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1. Lin J, Zhang W, Xie B, Li L, Zhang L, Zheng J, Wang X: [Clinical investigation of IRESSA in the treatment of patients with advanced refractory non-small cell lung cancer]. Zhongguo Fei Ai Za Zhi; 2006 Oct 20;9(5):455-7
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  • [Title] [Clinical investigation of IRESSA in the treatment of patients with advanced refractory non-small cell lung cancer].
  • BACKGROUND: Chemotherapy is a main method for patients with advanced non-small cell lung cancer (NSCLC).
  • NSCLC is usually a drug-resistant neoplasm.
  • Innate or acquired drug-resis-tance contributes to the chief cause for bad effect in the treatment of patients with NSCLC.
  • To search for a new anti-cancer drug becomes a goal of clinical oncologists.
  • RESULTS: Totally 33 patients enrolled in this study and all were stage IV.
  • The curative effect was correlated with the pathological type, in sequence of alveolar cell carcinoma, adenocarcinoma and squamous cell carcinoma.
  • No electrocardiogram abnormality was found.
  • CONCLUSIONS: IRESSA takes better effect on the advanced drug-resistant patients with NSCLC.

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  • (PMID = 21176471.001).
  • [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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2. Lafferty-Whyte K, Bilsland A, Cairney CJ, Hanley L, Jamieson NB, Zaffaroni N, Oien KA, Burns S, Roffey J, Boyd SM, Keith WN: Scoring of senescence signalling in multiple human tumour gene expression datasets, identification of a correlation between senescence score and drug toxicity in the NCI60 panel and a pro-inflammatory signature correlating with survival advantage in peritoneal mesothelioma. BMC Genomics; 2010 Oct 01;11:532
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  • [Title] Scoring of senescence signalling in multiple human tumour gene expression datasets, identification of a correlation between senescence score and drug toxicity in the NCI60 panel and a pro-inflammatory signature correlating with survival advantage in peritoneal mesothelioma.
  • RESULTS: We first show that scoring captures differential induction of damage or inflammatory pathways in a series of public datasets involving radiotherapy of colon adenocarcinoma, chemotherapy of breast cancer cells, replicative senescence of mesenchymal stem cells, and progression of melanoma.
  • [MeSH-major] Antineoplastic Agents / toxicity. Cell Aging / genetics. Gene Expression Regulation, Neoplastic / drug effects. Inflammation / genetics. Mesothelioma / genetics. Peritoneal Neoplasms / genetics. Signal Transduction / genetics
  • [MeSH-minor] Breast Neoplasms / drug therapy. Breast Neoplasms / genetics. Breast Neoplasms / pathology. Breast Neoplasms / radiotherapy. Cell Line, Tumor. Cluster Analysis. Databases, Genetic. Disease Progression. Female. Gene Expression Profiling. Humans. Mesenchymal Stromal Cells / drug effects. Mesenchymal Stromal Cells / metabolism. Prognosis. Research Design. Survival Analysis

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  • [Cites] Cell. 2006 Mar 24;124(6):1169-81 [16564011.001]
  • [Cites] Hum Mol Genet. 2006 Mar 1;15(5):725-33 [16421168.001]
  • [Cites] PLoS One. 2009;4(7):e6459 [19649288.001]
