[X] Close
You are about to erase all the values you have customized, search history, page format, etc.
Click here to RESET all values       Click here to GO BACK without resetting any value
Items 1 to 55 of about 55
1. Ye Q, Zhou J, Zhang W: [Effect of endothelin-1 on the proliferation of human lung adenocarcinoma cell SPC-A1]. Zhongguo Fei Ai Za Zhi; 2007 Feb 20;10(1):1-4

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Effect of endothelin-1 on the proliferation of human lung adenocarcinoma cell SPC-A1].
  • BACKGROUND: Endothelin-1 (ET-1) is a potent mitogen involved in tumor cell growth and angiogenesis.
  • The aim of this study is to explore the effect of ET-1 on the proliferation of human lung adenocarcinoma cells SPC-A1.
  • METHODS: Cell number was measured by MTT [3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide] assay.
  • Cell cycle was detected by flow cytometry.
  • RESULTS: ET-1 (1×10⁻¹⁵ -1×10⁻⁸ mol/L) enhanced SPC-A1 cell growth in a dose-dependent manner in vitro, with the greatest effect beginning at 1×10⁻¹¹ mol/L.
  • BQ123 could significantly reduce the basal growth of SPC-A1 cells (P < 0.05), but BQ788 had no such effect.
  • ET-1 had no significant effect on SPC-A1 cell cycle.
  • CONCLUSIONS: ET-1 enhances SPC-A1 cell proliferation by the activation of ETA receptor.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21110923.001).
  • [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
  •  go-up   go-down


2. DiMeo TA, Anderson K, Phadke P, Fan C, Perou CM, Naber S, Kuperwasser C: A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer. Cancer Res; 2009 Jul 1;69(13):5364-73
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] A novel lung metastasis signature links Wnt signaling with cancer cell self-renewal and epithelial-mesenchymal transition in basal-like breast cancer.
  • In epithelial cancers, such as those of the breast, the epithelial-mesenchymal transition (EMT) is associated with basal-like breast cancers, generates cells with stem-like properties, and enables cancer cell dissemination and metastasis.
  • However, the molecular mechanism(s) that connects stem cell-like characteristics with EMT has yet to be defined.
  • Using an orthotopic model of human breast cancer metastasis to lung, we identified a poor prognosis gene signature, in which several components of the wnt signaling pathway were overexpressed in early lung metastases.
  • The wnt genes identified in this signature were strongly associated with human basal-like breast cancers.
  • Collectively, these results provide a molecular link between self-renewal, EMT, and metastasis in basal-like breast cancers.

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Breast Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] J Mammary Gland Biol Neoplasia. 2007 Sep;12(2-3):153-62 [17566854.001]
  • [Cites] Oncogene. 2007 Aug 16;26(38):5680-91 [17353908.001]
  • [Cites] J Cell Biochem. 2007 Dec 15;102(6):1519-28 [17471511.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Dec 4;104(49):19506-11 [18048329.001]
  • [Cites] Br J Cancer. 2008 Mar 25;98(6):1147-56 [18283316.001]
  • [Cites] Cancer Res. 2008 May 1;68(9):3108-14 [18451135.001]
  • [Cites] Cell. 2008 May 16;133(4):704-15 [18485877.001]
  • [Cites] Breast Cancer Res. 2008;10(2):R25 [18366788.001]
  • [Cites] Clin Exp Metastasis. 2008;25(6):629-42 [18461285.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4262-6 [10759547.001]
  • [Cites] J Biol Chem. 2001 Aug 10;276(32):30350-8 [11402039.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10869-74 [11553815.001]
  • [Cites] Nature. 2002 Jan 31;415(6871):530-6 [11823860.001]
  • [Cites] Nat Rev Cancer. 2002 Aug;2(8):563-72 [12154349.001]
  • [Cites] N Engl J Med. 2002 Dec 19;347(25):1999-2009 [12490681.001]
  • [Cites] Breast Cancer Res. 2003;5(2):101-6 [12631389.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Apr 1;100(7):3983-8 [12629218.001]
  • [Cites] Cancer Res. 2003 Apr 15;63(8):1906-13 [12702582.001]
  • [Cites] Cancer Cell. 2003 Jun;3(6):537-49 [12842083.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10393-8 [12917485.001]
  • [Cites] Cancer Res. 2003 Sep 15;63(18):5679-84 [14522883.001]
  • [Cites] J Cell Biol. 2003 Nov 24;163(4):847-57 [14623871.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Dec 23;100(26):15901-5 [14665696.001]
  • [Cites] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665.001]
  • [Cites] Cancer Cell. 2004 Jun;5(6):607-16 [15193263.001]
  • [Cites] Cell. 2004 Jun 25;117(7):927-39 [15210113.001]
  • [Cites] Int J Oncol. 2004 Sep;25(3):641-9 [15289865.001]
  • [Cites] Cell. 2004 Aug 6;118(3):277-9 [15294153.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Sep 21;101(38):13756-61 [15356343.001]
  • [Cites] Int J Cancer. 2005 Feb 10;113(4):515-24 [15472907.001]
  • [Cites] Oncogene. 2005 Jul 7;24(29):4660-71 [15897907.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6130-8 [16024614.001]
  • [Cites] Nature. 2005 Jul 28;436(7050):518-24 [16049480.001]
  • [Cites] Cancer Biol Ther. 2005 Apr;4(4):365-70 [15846061.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 20;102(38):13550-5 [16141321.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):13909-14 [16172383.001]
  • [Cites] Nat Genet. 2005 Oct;37(10):1047-54 [16142232.001]
  • [Cites] Mol Biol Cell. 2005 Nov;16(11):5283-93 [16135532.001]
  • [Cites] J Leukoc Biol. 2006 Feb;79(2):339-50 [16282532.001]
  • [Cites] Breast Cancer Res. 2005;7(6):R953-64 [16280042.001]
  • [Cites] Cancer Cell. 2006 Feb;9(2):121-32 [16473279.001]
  • [Cites] Cancer Biol Ther. 2006 Mar;5(3):281-6 [16410723.001]
  • [Cites] BMC Genomics. 2006;7:96 [16643655.001]
  • [Cites] J Clin Oncol. 2006 Sep 10;24(26):4236-44 [16896004.001]
  • [Cites] Cancer Res. 2006 Nov 1;66(21):10292-301 [17079448.001]
  • [Cites] Cell. 2006 Nov 3;127(3):469-80 [17081971.001]
  • [Cites] Nat Cell Biol. 2006 Dec;8(12):1398-406 [17072303.001]
  • [Cites] Oncogene. 2006 Dec 4;25(57):7469-81 [17143291.001]
  • [Cites] Oncogene. 2006 Dec 4;25(57):7531-7 [17143297.001]
  • [Cites] Breast Cancer Res. 2006;8(5):R59 [17062128.001]
  • [Cites] Cancer Cell. 2007 Mar;11(3):259-73 [17349583.001]
  • [Cites] Clin Cancer Res. 2007 Jun 1;13(11):3207-14 [17545524.001]
  • [Cites] Genome Biol. 2007;8(5):R76 [17493263.001]
  • [ErratumIn] Cancer Res. 2009 Aug 1;69(15):6366. Feng, Chang [corrected to Fan, Cheng]
  • (PMID = 19549913.001).
  • [ISSN] 1538-7445
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA125554-02; United States / NCI NIH HHS / CA / R01 CA125554; United States / NCI NIH HHS / CA / R01 CA125554-02; United States / NCI NIH HHS / CA / R01CA12555
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nuclear Proteins; 0 / TWIST1 protein, human; 0 / Transcription Factors; 0 / Twist Transcription Factor; 0 / Wnt Proteins; 0 / snail family transcription factors
  • [Other-IDs] NLM/ NIHMS154900; NLM/ PMC2782448
  •  go-up   go-down


