ, Chen FH, Chen XG: [Studies on antitumor activity of rhEndostatin]. Yao Xue Xue Bao; 2002 Oct;37(10):763-6
MedlinePlus Health Information. consumer health - Cancer Chemotherapy.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • No inhibition was observed in HCT-8, BGC803 and EJ cells at 1 x 10(-4) g.L-1 rhEndostatin. rhEndostatin was shown to inhibit human xenograft in nude mice with human gastric cancer BGC803 and breast cancer B37 when administered subcutaneously at 5, 10, 20 mg.kg-1.d-1 for 24 days in a dose-dependent manner.
  • Mouse hepatoma H22 was also suppressed when given rhEndostatin subcutaneously 20 mg.kg-1.d-1 for 9 days, but it showed no inhibitory effect on Lewis lung carcinoma and B16 melanoma.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Endostatins / therapeutic use. Neoplasms, Experimental / drug therapy
  • [MeSH-minor] Animals. Breast Neoplasms / pathology. Cell Division / drug effects. Cells, Cultured. Disease Models, Animal. Endothelium, Vascular / cytology. Endothelium, Vascular / drug effects. Female. Humans. Male. Mice. Mice, Inbred C57BL. Mice, Nude. Neoplasm Transplantation. Recombinant Proteins / therapeutic use. Stomach Neoplasms / pathology. Tumor Cells, Cultured / drug effects. Umbilical Cord / cytology. Xenograft Model Antitumor Assays

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  • (PMID = 12567857.001).
  • [ISSN] 0513-4870
  • [Journal-full-title] Yao xue xue bao = Acta pharmaceutica Sinica
  • [ISO-abbreviation] Yao Xue Xue Bao
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Endostatins; 0 / Recombinant Proteins
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33. Wang X, Willén R, Wadström T: Astaxanthin-rich algal meal and vitamin C inhibit Helicobacter pylori infection in BALB/cA mice. Antimicrob Agents Chemother; 2000 Sep;44(9):2452-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Helicobacter pylori infection in humans is associated with chronic type B gastritis, peptic ulcer disease, and gastric carcinoma.
  • A high intake of carotenoids and vitamin C has been proposed to prevent development of gastric malignancies.
  • The aim of this study was to explore if the microalga Haematococcus pluvialis rich in the carotenoid astaxanthin and vitamin C can inhibit experimental H. pylori infection in a BALB/cA mouse model.
  • Six-week-old BALB/cA mice were infected with the mouse-passaged H. pylori strain 119/95.
  • Five mice from each group were sacrificed 1 day after the cessation of treatment, and the other five animals were sacrificed 10 days after the cessation of treatment.
  • Culture of H. pylori and determination of the inflammation score of the gastric mucosae were used to determine the outcome of the treatment.
  • Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment.
  • [MeSH-major] Ascorbic Acid / therapeutic use. Helicobacter Infections / drug therapy. Helicobacter pylori. beta Carotene / analogs & derivatives. beta Carotene / therapeutic use
  • [MeSH-minor] Agar / chemistry. Animals. Carotenoids / pharmacology. Disease Models, Animal. Lipid Peroxidation / drug effects. Mice. Mice, Inbred BALB C. Xanthophylls

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  • MedlinePlus Health Information. consumer health - Vitamin C.
  • Hazardous Substances Data Bank. Sodium ascorbate .
  • Hazardous Substances Data Bank. ASTAXANTHINE .
  • Hazardous Substances Data Bank. L-Ascorbic Acid .
  • Hazardous Substances Data Bank. BETA-CAROTENE .
  • Hazardous Substances Data Bank. AGAR-AGAR .
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  • (PMID = 10952594.001).
  • [ISSN] 0066-4804
  • [Journal-full-title] Antimicrobial agents and chemotherapy
  • [ISO-abbreviation] Antimicrob. Agents Chemother.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Xanthophylls; 01YAE03M7J / beta Carotene; 36-88-4 / Carotenoids; 8XPW32PR7I / astaxanthine; 9002-18-0 / Agar; PQ6CK8PD0R / Ascorbic Acid
  • [Other-IDs] NLM/ PMC90084
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34. Yoshida T, Endo Y, Obata T, Kosugi Y, Sakamoto K, Sasaki T: Influence of cytidine deaminase on antitumor activity of 2'-deoxycytidine analogs in vitro and in vivo. Drug Metab Dispos; 2010 Oct;38(10):1814-9