  • [Cites] Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9363-7 [7568133.001]
  • [Cites] Histopathology. 2001 Aug;39(2):187-97 [11493336.001]
  • [Cites] Cancer Cell. 2010 Mar 16;17(3):262-72 [20227040.001]
  • [Cites] Int J Radiat Biol. 2005 Jun;81(6):445-58 [16308915.001]
  • [Cites] Environ Health Perspect. 2004 Nov;112(16):1607-13 [15598611.001]
  • [Cites] Cancer Biol Ther. 2008 Mar;7(3):392-6 [18075305.001]
  • [Cites] PLoS Biol. 2008 Dec 2;6(12):2853-68 [19053174.001]
  • [Cites] Cancer Res. 2005 Apr 1;65(7):2795-803 [15805280.001]
  • [Cites] Clin J Am Soc Nephrol. 2010 Jan;5(1):56-61 [19833906.001]
  • [Cites] Mol Divers. 2006 Feb;10(1):39-79 [16404528.001]
  • [Cites] Cancer Res. 2006 Mar 15;66(6):2881-4 [16540631.001]
  • [Cites] Trends Biochem Sci. 2002 Jul;27(7):339-44 [12114022.001]
  • [Cites] EMBO Rep. 2009 Mar;10(3):228-30 [19218920.001]
  • [Cites] Mech Ageing Dev. 2009 Jan-Feb;130(1-2):24-32 [18538372.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Aug 12;105(32):11299-304 [18695223.001]
  • [Cites] Curr Opin Cell Biol. 2008 Apr;20(2):150-5 [18353625.001]
  • [Cites] Nat Cell Biol. 2009 Aug;11(8):973-9 [19597488.001]
  • [Cites] Annu Rev Genet. 2008;42:301-34 [18680434.001]
  • [Cites] J Pathol. 2005 Dec;207(4):410-21 [16177957.001]
  • [Cites] FEBS Lett. 2008 Apr 30;582(10):1451-8 [18381073.001]
  • [Cites] Nat Rev Mol Cell Biol. 2007 Sep;8(9):729-40 [17667954.001]
  • [Cites] Eur J Cancer. 2009 Aug;45(12):2138-45 [19409772.001]
  • [Cites] Br J Cancer. 2007 Mar 12;96(5):686-91 [17311013.001]
  • [Cites] Nat Rev Cancer. 2006 Jun;6(6):472-6 [16723993.001]
  • [Cites] Nat Genet. 2000 Mar;24(3):236-44 [10700175.001]
  • [Cites] Pigment Cell Melanoma Res. 2008 Feb;21(1):27-38 [18353141.001]
  • [Cites] Cell. 2002 May 3;109(3):335-46 [12015983.001]
  • [Cites] Exp Cell Res. 2008 Jun 10;314(9):1909-17 [18423606.001]
  • [Cites] Cell. 2008 Jun 13;133(6):1019-31 [18555778.001]
  • [Cites] PLoS Biol. 2007 May;5(5):e110 [17472436.001]
  • [Cites] Life Sci. 2008 Sep 26;83(13-14):475-80 [18723031.001]
  • [Cites] Dev Cell. 2005 Jan;8(1):19-30 [15621527.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3303-8 [15867227.001]
  • [Cites] PLoS One. 2008;3(5):e2213 [18493317.001]
  • [Cites] Oncogene. 2009 Oct 29;28(43):3765-74 [19684619.001]
  • [Cites] Clin Cancer Res. 2008 Jul 1;14(13):4134-40 [18593991.001]
  • [Cites] Biochem Pharmacol. 2008 Oct 15;76(8):947-57 [18657518.001]
  • [Cites] Aging Cell. 2010 Apr;9(2):220-35 [20089118.001]
  • [Cites] Mol Oncol. 2010 Feb;4(1):52-64 [19969511.001]
  • [Cites] Cancer Biol Ther. 2005 Sep;4(9):1018-29 [16251803.001]
  • [Cites] Mol Cell Biol. 2007 Mar;27(6):2343-58 [17242207.001]
  • [Cites] Oncogene. 2008 Oct 9;27(46):5975-87 [18711403.001]
  • [Cites] Nat Rev Cancer. 2009 Feb;9(2):81-94 [19132009.001]
  • [Cites] Genes Dev. 2009 Apr 1;23(7):798-803 [19279323.001]
  • [Cites] Neoplasia. 2010 May;12(5):405-14 [20454512.001]
  • [Cites] Endocr Relat Cancer. 1999 Mar;6(1):41-4 [10732785.001]
  • [Cites] EMBO J. 2003 Aug 15;22(16):4212-22 [12912919.001]
  • [Cites] Cancer Inform. 2007 Feb 04;3:11-7 [19455231.001]
  • [Cites] J Neurosurg. 2006 Jul;105(1):111-8 [16871885.001]
  • [Cites] Br J Cancer. 2008 Apr 22;98(8):1467-74 [18414473.001]
  • (PMID = 20920304.001).