3. Wei J, Yan W, Li X, Chang WC, Tai HH: Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells. Biochem Pharmacol; 2007 Sep 1;74(5):787-800
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] Activation of thromboxane receptor alpha induces expression of cyclooxygenase-2 through multiple signaling pathways in A549 human lung adenocarcinoma cells.
  • Human lung adenocarcinoma A549 cells stably transfected with TPalpha (A549-TPalpha) were used to study agonist I-BOP-induced expression of cyclooxygenase-2 (COX-2) and the related mechanisms of induced expression.
  • Distal NF-kappaB site is essential for the basal induction of the COX-2 transcription, whereas CRE and proximal NF-kappaB sites are important for the induced transcription.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Biochem Biophys Res Commun. 2000 Jan 7;267(1):245-51 [10623605.001]
  • [Cites] J Biol Chem. 1998 Apr 3;273(14):8389-97 [9525949.001]
  • [Cites] N Engl J Med. 2000 Jun 29;342(26):1946-52 [10874062.001]
  • [Cites] Biochem J. 2000 Dec 1;352 Pt 2:419-24 [11085935.001]
  • [Cites] Cancer Lett. 2006 Mar 28;234(2):193-8 [15876485.001]
  • [Cites] J Pharmacol Exp Ther. 2006 Apr;317(1):267-74 [16352701.001]
  • [Cites] J Immunol. 2006 Apr 15;176(8):5050-9 [16585602.001]
  • [Cites] Cell Signal. 2006 Aug;18(8):1235-43 [16289764.001]
  • [Cites] Carcinogenesis. 2006 Nov;27(11):2170-9 [16632868.001]
  • [Cites] Ann Intern Med. 1994 Aug 15;121(4):241-6 [8037405.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Feb;296(2):426-33 [11160627.001]
  • [Cites] J Biol Chem. 2001 May 25;276(21):18075-81 [11278548.001]
  • [Cites] Biochim Biophys Acta. 2001 May 28;1539(1-2):147-62 [11389977.001]
  • [Cites] J Pharmacol Exp Ther. 2001 Sep;298(3):1243-51 [11504827.001]
  • [Cites] Clin Cancer Res. 2001 Sep;7(9):2669-74 [11555578.001]
  • [Cites] J Biol Chem. 2001 Oct 12;276(41):37839-45 [11483590.001]
  • [Cites] Br J Pharmacol. 2001 Nov;134(6):1137-50 [11704632.001]
  • [Cites] Chem Rev. 2001 Aug;101(8):2449-76 [11749383.001]
  • [Cites] Am J Pathol. 2002 Feb;160(2):389-401 [11839557.001]
  • [Cites] Mol Pharmacol. 2002 Apr;61(4):817-31 [11901221.001]
  • [Cites] Biochem J. 2003 May 1;371(Pt 3):733-42 [12534349.001]
  • [Cites] Oncogene. 2003 Jul 3;22(27):4150-65 [12833138.001]
  • [Cites] J Biol Chem. 2004 Jan 9;279(2):1323-9 [14581482.001]
  • [Cites] Biochim Biophys Acta. 2004 Jul 5;1683(1-3):38-48 [15238218.001]
  • [Cites] Proc Natl Acad Sci U S A. 1975 Aug;72(8):2994-8 [1059088.001]
  • [Cites] Nature. 1976 Jun 17;261(5561):558-60 [934294.001]
  • [Cites] Science. 1976 Jul 9;193(4248):163-5 [945611.001]
  • [Cites] Nature. 1991 Feb 14;349(6310):617-20 [1825698.001]
  • [Cites] J Biol Chem. 1991 May 15;266(14):9309-13 [1851174.001]
  • [Cites] J Biol Chem. 1994 Feb 25;269(8):5693-8 [8119906.001]
  • [Cites] Nature. 1994 May 12;369(6476):156-60 [8177321.001]
  • [Cites] J Biol Chem. 1994 Jul 29;269(30):19256-61 [8034687.001]
  • [Cites] Biochim Biophys Acta. 1996 Jan 5;1299(1):125-40 [8555245.001]
  • [Cites] Cancer Res. 1998 Sep 1;58(17):3761-4 [9731479.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1395-413 [9779987.001]
  • [Cites] Cancer Res. 1998 Nov 15;58(22):4997-5001 [9823297.001]
  • [Cites] Cancer Res. 1999 Sep 15;59(18):4574-7 [10493510.001]
  • [Cites] Carcinogenesis. 2005 Jan;26(1):65-72 [15358636.001]
  • [Cites] J Neurochem. 2005 Apr;93(2):257-68 [15816849.001]
  • [Cites] Cancer Res. 2005 Jul 15;65(14):6275-81 [16024629.001]
  • [Cites] Nat Cell Biol. 2005 Aug;7(8):758-65 [16056267.001]
  • [Cites] Biochem Biophys Res Commun. 2005 Dec 16;338(2):1171-8 [16256948.001]
  • [Cites] Cancer Res. 2005 Dec 15;65(24):11581-7 [16357168.001]
  • [Cites] Nucleic Acids Res. 2006;34(1):217-31 [16397300.001]
  • [Cites] J Biol Chem. 2006 Feb 24;281(8):4564-9 [16371352.001]
  • [Cites] Nature. 1996 Feb 8;379(6565):557-60 [8596637.001]
  • [Cites] J Clin Invest. 1996 Feb 15;97(4):949-56 [8613548.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 May 14;93(10):4816-20 [8643486.001]
  • [Cites] Kidney Int. 1996 May;49(5):1187-98 [8731081.001]
  • [Cites] J Biol Chem. 1997 Jan 3;272(1):601-8 [8995303.001]
  • [Cites] Eur J Neurosci. 1997 May;9(5):934-40 [9182946.001]
  • [Cites] Biochim Biophys Acta. 1996 Jan 10;1310(1):48-52 [9244174.001]
  • [Cites] Biochem Biophys Res Commun. 2000 Jun 16;272(3):744-8 [10860826.001]
  • (PMID = 17632087.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL046296-11; United States / NHLBI NIH HHS / HL / R01 HL046296-07; United States / NHLBI NIH HHS / HL / R01 HL046296; United States / NHLBI NIH HHS / HL / HL046296-06; United States / NHLBI NIH HHS / HL / HL046296-07; United States / NHLBI NIH HHS / HL / HL-46296; United States / NHLBI NIH HHS / HL / R01 HL046296-09; United States / NHLBI NIH HHS / HL / HL046296-08; United States / NHLBI NIH HHS / HL / R01 HL046296-11; United States / NHLBI NIH HHS / HL / R01 HL046296-08; United States / NHLBI NIH HHS / HL / HL046296-09; United States / NHLBI NIH HHS / HL / R01 HL046296-10; United States / NHLBI NIH HHS / HL / HL046296-10; United States / NHLBI NIH HHS / HL / R01 HL046296-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Bicyclo Compounds, Heterocyclic; 0 / Fatty Acids, Unsaturated; 0 / Protein Isoforms; 0 / Receptors, Thromboxane; 0 / Receptors, Thromboxane A2, Prostaglandin H2; 124924-85-2 / 7-(3-(3-hydroxy-4-(4'-iodophenoxy)-1-butenyl)-7-oxabicyclo(2.2.1)heptan-2-yl)-5-heptenoic acid; EC 1.14.99.1 / Cyclooxygenase 2
  • [Other-IDs] NLM/ NIHMS28713; NLM/ PMC1995664
  •  go-up   go-down