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • To elucidate the relationship between the chemosensitivity to antitumor dCyd nucleosides and CDA expression, we established a stable line of human gastric carcinoma TMK-1 cells constitutively overexpressing CDA (TMK-1/CDA) and examined its chemosensitivity to antitumor dCyd analogs in vitro and in vivo.
  • We observed comparable reactivity for dFdC and Ara-C, and the substrate reactivity of CNDAC to recombinant human CDA was more than 10 times less efficient than those of Ara-C and dFdC.
  • In addition, we transplanted TMK-1/CDA cells into a nude mouse xenograft model and examined their in vivo chemosensitivity to CNDAC.
  • [MeSH-minor] Animals. Blotting, Western. Cell Line, Tumor. Cell Survival / drug effects. Female. Humans. Mice. Mice, Nude. Neoplasms, Experimental / drug therapy. Neoplasms, Experimental / enzymology. Neoplasms, Experimental / metabolism. Recombinant Proteins / genetics. Recombinant Proteins / metabolism. Substrate Specificity. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 20587622.001).
  • [ISSN] 1521-009X
  • [Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals
  • [ISO-abbreviation] Drug Metab. Dispos.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Recombinant Proteins; 0W860991D6 / Deoxycytidine; EC 3.5.4.5 / Cytidine Deaminase
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35. Coburger C, Lage H, Molnár J, Langner A, Hilgeroth A: Multidrug resistance reversal properties and cytotoxic evaluation of representatives of a novel class of HIV-1 protease inhibitors. J Pharm Pharmacol; 2010 Dec;62(12):1704-10
Genetic Alliance. consumer health - HIV.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVES: P-Glycoprotein (P-gp) plays a central role in the development of resistance against cytostatics in anticancer therapy and against human immunodeficiency virus (HIV) therapeutics of the HIV-1 protease inhibitor type.
  • An approach to reverse the so-called multidrug resistance (MDR) phenomenon by the use of P-gp inhibiting agents is a challenge in the therapy of cancer and AIDS.
  • METHODS: Novel HIV-1 protease inhibitors (H17, JW41, JW33 and JW46) have been evaluated in comparison with ritonavir as P-gp inhibiting agents, in the exclusively P-gp overexpressing model cell line mouse T lymphoma using flow cytometry.
  • The cytotoxic properties against various cell lines were characterized in the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide) assay to estimate potential toxic effects in therapeutically relevant concentrations in metabolically active HepG2 cells, drug-sensitive Jurkat cells and in gastric carcinoma cells.
  • CONCLUSIONS: The novel compounds have been shown to be prospective AIDS therapeutics, acting as effective and nontoxic P-gp inhibitors compared with ritonavir, which is a known P-gp inhibitor with unfavourable toxic and P-gp substrate properties.
  • [MeSH-major] Cell Survival / drug effects. Drug Resistance, Multiple / drug effects. HIV Protease Inhibitors / pharmacology. P-Glycoprotein / antagonists & inhibitors. Ritonavir / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Hep G2 Cells. Humans. Jurkat Cells. Lymphoma, T-Cell. Mice. Mitochondria / drug effects. Mitochondria / metabolism

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  • [Copyright] © 2010 The Authors. JPP © 2010 Royal Pharmaceutical Society of Great Britain.
  • (PMID = 21054396.001).
  • [ISSN] 2042-7158
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / HIV Protease Inhibitors; 0 / P-Glycoprotein; O3J8G9O825 / Ritonavir
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36. [Tuberculosis in compromised hosts]. Kekkaku; 2003 Nov;78(11):717-22
MedlinePlus Health Information. consumer health - Tuberculosis.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Many new findings and useful reports for practical medical treatment are submitted; why these compromised hosts are predisposed to tuberculosis, tuberculosis diagnostic and remedial notes of those compromised hosts etc.
  • In 1980, Saiki and co-workers reported that host defense and delayed-type hypersensitivity response to M. tuberculosis was hampered in a mouse DM model established by injecting streptozotocin (Infect Immun.
  • Patients who have undergone gastric resection are considered at increased risk of developing pulmonary tuberculosis.
  • Of 654 pulmonary tuberculosis patients admitted to National Chiba-Higashi Hospital from January 1999 to December 2001, 55 patients (31-84 years old, mean 63.5 +/- 12.5 years, 48 males and 7 females) had the history of gastric resection.
  • The mean age of gastric resection was 50.2 +/- 16.6 years, and the mean interval from gastrectomy to pulmonary tuberculosis was 13.6 +/- 11.0 years.
  • Gastrectomy was done due to carcinoma of the stomach in 31 cases, gastric and/or duodenal ulcer in 21 cases, adenomatous polyp in two cases, and accidental injury in one case.
  • No one had recurrence of carcinoma of the stomach.
  • I calculated the odds of tuberculosis among gastrectomy patients to be 3.8 times that of appropriate controls.
  • It is easy to stay in the leaching lesion so that anti-tuberculosis drugs are much effective, and the patients recover easily.
  • However, if the treatment is delayed, it is fatally because hematogenous metastasis are easy to occur and become miliary tuberculosis.
  • With AIDS patients with tuberculosis, there are the following problems on the treatment. (1) The adverse reactions by antituberculosis drugs tend to occur in AIDS patients.
  • Eleven of 33 AIDS patients with tuberculosis had the adverse reactions (skin rash, fever, liver dysfunction) considered to be due to antituberculosis drugs.
  • It is a very large burden for the HIV infected persons to take simultaneously antituberculosis drugs, medicines for opportunistic infections, and anti-HIV medicines.
  • Since many medicines are taken, it is difficult to determine which drug is the cause once an adverse reaction occurs and all medicines should be often stopped. (2) The combined use with rifampicin (RFP) is difficult for the protease inhibitors and nonnuclear acid reverse transcriptase inhibitors.
  • RFP induces cytochrome P-450 in liver, accelerates the metabolism of some concomitant drug agents, and reduces blood concentration them remarkably.
  • When starting the two above-mentioned medicines during tuberculosis treatment, RFP should be changed to rifabutin (RFB) which has less induction of P-450 than RFP.
  • So, the treatment with EFV and RFP is recently chosen.
  • However, the monitor of the blood concentration of EFV is required, and the dose of EFV should be increased if it is a low value. (3) When a highly active antiretroviral therapy (HAART) is given to AIDS patients with tuberculosis, transient worsening of tuberculosis may develop after about two weeks. (ABSTRACT TRUNCATED)

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  • (PMID = 14672050.001).
  • [ISSN] 0022-9776
  • [Journal-full-title] Kekkaku : [Tuberculosis]
  • [ISO-abbreviation] Kekkaku
  • [Language] jpn
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Japan
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