  • [ISSN] 1471-2164
  • [Journal-full-title] BMC genomics
  • [ISO-abbreviation] BMC Genomics
  • [Language] eng
  • [Grant] United Kingdom / Chief Scientist Office / / CAF/06/24; United Kingdom / Cancer Research UK / / F2-2007-200950
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents
  • [Other-IDs] NLM/ PMC3091681
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3. Takemura M, Osugi H, Lee S, Taguchi S, Kaneko M, Tanaka Y, Fukuhara K, Fujiwara Y, Nishizawa S, Kinoshita H, Harada S: [A case of synchronous esophageal and gastric cancer successfully treated by combination TS-1/CDDP therapy with irradiation]. Gan To Kagaku Ryoho; 2004 Feb;31(2):251-4
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  • A 56-year-old man with a chief complaint of dysphagia was diagnosed with thoracic esophageal cancer by endoscopy, and was referred to our hospital.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Esophageal Neoplasms / drug therapy. Esophageal Neoplasms / radiotherapy. Neoplasms, Multiple Primary. Stomach Neoplasms / drug therapy. Stomach Neoplasms / radiotherapy
  • [MeSH-minor] Adenocarcinoma / drug therapy. Adenocarcinoma / radiotherapy. Administration, Oral. Carcinoma, Squamous Cell / drug therapy. Carcinoma, Squamous Cell / radiotherapy. Cisplatin / administration & dosage. Combined Modality Therapy. Drug Administration Schedule. Drug Combinations. Humans. Male. Middle Aged. Oxonic Acid / administration & dosage. Pyridines / administration & dosage. Radiotherapy Dosage. Tegafur / administration & dosage

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  • (PMID = 14997762.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Pyridines; 150863-82-4 / S 1 (combination); 1548R74NSZ / Tegafur; 5VT6420TIG / Oxonic Acid; Q20Q21Q62J / Cisplatin
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4. Morton JP, Karim SA, Graham K, Timpson P, Jamieson N, Athineos D, Doyle B, McKay C, Heung MY, Oien KA, Frame MC, Evans TR, Sansom OJ, Brunton VG: Dasatinib inhibits the development of metastases in a mouse model of pancreatic ductal adenocarcinoma. Gastroenterology; 2010 Jul;139(1):292-303
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Dasatinib inhibits the development of metastases in a mouse model of pancreatic ductal adenocarcinoma.
  • BACKGROUND & AIMS: Pancreatic ductal adenocarcinoma (PDAC) is a highly invasive and metastatic disease for which conventional treatments are of limited efficacy.
  • A number of agents in development are potential anti-invasive and antimetastatic agents, including the Src kinase inhibitor dasatinib.
  • The aim of this study was to assess the importance of Src in human PDAC and to use a genetically engineered mouse model of PDAC to determine the effects of dasatinib on PDAC progression.
  • Cell lines were derived from mouse PDACs, and in vitro effects of dasatinib assessed.
  • Dasatinib inhibited the migration and invasion of PDAC cell lines, although no effects on proliferation were seen at concentrations that inhibited Src kinase activity.
  • However, there was no survival advantage in the dasatinib-treated animals owing to continued growth of the primary tumor.
  • CONCLUSIONS: This study confirms the importance of Src in human PDAC and shows the usefulness of a genetically engineered mouse model of PDAC for assessing the activity of potential antimetastatic agents and suggests that dasatinib should be evaluated further as monotherapy after resection of localized invasive PDAC.