Advertisement
4. Paschoud S, Bongiovanni M, Pache JC, Citi S: Claudin-1 and claudin-5 expression patterns differentiate lung squamous cell carcinomas from adenocarcinomas. Mod Pathol; 2007 Sep;20(9):947-54
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Claudin-1 and claudin-5 expression patterns differentiate lung squamous cell carcinomas from adenocarcinomas.
  • We investigated the expression of tight junction proteins in human lung squamous cell carcinomas and adenocarcinomas by immunohistochemistry and quantitative real-time reverse transcription-polymerase chain reaction (RT-PCR).
  • We found a statistically significant correlation between diagnosis and positivity of tumors with either claudin (CLDN)-1 or CLDN-5.
  • Squamous cell carcinomas and basal cells of bronchial epithelium were positive for CLDN-1 and negative for CLDN-5, whereas adenocarcinomas, normal cylindrical cells and pneumocytes were positive for CLDN-5 and negative for CLDN-1, suggesting different pathways in tumor development and progression.
  • CLDN-4 and ZO-1 staining were detected in both types of tumors, whereas cingulin (CGN) was not detected in squamous cell carcinomas.
  • In squamous cell carcinomas, we observed statistically significant decreases in the mRNA levels of JAM-1, occludin, CLDN-3, CLDN-4, CLDN-7, CGN, ZO-2 and ZO-3, and an increase in CLDN-1 mRNA.
  • These results indicate that characterization of tight junction protein expression in human lung tumors can be an additional diagnostic tool and provide new insights on their histogenesis.
  • [MeSH-major] Adenocarcinoma / diagnosis. Carcinoma, Squamous Cell / diagnosis. Lung Neoplasms / diagnosis. Membrane Proteins / analysis. Tight Junctions / chemistry
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / analysis. Biomarkers, Tumor / genetics. Claudin-1. Claudin-4. Claudin-5. Diagnosis, Differential. Female. Gene Expression Regulation, Neoplastic. Humans. Immunohistochemistry. Male. Microfilament Proteins / analysis. Middle Aged. Neoplasm Staging. Phosphoproteins / analysis. RNA, Messenger / analysis. Reverse Transcriptase Polymerase Chain Reaction. Zonula Occludens-1 Protein

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17585317.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CGN protein, human; 0 / CLDN1 protein, human; 0 / CLDN4 protein, human; 0 / CLDN5 protein, human; 0 / Claudin-1; 0 / Claudin-4; 0 / Claudin-5; 0 / Membrane Proteins; 0 / Microfilament Proteins; 0 / Phosphoproteins; 0 / RNA, Messenger; 0 / TJP1 protein, human; 0 / Zonula Occludens-1 Protein
  •  go-up   go-down


5. Saad RS, Liu YL, Silverman JF: Distribution of basal/myoepithelial markers in benign and malignant bronchioloalveolar proliferations of the lung. Appl Immunohistochem Mol Morphol; 2010 May;18(3):219-25
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Distribution of basal/myoepithelial markers in benign and malignant bronchioloalveolar proliferations of the lung.
  • We investigated the staining pattern of commonly used basal cell/myoepithelial markers, such as p63 (a p53-homologous nuclear protein), basal cell-specific cytokeratin antibody (34betaE12, K903), and smooth muscle myosin heavy chain (SMMHC) in benign and malignant bronchioloalveolar proliferations of the lung.
  • We studied 85 lung lesions consisting of 35 bronchioloalveolar carcinoma, 30 well-differentiated adenocarcinoma, and 20 cases of benign lung lesions.
  • In normal lung, p63, K903, and SMMHC decorated the basal cells of large and small airways and occasional cells of terminal bronchioles.
  • In reactive processes, a distinctive staining pattern was present in 19/20 (95%) of the cases characterized by staining of basal cells of the airways and bronchiolar epithelium and squamous metaplastic epithelium for p63 and K903, whereas 12/20 (60%) stained with SMMHC.
  • For adenocarcinoma, a majority of the cases (28/30, 93%) were negative for p63 and K903; however, SMMHC showed artifactual staining in the desmoplastic stroma in 6/30 (20%) cases.
  • Our results highlighted the differential expression of basal cell markers across various bronchioloalveolar lesions.
  • The staining pattern of basal cells in bronchioloalveolar carcinoma supports that these neoplasms may actually be carcinoma in-situ.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 20065853.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / CKAP4 protein, human; 0 / Membrane Proteins; 68238-35-7 / Keratins; EC 3.6.1.- / Smooth Muscle Myosins
  •  go-up   go-down


6. Boelens MC, van den Berg A, Vogelzang I, Wesseling J, Postma DS, Timens W, Groen HJ: Differential expression and distribution of epithelial adhesion molecules in non-small cell lung cancer and normal bronchus. J Clin Pathol; 2007 Jun;60(6):608-14
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] Differential expression and distribution of epithelial adhesion molecules in non-small cell lung cancer and normal bronchus.
  • BACKGROUND: Changes in epithelial cell interactions have been implicated in carcinogenesis, tumour invasion and metastasis.
  • AIM: To screen for altered expression of epithelial adhesion genes in lung cancer development.
  • METHODS: Gene expression profiles were assessed with cDNA expression arrays in eight non-small cell lung cancer (NSCLC) and eight normal bronchi obtained from the same patient.
  • RESULTS: 43 differentially expressed cancer-related genes were identified in adenocarcinoma, squamous cell carcinoma (SCC) and normal bronchus.
  • ITGA3 and ITGB4, showing predominantly cell-matrix staining, were up regulated in adenocarcinoma and SCC, respectively.
  • Components of the desmosome adhesion complex DSP, plakoglobin and DSC3 were strongly up regulated in SCC and showed a distinct cell-cell staining pattern.
  • DSP and plakoglobin were predominantly present at central, more differentiated tumour cells, whereas DSC3 showed a stronger staining in the peripheral basal cells of SCC tumour areas.
  • A possible association of strong presence and normal-distributed desmosomal molecules in SCC with the less frequent and late pattern of metastasis in SCC as compared with adenocarcinoma is suggested.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Cell Adhesion Molecules / metabolism. Lung Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Aged. Bronchi / metabolism. Carcinoma, Small Cell / metabolism. Desmosomes / metabolism. Female. Gene Expression Profiling / methods. Gene Expression Regulation, Neoplastic. Humans. Immunoenzyme Techniques. In Situ Hybridization. Integrins / metabolism. Male. RNA, Messenger / genetics. RNA, Neoplasm / genetics. Up-Regulation