  • [MeSH-major] Carcinoma, Pancreatic Ductal / drug therapy. Pancreatic Neoplasms / drug therapy. Protein Kinase Inhibitors / therapeutic use. Pyrimidines / therapeutic use. Thiazoles / therapeutic use. src-Family Kinases / antagonists & inhibitors
  • [MeSH-minor] Animals. Cell Line, Tumor. Cell Movement / drug effects. Dasatinib. Disease Models, Animal. Female. Mice. Neoplasm Invasiveness. Neoplasm Metastasis

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  • [Copyright] Copyright 2010 AGA Institute. Published by Elsevier Inc. All rights reserved.
  • (PMID = 20303350.001).
  • [ISSN] 1528-0012
  • [Journal-full-title] Gastroenterology
  • [ISO-abbreviation] Gastroenterology
  • [Language] eng
  • [Grant] United Kingdom / Chief Scientist Office / / CAF/06/24; United Kingdom / Cancer Research UK / / C157/A9148; United Kingdom / Chief Scientist Office / / ; United Kingdom / Cancer Research UK / / C2193/A7603
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Protein Kinase Inhibitors; 0 / Pyrimidines; 0 / Thiazoles; EC 2.7.10.2 / src-Family Kinases; RBZ1571X5H / Dasatinib
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5. Theoharides TC, Rozniecki JJ, Sahagian G, Jocobson S, Kempuraj D, Conti P, Kalogeromitros D: Impact of stress and mast cells on brain metastases. J Neuroimmunol; 2008 Dec 15;205(1-2):1-7
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  • Metastases continue to be the chief cause of morbidity and mortality for many tumors, including brain metastases of lung and mammary adenocarcinoma.
  • Recent evidence suggests that local inflammation is conducive for cancer growth and a unique immune cell, the mast cell, accumulates in the stroma surrounding tumors and is critically located at the blood-brain-barrier (BBB).
  • Stress and mast cells could serve as new targets for drug development to prevent brain metastases, especially since CRH receptor antagonists and brain mast cell inhibitors have recently been developed.
  • [MeSH-minor] Animals. Blood-Brain Barrier / drug effects. Blood-Brain Barrier / physiopathology. Humans. Inflammation / pathology. Inflammation / physiopathology. Inflammation Mediators / metabolism. Inflammation Mediators / pharmacology

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  • [CommentIn] J Neuroimmunol. 2009 Apr 30;209(1-2):121-2 [19195717.001]
  • (PMID = 18977036.001).
  • [ISSN] 0165-5728
  • [Journal-full-title] Journal of neuroimmunology
  • [ISO-abbreviation] J. Neuroimmunol.
  • [Language] eng
  • [Grant] United States / NIAMS NIH HHS / AR / AR47658; United States / NCI NIH HHS / BC / BC24430; United States / NIDDK NIH HHS / DK / DK62861; United States / NINDS NIH HHS / NS / NS38326; United States / NINDS NIH HHS / NS / NS55681
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Inflammation Mediators
  • [Number-of-references] 173
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6. Clemons NJ, McColl KE, Fitzgerald RC: Nitric oxide and acid induce double-strand DNA breaks in Barrett's esophagus carcinogenesis via distinct mechanisms. Gastroenterology; 2007 Oct;133(4):1198-209
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  • METHODS: Transformed and primary Barrett's esophagus and adenocarcinoma cells were exposed to either acid, (pH 3.5), +/- antioxidant or NO from a donor or generated by acidification of nitrite in the presence of ascorbate +/- NO scavenger.
  • RESULTS: Exposure to acid (pH 3.5) for > or =15 minutes induced DSBs in all cell lines (P < .05).
  • Exposure to physiologic concentrations of NO produced from the NO donor or acidification of salivary nitrite induced DSBs in a dose- (>25 micromol/L) and cell-dependent manner (adenocarcinoma >Barrett's esophagus, P < .05).