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Nat Cell Biol. 2001 Sep;3(9):823-30 [11533662.001]
  • [Cites] Ann N Y Acad Sci. 2000;915:144-50 [11193570.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13784-9 [11707590.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3005-8 [12036904.001]
  • [Cites] Cancer Res. 2002 Jun 1;62(11):3244-50 [12036940.001]
  • [Cites] Mol Membr Biol. 2002 Apr-Jun;19(2):81-94 [12126234.001]
  • [Cites] Nat Med. 2002 Aug;8(8):816-24 [12118244.001]
  • [Cites] Curr Opin Cell Biol. 2002 Oct;14(5):537-45 [12231347.001]
  • [Cites] Oncogene. 2003 Apr 10;22(14):2192-205 [12687021.001]
  • [Cites] Cancer Biol Ther. 2003 May-Jun;2(3):291-8 [12878869.001]
  • [Cites] Annu Rev Cell Dev Biol. 2003;19:207-35 [14570569.001]
  • [Cites] Cancer Biol Ther. 2003 Sep-Oct;2(5):566-71 [14614329.001]
  • [Cites] Oncol Rep. 2004 May;11(5):1041-4 [15069544.001]
  • [Cites] Nat Rev Mol Cell Biol. 2004 Apr;5(4):271-81 [15071552.001]
  • [Cites] J Thorac Cardiovasc Surg. 2004 May;127(5):1332-41; discussion 1342 [15115990.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Jul 6;101(27):10143-8 [15210990.001]
  • [Cites] Cell. 1986 Sep 26;46(7):1063-73 [3530498.001]
  • [Cites] Am J Respir Cell Mol Biol. 1992 Feb;6(2):197-206 [1540382.001]
  • [Cites] Int J Cancer. 1995 Aug 22;64(4):248-52 [7657388.001]
  • [Cites] J Exp Ther Oncol. 2004 Jul;4(2):155-60 [15500010.001]
  • [Cites] Cancer Metastasis Rev. 1995 Sep;14(3):229-39 [8548871.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jul 23;93(15):7701-5 [8755539.001]
  • [Cites] Chest. 1997 Jun;111(6):1710-7 [9187198.001]
  • [Cites] Hum Pathol. 1997 Sep;28(9):1018-25 [9308725.001]
  • [Cites] J Clin Oncol. 1998 Mar;16(3):1060-7 [9508191.001]
  • [Cites] J Pathol. 1998 Apr;184(4):369-81 [9664902.001]
  • [Cites] Differentiation. 1998 Sep;63(5):295-304 [9810708.001]
  • [Cites] Hum Pathol. 1998 Nov;29(11):1208-15 [9824097.001]
  • [Cites] J Surg Res. 2004 Nov;122(1):61-9 [15522316.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
  • (PMID = 16489176.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Integrins; 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm
  • [Other-IDs] NLM/ PMC1955047
  •  go-up   go-down


7. Kim IM, Ackerson T, Ramakrishna S, Tretiakova M, Wang IC, Kalin TV, Major ML, Gusarova GA, Yoder HM, Costa RH, Kalinichenko VV: The Forkhead Box m1 transcription factor stimulates the proliferation of tumor cells during development of lung cancer. Cancer Res; 2006 Feb 15;66(4):2153-61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The Forkhead Box m1 transcription factor stimulates the proliferation of tumor cells during development of lung cancer.
  • The proliferation-specific Forkhead Box m1 (Foxm1 or Foxm1b) transcription factor (previously called HFH-11B, Trident, Win, or MPP2) regulates expression of cell cycle genes essential for progression into DNA replication and mitosis.
  • Expression of Foxm1 is found in a variety of distinct human cancers including hepatocellular carcinomas, intrahepatic cholangiocarcinomas, basal cell carcinomas, ductal breast carcinomas, and anaplastic astrocytomas and glioblastomas.
  • In this study, we show that human Foxm1 protein is abundantly expressed in highly proliferative human non-small cell lung cancers (NSCLC) as well as in mouse lung tumors induced by urethane.
  • To determine the role of Foxm1 during the development of mouse lung tumors, we used IFN-inducible Mx-Cre recombinase transgene to delete mouse Foxm1 fl/fl-targeted allele before inducing lung tumors with urethane.
  • We show that Mx-Cre Foxm1-/- mice exhibit diminished proliferation of lung tumor cells causing a significant reduction in number and size of lung adenomas.
  • Transient transfection experiments with A549 lung adenocarcinoma cells show that depletion of Foxm1 levels by short interfering RNA caused diminished DNA replication and mitosis and reduced anchorage-independent growth of cell colonies on soft agar.
  • Foxm1-depleted A549 cells exhibit reduced expression of cell cycle-promoting cyclin A2 and cyclin B1 genes.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / pathology. Forkhead Transcription Factors / physiology. Lung Neoplasms / pathology
  • [MeSH-minor] Adenocarcinoma / chemically induced. Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Alleles. Animals. Cell Adhesion. Cell Growth Processes / physiology. Cyclin A / biosynthesis. Cyclin A / genetics. Cyclin A2. Cyclin B / biosynthesis. Cyclin B / genetics. Cyclin B1. DNA Replication. DNA, Neoplasm / biosynthesis. Gene Deletion. Humans. Mice. Mice, Inbred C57BL. Mice, Transgenic. Mitosis. RNA, Small Interfering / genetics. Urethane

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. ETHYL CARBAMATE .
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16489016.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NIDDK NIH HHS / DK / DK 54687-06
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CCNA2 protein, human; 0 / CCNB1 protein, human; 0 / Ccnb1 protein, mouse; 0 / Cyclin A; 0 / Cyclin A2; 0 / Cyclin B; 0 / Cyclin B1; 0 / DNA, Neoplasm; 0 / FOXM1 protein, human; 0 / Forkhead Transcription Factors; 0 / Foxm1 protein, mouse; 0 / RNA, Small Interfering; 3IN71E75Z5 / Urethane
  •  go-up   go-down


8. Emuss V, Garnett M, Mason C, Marais R: Mutations of C-RAF are rare in human cancer because C-RAF has a low basal kinase activity compared with B-RAF. Cancer Res; 2005 Nov 1;65(21):9719-26
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Mutations of C-RAF are rare in human cancer because C-RAF has a low basal kinase activity compared with B-RAF.
  • Here we show that presumptive mutants of the closely related kinase, C-RAF, were detected in only 4 of 545 (0.7%) cancer cell lines.
  • The basal and B-RAF-stimulated kinase activities of a third variant are unaltered but its activation by RAS is significantly reduced, suggesting that it may act in a dominant-negative manner to modulate pathway signaling.
  • The fourth variant has elevated basal kinase activity and is hypersensitive to activation by RAS but does not transform mammalian cells.
  • [MeSH-minor] Adenocarcinoma / enzymology. Adenocarcinoma / genetics. Amino Acid Sequence. Animals. COS Cells. Carcinoma / enzymology. Carcinoma / genetics. Cercopithecus aethiops. Colorectal Neoplasms / enzymology. Colorectal Neoplasms / genetics. Enzyme Activation. Fibrosarcoma / enzymology. Fibrosarcoma / genetics. Humans. Lung Neoplasms / enzymology. Lung Neoplasms / genetics. Mice. Molecular Sequence Data. Mutagenesis, Site-Directed. NIH 3T3 Cells


9. Marci V, Volante M, Cappia S, Righi L, Novello C, Scagliotti GV, Brambilla E, Papotti M: Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma. Virchows Arch; 2007 Sep;451(3):729-36
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] Basaloid adenocarcinoma. A new variant of pulmonary adenocarcinoma.
  • The 2004 WHO classification of lung tumours recognised basaloid carcinoma as a variant of squamous and large cell carcinoma.
  • We report a unique case of primary pulmonary adenocarcinoma with a basaloid component.
  • The patient is disease-free 13 months after diagnosis.
  • The former was an adenocarcinoma with mucus containing spaces lined by columnar mucinous cells and basaloid cells.
  • The solid component was an organoid proliferation of basaloid-type cells, as in cutaneous basal cell carcinoma.
  • (1) The solid areas resemble a conventional basaloid carcinoma, except for the presence of small mucin-containing spaces. (2) The mucinous adenocarcinoma areas contain two layers of columnar and basaloid cells. (3) Both components are neoplastic based on cell morphology, invasive properties and phenotypic profile.
  • These findings indicate that a basaloid variant of adenocarcinoma is also existing in the spectrum of basaloid carcinomas of the lung.
  • [MeSH-major] Adenocarcinoma / pathology. Lung Neoplasms / pathology
  • [MeSH-minor] Aged, 80 and over. Carcinoma, Basal Cell. Humans. Keratins / analysis. Male. Mucins / analysis. Neoplasm Invasiveness. Phenotype. World Health Organization