  • [MeSH-major] Adenocarcinoma / metabolism. Barrett Esophagus / complications. Cell Transformation, Neoplastic / metabolism. DNA Breaks, Single-Stranded. Esophageal Neoplasms / metabolism. Gastric Acid / metabolism. Nitric Oxide / metabolism
  • [MeSH-minor] Antioxidants / pharmacology. Ascorbic Acid / pharmacology. Cell Line, Tumor. Cell Survival. Comet Assay. Dose-Response Relationship, Drug. Histones / metabolism. Humans. Hydrazines / pharmacology. Hydrogen-Ion Concentration. Mitochondria / metabolism. Mitochondria / pathology. Nitric Oxide Donors / pharmacology. Phosphorylation. Reactive Oxygen Species / metabolism. S Phase. Sodium Nitrite / pharmacology. Time Factors


7. Shimizu K, Watanabe E, Hamanaka S, Onuma S, Nakano M, Yamazaki T, Higa M, Yamamuro W, Kiguchi E: [A case of non-small-cell lung cancer successfully treated using combination chemotherapy with CDDP and vinorelbine]. Gan To Kagaku Ryoho; 2000 Sep;27(10):1565-8
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  • [Title] [A case of non-small-cell lung cancer successfully treated using combination chemotherapy with CDDP and vinorelbine].
  • A 67-year-old woman presented to our hospital with a chief complaint of bloody sputum.
  • A tumor biopsy done under bronchoscopy revealed poorly differentiated adenocarcinoma of the lungs (cT2N3M1).
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Carcinoma, Non-Small-Cell Lung / drug therapy. Lung Neoplasms / drug therapy
  • [MeSH-minor] Aged. Cisplatin / administration & dosage. Drug Administration Schedule. Female. Humans. Vinblastine / analogs & derivatives

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  • (PMID = 11016002.001).
  • [ISSN] 0385-0684
  • [Journal-full-title] Gan to kagaku ryoho. Cancer & chemotherapy
  • [ISO-abbreviation] Gan To Kagaku Ryoho
  • [Language] jpn
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] JAPAN
  • [Chemical-registry-number] 5V9KLZ54CY / Vinblastine; Q20Q21Q62J / Cisplatin
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8. 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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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [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.
  • 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.
  • 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.
  • [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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9. Yamaguchi H, Goldenring JR, Kaminishi M, Lee JR: Association of spasmolytic polypeptide-expressing metaplasia with carcinogen administration and oxyntic atrophy in rats. Lab Invest; 2002 Aug;82(8):1045-52
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  • Spasmolytic polypeptide (TFF2)-expressing metaplasia (SPEM) is a gastric metaplastic lineage associated with the development of intestinal-type gastric adenocarcinoma.
  • To study the etiology of this potential neoplastic precursor metaplasia, we used surgical rat models of remnant gastric adenocarcinoma studied with and without exposure to nitroso carcinogen.
  • Animals with truncal vagotomy without duodenogastric reflux procedures demonstrated normal mucous neck cell spasmolytic polypeptide (SP) immunostaining.
  • In these animals, anti-proliferating cell nuclear antigen (PCNA)-labeled nuclei were found in the normal midgland progenitor zone.
  • Seventy percent of animals with antrectomy and carcinogen (with or without vagotomy) developed SPEM at the base of the gastric mucosa.
  • Of interest, three animals demonstrating these changes developed intestinal-type gastric adenocarcinoma.
  • Finally, we studied the immunostaining pattern of intrinsic factor, normally a chief cell marker in rat fundic mucosa.
  • In animals with SPEM, we observed coexpression of SP and intrinsic factor in SPEM cells at the base of the mucosa.
  • These findings support our hypothesis that SPEM develops from a second progenitor cell population, reflecting either the unmasking of a cryptic zone or transdifferentiation of chief cells.
  • [MeSH-minor] Animals. Carcinogens / toxicity. Cell Differentiation. Cell Transformation, Neoplastic. Male. Metaplasia. Nitroso Compounds / toxicity. Rats. Rats, Wistar. Stomach / drug effects. Stomach / metabolism. Stomach / pathology

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  • (PMID = 12177243.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Nitroso Compounds; 0 / Peptides; 0 / spasmolytic polypeptide
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