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17618455.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Mucins; 68238-35-7 / Keratins
  •  go-up   go-down


10. Hira A, Watanabe H, Maeda Y, Yokoo K, Sanematsu E, Fujii J, Sasaki J, Hamada A, Saito H: Role of P-glycoprotein in accumulation and cytotoxicity of amrubicin and amrubicinol in MDR1 gene-transfected LLC-PK1 cells and human A549 lung adenocarcinoma cells. Biochem Pharmacol; 2008 Feb 15;75(4):973-80
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role of P-glycoprotein in accumulation and cytotoxicity of amrubicin and amrubicinol in MDR1 gene-transfected LLC-PK1 cells and human A549 lung adenocarcinoma cells.
  • Amrubicin is a completely synthetic 9-aminoanthracycline agent for the treatment of lung cancer in Japan.
  • Cytotoxicity and intracellular accumulation of amrubicin and amrubicinol were evaluated by LLC-PK1 cells, MDR1 gene-transfected LLC-PK1 (L-MDR1) cells overexpressing P-gp, and human A549 lung adenocarcinoma cells.
  • The basal-to-apical transepithelial transport of both drugs markedly exceeded, whereas the apical-to-basal transport of both drugs was significantly lower in L-MDR1 cells than LLC-PK1 cells.
  • These findings indicated that P-gp is responsible for cellular accumulation and cytotoxicity of both amrubicin and amrubicinol, therefore suggesting that the antitumor effect of amrubicin could be affected by the expression level of P-gp in lung cancer cells in chemotherapeutic treatments.
  • [MeSH-minor] Adenocarcinoma. Animals. Biological Transport. Cell Line, Tumor. Cell Survival / drug effects. Humans. LLC-PK1 Cells. Lung Neoplasms. Molecular Structure. Swine. Transfection

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18054347.001).
  • [ISSN] 1873-2968
  • [Journal-full-title] Biochemical pharmacology
  • [ISO-abbreviation] Biochem. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anthracyclines; 0 / Antineoplastic Agents; 0 / P-Glycoprotein; 0 / amrubicinol; 93N13LB4Z2 / amrubicin
  •  go-up   go-down


11. Peterson MR, Piao Z, Bazhenova LA, Weidner N, Yi ES: Terminal respiratory unit type lung adenocarcinoma is associated with distinctive EGFR immunoreactivity and EGFR mutations. Appl Immunohistochem Mol Morphol; 2007 Sep;15(3):242-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Terminal respiratory unit type lung adenocarcinoma is associated with distinctive EGFR immunoreactivity and EGFR mutations.
  • Approximately 10% to 20% of nonsmall cell lung cancer patients respond to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors, such as gefitinib.
  • A recent study reported that the terminal respiratory unit (TRU)-type adenocarcinoma shares the clinical profile and EGFR mutations of gefitinib responders.
  • We performed a detailed immunohistochemical analysis of EGFR expression on 124 consecutive lung resection specimens for malignancy, to survey the EGFR immunoreactivity in lung cancers in general and to correlate EGFR immunoreactivity with EGFR mutations and TRU-type histology.
  • EGFR positivity was seen most frequently in squamous cell carcinomas (77%), followed by TRU-type adenocarcinomas (63%), large cell carcinomas (23%), and non-TRU-type adenocarcinomas (12%).
  • Five of six cases with EGFR mutation were positive for EGFR immunostain with the basal cytoplasmic localization.
  • In conclusion, EGFR immunoreactivity with basal cytoplasmic pattern was exclusively seen in TRU-type adenocarcinoma and a subset of these cases was seen with EGFR mutations in the responders to EGFR inhibitor therapy.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17721266.001).
  • [ISSN] 1541-2016
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] EC 2.7.10.1 / Receptor, Epidermal Growth Factor
  •  go-up   go-down


12. Gao M, Yeh PY, Lu YS, Chang WC, Kuo ML, Cheng AL: NF-kappaB p50 promotes tumor cell invasion through negative regulation of invasion suppressor gene CRMP-1 in human lung adenocarcinoma cells. Biochem Biophys Res Commun; 2008 Nov 14;376(2):283-7
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] NF-kappaB p50 promotes tumor cell invasion through negative regulation of invasion suppressor gene CRMP-1 in human lung adenocarcinoma cells.
  • Lung adenocarcinoma Cl1-5 cells were selected from parental Cl1-0 cells based on their high metastatic potential.
  • The electromobility shift assay showed that while Cl1-0 cells exhibited low NF-kappaB activity in response to TNF-alpha, an abundance of basal and TNF-alpha-induced NF-kappaB-DNA complex was detected in Cl1-5 cells.
  • [MeSH-major] Adenocarcinoma / pathology. Gene Expression Regulation, Neoplastic. Genes, Tumor Suppressor. Lung Neoplasms / pathology. NF-kappa B p50 Subunit / metabolism. Nerve Tissue Proteins / genetics
  • [MeSH-minor] Cell Line, Tumor. Electrophoretic Mobility Shift Assay. Humans. Neoplasm Invasiveness. Promoter Regions, Genetic. Transcription Factor RelA / metabolism. Tumor Necrosis Factor-alpha / pharmacology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18782567.001).
  • [ISSN] 1090-2104
  • [Journal-full-title] Biochemical and biophysical research communications
  • [ISO-abbreviation] Biochem. Biophys. Res. Commun.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / CRMP1 protein, human; 0 / NF-kappa B p50 Subunit; 0 / Nerve Tissue Proteins; 0 / Transcription Factor RelA; 0 / Tumor Necrosis Factor-alpha
  •  go-up   go-down


13. Trivunić S, Budakov P, Vucković N, Zivojinov M: [Morphological parameters of prostatic adenocarcinoma]. Med Pregl; 2007 Nov-Dec;60(11-12):549-52
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Morphological parameters of prostatic adenocarcinoma].
  • INTRODUCTION: Prostatic carcinoma is one of the most common malignancies in men and the second most common cause of cancer-related deaths, after lung cancer.
  • The following histologic changes are associated with prostatic carcinomas. prostatic acini are close to one another and present with linear infiltrates in the fibromuscular tissue; cells lining the acini often consist of a single layer, and the basal cell layer is absent; prominent large eosinophilic nucleoli are usually present in malignant cells; nuclear hyperchromatism is rare and it depends on the quality of the tissue fixation; perineural invasion is often observed.
  • Immunohistochemistry is widely used in pathology and clinical diagnosis of prostatic carcinoma, metastases of prostatic origin in staging malignant tumors and in the prognosis.
  • [MeSH-major] Adenocarcinoma / pathology. Prostatic Neoplasms / pathology

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18666594.001).
  • [ISSN] 0025-8105
  • [Journal-full-title] Medicinski pregled
  • [ISO-abbreviation] Med. Pregl.
  • [Language] srp
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] Serbia
  •  go-up   go-down


14. Akino Y, Teshima T, Kihara A, Kodera-Suzumoto Y, Inaoka M, Higashiyama S, Furusawa Y, Matsuura N: Carbon-ion beam irradiation effectively suppresses migration and invasion of human non-small-cell lung cancer cells. Int J Radiat Oncol Biol Phys; 2009 Oct 1;75(2):475-81
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Carbon-ion beam irradiation effectively suppresses migration and invasion of human non-small-cell lung cancer cells.
  • The purpose of this study was to investigate the effect of carbon beam on non-small-cell lung cancer (NSCLC) cell aggressiveness and gene expression.
  • METHODS AND MATERIALS: A549 (lung adenocarcinoma) and EBC-1 (lung squamous cell carcinoma) cells were treated with 290 MeV/nucleon carbon ion beam at the Heavy Ion Medical Accelerator in Chiba or with 4-MV X-ray at Osaka University.
  • We tested proliferative, migratory, and invasive activities by cell proliferation assay, Boyden chamber assay, and Matrigel chemoinvasion assay, respectively. cDNA microarray and reverse transcription polymerase chain reaction were also performed to assess mRNA expression alteration.
  • RESULTS: X-irradiation increased cell proliferation of A549 cells at 0.5 Gy, whereas high-dose X-ray reduced migration and invasion of A549 cells.
  • Carbon beam irradiation induced alteration of various gene expression profiles differently from X-ray irradiation. mRNA expression of ANLN, a homologue of anillin, was suppressed to 60% levels of basal expression in carbon beam-irradiated A549 cells after 12 h.
  • [MeSH-major] Carbon Radioisotopes / therapeutic use. Carcinoma, Non-Small-Cell Lung / radiotherapy. Cell Movement / radiation effects. Lung Neoplasms / radiotherapy
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / pathology. Adenocarcinoma / radiotherapy. Adenocarcinoma / secondary. Carcinoma, Squamous Cell / genetics. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / radiotherapy. Carcinoma, Squamous Cell / secondary. Cell Adhesion / radiation effects. Cell Line, Tumor. Cell Proliferation / radiation effects. Collagen. Drug Combinations. Gene Expression Profiling / methods. Humans. Laminin. Neoplasm Invasiveness / prevention & control. Proteoglycans. RNA, Messenger / metabolism. Relative Biological Effectiveness. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19735871.001).
  • [ISSN] 1879-355X
  • [Journal-full-title] International journal of radiation oncology, biology, physics
  • [ISO-abbreviation] Int. J. Radiat. Oncol. Biol. Phys.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carbon Radioisotopes; 0 / Drug Combinations; 0 / Laminin; 0 / Proteoglycans; 0 / RNA, Messenger; 119978-18-6 / matrigel; 9007-34-5 / Collagen
  •  go-up   go-down


15. Hao J, Xu A, Xie X, Hao J, Tian T, Gao S, Xiao X, He D: Elevated expression of UBE2T in lung cancer tumors and cell lines. Tumour Biol; 2008;29(3):195-203
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Elevated expression of UBE2T in lung cancer tumors and cell lines.
  • The aim of this study was to investigate the association between UBE2T, a member of the ubiquitin-conjugating E2 family, and lung cancer, which has never been reported to date.
  • Therefore, the expression of UBE2T mRNA was examined in normal human tissues and 8 lung cancer cell lines.
  • Subsequently, UBE2T expression was analyzed in 41 lung cancer tissues by PCR and Western blots, as well as in 103 lung cancer specimens by immunohistochemistry.
  • UBE2T mRNA was highly expressed in all lung cancer cell lines examined, while it could not be detected in normal lung tissue.
  • UBE2T was detected in 75.6% of primary lung cancer tissue samples (n = 41) at mRNA level and in 60.9% at protein level.
  • In addition, positive UBE2T staining was observed in 61% of lung cancer specimens (n = 103), particularly in all immunohistochemically stained small cell carcinoma tissues.
  • In normal lung tissue, only weak staining was observed in the basal cells of bronchial epithelium.
  • In conclusion, UBE2T was significantly upregulated in lung cancer tissue and cell lines, suggesting involvement of UBE2T in the malignant cell phenotype.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Large Cell / metabolism. Carcinoma, Small Cell / metabolism. Carcinoma, Squamous Cell / metabolism. Lung Neoplasms / metabolism. Ubiquitin-Conjugating Enzymes / metabolism
  • [MeSH-minor] Animals. Cell Line. Cell Line, Tumor. Gene Expression Regulation. Gene Expression Regulation, Neoplastic. Humans. Lung / cytology. Lung / metabolism. Mice. NIH 3T3 Cells. Phenotype. RNA, Messenger / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2008 S. Karger AG, Basel.
  • (PMID = 18667844.001).
  • [ISSN] 1423-0380
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; EC 2.3.2.23 / UBE2T protein, human; EC 2.3.2.23 / Ubiquitin-Conjugating Enzymes
  •  go-up   go-down


16. Sato T, Murakumo Y, Hagiwara S, Jijiwa M, Suzuki C, Yatabe Y, Takahashi M: High-level expression of CD109 is frequently detected in lung squamous cell carcinomas. Pathol Int; 2007 Nov;57(11):719-24
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] High-level expression of CD109 is frequently detected in lung squamous cell carcinomas.
  • CD109 is a glycosylphosphatidylinositol (GPI)-anchored cell surface protein, which is a member of the alpha2-macroglobulin/C3, C4, C5 family of thioester-containing proteins.
  • Herein it is reported that the CD109 protein is preferentially expressed in lung squamous cell carcinomas compared with other types of lung carcinoma including adenocarcinomas, large cell carcinomas and small cell carcinomas.
  • Immunohistochemical staining of surgically resected lung specimens using an anti-CD109 antibody detected CD109 expression in basal cells of bronchial and bronchiolar epithelia and myoepithelial cells of bronchial secretary glands, but not in bronchial and bronchiolar apical epithelial cells and alveolar epithelial cells.
  • Furthermore, the CD109 immunoreactivity was observed in squamous cell carcinomas at a high frequency compared with other types of lung carcinoma.
  • Although the detailed function of CD109 protein is unclear, these results suggest that CD109 expression may play a role in the development of lung squamous cell carcinoma.
  • [MeSH-major] Antigens, CD / metabolism. Biomarkers, Tumor / analysis. Carcinoma, Squamous Cell / metabolism. Lung Neoplasms / metabolism. Neoplasm Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Aged, 80 and over. Blotting, Western. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Small Cell / metabolism. Carcinoma, Small Cell / pathology. Female. GPI-Linked Proteins. Gene Expression. Humans. Immunohistochemistry. Male. Middle Aged. RNA, Small Interfering

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17922683.001).
  • [ISSN] 1320-5463
  • [Journal-full-title] Pathology international
  • [ISO-abbreviation] Pathol. Int.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antigens, CD; 0 / Biomarkers, Tumor; 0 / CD109 protein, human; 0 / GPI-Linked Proteins; 0 / Neoplasm Proteins; 0 / RNA, Small Interfering
  •  go-up   go-down


17. Lal DR, Clark I, Shalkow J, Downey RJ, Shorter NA, Klimstra DS, La Quaglia MP: Primary epithelial lung malignancies in the pediatric population. Pediatr Blood Cancer; 2005 Oct 15;45(5):683-6
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Primary epithelial lung malignancies in the pediatric population.
  • BACKGROUND: Primary epithelial lung malignancies are rare in childhood and adolescence.
  • We reviewed the Memorial Sloan-Kettering Cancer Center experience with these tumors to better understand their histology, time to diagnosis, treatment, and outcome.
  • PROCEDURE: A retrospective review was performed on all patients 21 years of age or younger at diagnosis, treated for primary epithelial lung malignancies at Memorial Sloan-Kettering Cancer Center between 1980 and 2001.
  • RESULTS: We identified 11 patients with primary epithelial lung malignancy.
  • The median age at diagnosis was 19 (range: 12-21) years.
  • Seven patients (64%) were initially diagnosed as having pneumonia which contributed to a delay in diagnosis.
  • Final pathologic diagnoses included adenocarcinoma (four), carcinoid tumor (three typical, one atypical), basaloid carcinoma (two), and mucoepidermoid carcinoma (one).
  • CONCLUSIONS: When children and adolescents present with primary epithelial lung malignancy a majority will have advanced disease and experience a delay in diagnosis.
  • The histologic types of tumors encountered are similar to lung tumors occurring in adults, although the frequency of the various types differs.
  • Patients with carcinoid tumors seem to have the best prognosis, followed by adenocarcinoma.
  • [MeSH-major] Carcinoma / diagnosis. Lung Neoplasms / diagnosis
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Adolescent. Adult. Carcinoid Tumor / diagnosis. Carcinoid Tumor / pathology. Carcinoma, Basal Cell / diagnosis. Carcinoma, Basal Cell / pathology. Child. Diagnostic Errors. Female. Humans. Male. Pneumonia / diagnosis

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15714450.001).
  • [ISSN] 1545-5009
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


18. Toulany M, Dittmann K, Fehrenbacher B, Schaller M, Baumann M, Rodemann HP: PI3K-Akt signaling regulates basal, but MAP-kinase signaling regulates radiation-induced XRCC1 expression in human tumor cells in vitro. DNA Repair (Amst); 2008 Oct 1;7(10):1746-56
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] PI3K-Akt signaling regulates basal, but MAP-kinase signaling regulates radiation-induced XRCC1 expression in human tumor cells in vitro.
  • In contrast to the DNA-PKcs-deficient glioblastoma cell line MO59J, the DNA-PKcs-proficient counterpart MO59K as well as human lung adenocarcinoma A549 cells presented a high basal level of XRCC1 expression.
  • Targeting of DNA-PKcs as well as PI3K/Akt pathway by specific kinase inhibitors and/or siRNA reduced basal XRCC1 expression in un-irradiated DNA-PKcs-proficient cells to the level observed in DNA-PKcs-deficient cells.
  • Reduction of basal expression of XRCC1 by XRCC1-siRNA, AKT-siRNA as well as DNA-PKcs inhibitor facilitated IR-induced XRCC1 expression.
  • Applying gamma-H2AX foci analysis it was shown that basal expression of XRCC1 is important for the repair of IR-induced DNA-double strand breaks (DNA-DSBs).
  • These data indicate that IR-induced XRCC1 expression is dependent on the expression level of DNA-PKcs and basal activity status of PI3K/Akt signaling.
  • Likewise, potential of IR-induced XRCC1 expression depends on its basal expression level.
  • [MeSH-minor] Cell Line, Tumor. DNA Breaks, Double-Stranded / drug effects. DNA Breaks, Double-Stranded / radiation effects. DNA Repair / drug effects. DNA Repair / radiation effects. DNA-Activated Protein Kinase / deficiency. DNA-Activated Protein Kinase / metabolism. Extracellular Signal-Regulated MAP Kinases / metabolism. Humans. Mitogen-Activated Protein Kinases / metabolism. Protein Binding / drug effects. Protein Binding / radiation effects. Protein Kinase Inhibitors / pharmacology. Radiation, Ionizing. Receptor, Epidermal Growth Factor / metabolism. Recombinant Fusion Proteins / metabolism. Recombination, Genetic / drug effects. Recombination, Genetic / radiation effects

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18678286.001).
  • [ISSN] 1568-7864
  • [Journal-full-title] DNA repair
  • [ISO-abbreviation] DNA Repair (Amst.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; 0 / Protein Kinase Inhibitors; 0 / Recombinant Fusion Proteins; 0 / X-ray repair cross complementing protein 1; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.10.1 / Receptor, Epidermal Growth Factor; EC 2.7.11.1 / DNA-Activated Protein Kinase; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  •  go-up   go-down


19. Weng YL, Liao HF, Li AF, Chang JC, Chiou RY: Oral administration of resveratrol in suppression of pulmonary metastasis of BALB/c mice challenged with CT26 colorectal adenocarcinoma cells. Mol Nutr Food Res; 2010 Feb;54(2):259-67
Hazardous Substances Data Bank. RESVERATROL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oral administration of resveratrol in suppression of pulmonary metastasis of BALB/c mice challenged with CT26 colorectal adenocarcinoma cells.
  • Suppression of pulmonary metastasis of BALB/c mice challenged with CT26 colorectal adenocarcinoma cells achieved by oral administration of resveratrol was assessed in three separate experiments.
  • Prior to challenge, 8-wk-old mice were fed with a basal diet and orally administered with resveratrol (30 mg/kg/2 days) eight or twelve times.
  • The surviving mice were challenged with CT26 cells by hypodermic injection, fed with a basal diet for an additional 30 days, and sacrificed.
  • [MeSH-major] Adenocarcinoma / prevention & control. Antineoplastic Agents, Phytogenic / administration & dosage. Antineoplastic Agents, Phytogenic / therapeutic use. Lung Neoplasms / prevention & control. Stilbenes / administration & dosage. Stilbenes / therapeutic use
  • [MeSH-minor] Administration, Oral. Animals. Cell Line, Tumor. Colorectal Neoplasms / pathology. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Immunologic Factors / administration & dosage. Immunologic Factors / therapeutic use. Mice. Mice, Inbred BALB C. Neoplasm Recurrence, Local / prevention & control. Neoplasm Transplantation. Random Allocation. Survival Analysis. Tumor Burden / drug effects

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19862773.001).
  • [ISSN] 1613-4133
  • [Journal-full-title] Molecular nutrition & food research
  • [ISO-abbreviation] Mol Nutr Food Res
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Phytogenic; 0 / Immunologic Factors; 0 / Stilbenes; Q369O8926L / resveratrol
  •  go-up   go-down


20. Stathopoulos GT, Sherrill TP, Han W, Sadikot RT, Polosukhin VV, Fingleton B, Yull FE, Blackwell TS: Use of bioluminescent imaging to investigate the role of nuclear factor-kappaBeta in experimental non-small cell lung cancer metastasis. Clin Exp Metastasis; 2008;25(1):43-51
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Use of bioluminescent imaging to investigate the role of nuclear factor-kappaBeta in experimental non-small cell lung cancer metastasis.
  • Nuclear factor (NF)-kappaB is frequently over-expressed in non-small cell lung cancer (NSCLC), but the exact role of this observation remains unclear.
  • Stable integration of a NF-kappaBeta reporter confirmed high basal activation of the transcription factor in mouse NSCLC cells in vitro and during experimental metastasis to the lungs, like human NSCLC.
  • In the mouse model of NSCLC metastasis, NF-kappaBeta-dependent luciferase expression served as a reliable indicator of tumor cell delivery to the lungs, establishment of metastatic tumors, and lung tumor burden.
  • In vitro transient p65/RelA and IkappaBetaalpha gene transfer to mouse NSCLC cells resulted, respectively, in significant NF-kappaB activation and inhibition, without affecting cell growth.
  • In conclusion, using bioluminescent detection of NF-kappaB activation in mouse lug adenocarcinoma cells, we found a negative impact of p65/RelA on NSCLC metastasis.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / metabolism. Luciferases / metabolism. Luminescent Agents / metabolism. Lung Neoplasms / metabolism. NF-kappa B / metabolism. Neoplasm Metastasis / physiopathology
  • [MeSH-minor] Animals. Carcinoma, Lewis Lung / metabolism. Carcinoma, Lewis Lung / pathology. Humans. I-kappa B Kinase / metabolism. Mice. Synaptotagmin I / metabolism

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18008176.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / NIH HL61419; United States / NHLBI NIH HHS / HL / NIH HL66196
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Luminescent Agents; 0 / NF-kappa B; 0 / Synaptotagmin I; EC 1.13.12.- / Luciferases; EC 2.7.11.10 / I-kappa B Kinase
  •  go-up   go-down


21. Torky AR, Stehfest E, Viehweger K, Taege C, Foth H: Immuno-histochemical detection of MRPs in human lung cells in culture. Toxicology; 2005 Feb 28;207(3):437-50
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Immuno-histochemical detection of MRPs in human lung cells in culture.
  • For this purpose we used normal human lung cells (bronchial epithelial cells, NHBEC, and peripheral lung cells, PLC) as well as tumor cell cultures as test tools to investigate the intracelluar localization of these proteins under classical culture conditions and under air-liquid interface by means of indirect fluorescence microscopy.
  • Characterization of the cultured cells as lung epithelial cells was performed by means of immuno-histochemical analysis.
  • MRP1 and MRP3 were localised to the cellular membrane in all tested lung cell types.
  • All MRP1-MRP5 isoforms could be characterized in A549 tumor cell line as membrane proteins.
  • In order to imitate the physiological in vivo circumstances in the lung, we have established a dry/wet method (air-liquid interface) for cell cultivation so that cultured cells have the option to polarize between air and basal membrane and this might influence the distribution pattern of MRP1 and MRP2 in NHBEC.
  • Using confocal laser scanning techniques we could show that in cells kept under dry/wet conditions MRP1 was found to be localised to baso-lateral cell regions while MRP2 was localised to all cell regions.
  • [MeSH-major] Adenocarcinoma / metabolism. Bronchi / metabolism. Cell Culture Techniques / methods. Lung Neoplasms / metabolism. P-Glycoproteins / metabolism. Respiratory Mucosa / metabolism
  • [MeSH-minor] Cell Line, Tumor. Humans. Immunohistochemistry. Microscopy, Confocal. Protein Isoforms

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15664271.001).
  • [ISSN] 0300-483X
  • [Journal-full-title] Toxicology
  • [ISO-abbreviation] Toxicology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / P-Glycoproteins; 0 / Protein Isoforms
  •  go-up   go-down


22. Zheng HC, Saito H, Masuda S, Wang ZG, Takano Y: Cytoplasmic and nuclear maspin expression in lung carcinomas: an immunohistochemical study using tissue microarrays. Appl Immunohistochem Mol Morphol; 2008 Oct;16(5):459-65
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cytoplasmic and nuclear maspin expression in lung carcinomas: an immunohistochemical study using tissue microarrays.
  • Here, maspin expression was examined on tissue microarrays containing lung carcinoma (n=155) and adjacent noncancerous tissue (n=20) and also 4 lung carcinoma cell lines (LC-1/Sq, LC-IF, PC-14, and AoI) by immunohistochemistry.
  • Maspin expression showed positive nuclear staining in basal cells, LC-IF, and PC-14 cell lines, and also cytoplasmic immunoreactivity in secretory and ciliated cells, LC-1/Sq cell line.
  • Cytoplasmic staining was the lowest in adenocarcinoma (AD) and the highest in squamous cell carcinoma as compared with other types of lung carcinoma (P<0.05), and positively correlated with expression of p53 and caspase-3 (P<0.05).
  • The nuclear maspin expression gradually increased through squamous cell carcinoma, AD, large cell carcinoma to small cell carcinoma (P<0.05) and was also positively associated with the levels of vascular epithelial growth factor and extracellular matrix metalloproteinase inducer expression (P<0.05).
  • Kaplan-Meier analysis indicated that the cytoplasmic or nuclear maspin expression was not a good prognostic marker for lung carcinomas overall (P>0.05), but the cytoplasmic pattern pointed to good survival for AD cases (P<0.05).
  • It was concluded that the cytoplasmic and nuclear expression patterns of maspin are involved in the cellular differentiation of normal lung tissue and the histogenesis of different lung carcinomas.
  • The cytoplasmic maspin may play an important role in lung carcinomas by regulating apoptosis and thus is a favorable prognostic marker for AD patients, whereas the nuclear location may be linked to promotion of angiogenesis.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18665036.001).
  • [ISSN] 1533-4058
  • [Journal-full-title] Applied immunohistochemistry & molecular morphology : AIMM
  • [ISO-abbreviation] Appl. Immunohistochem. Mol. Morphol.
  • [Language] ENG
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / SERPIN-B5; 0 / Serpins
  •  go-up   go-down


23. Liu YL, Matsuzaki T, Nakazawa T, Murata S, Nakamura N, Kondo T, Iwashina M, Mochizuki K, Yamane T, Takata K, Katoh R: Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues. Hum Pathol; 2007 Jan;38(1):171-8
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Expression of aquaporin 3 (AQP3) in normal and neoplastic lung tissues.
  • To investigate the expression of AQP3 in normal and neoplastic lung tissues, we studied a series of 149 lung carcinoma tissues and 2 cell lines by immunohistochemistry, Western blotting, and reverse transcriptase-polymerase chain reaction.
  • In normal lung tissues, immunohistochemical expression of AQP3 was demonstrated in bronchial basal cells, alveolar type II cells, bronchiolar epithelial cells, and secretory cells of submucosal glands.
  • In lung carcinomas, AQP3 expression was observed in 59 (70.2%) of 84 adenocarcinomas.
  • Squamous cell carcinoma and large cell carcinoma had rather low positive ratios (35.8% and 13.4%, respectively).
  • No AQP3 expression was demonstrated in small cell carcinoma, pleomorphic carcinoma, or metastatic colon adenocarcinoma.
  • Western blotting and reverse transcriptase-polymerase chain reaction analyses confirmed the expression of AQP3 protein and messenger RNA in cell lines and tissues of lung adenocarcinoma.
  • In addition, lung carcinomas, especially adenocarcinomas, can produce AQP3, possibly in connection with their functional and/or biological nature, although the detailed mechanism of AQP3 expression in lung carcinomas remains to be clarified.
  • [MeSH-major] Aquaporin 3 / genetics. Lung / metabolism. Lung Neoplasms / genetics
  • [MeSH-minor] Adenocarcinoma / genetics. Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Blotting, Western. Cell Line, Tumor. Female. Gene Expression. Humans. Immunohistochemistry. Male. Reverse Transcriptase Polymerase Chain Reaction

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17056099.001).
  • [ISSN] 0046-8177
  • [Journal-full-title] Human pathology
  • [ISO-abbreviation] Hum. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 158801-98-0 / Aquaporin 3
  •  go-up   go-down


24. Yuan P, Kadara H, Behrens C, Tang X, Woods D, Solis LM, Huang J, Spinola M, Dong W, Yin G, Fujimoto J, Kim E, Xie Y, Girard L, Moran C, Hong WK, Minna JD, Wistuba II: Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung. PLoS One; 2010 Feb 09;5(2):e9112
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] Sex determining region Y-Box 2 (SOX2) is a potential cell-lineage gene highly expressed in the pathogenesis of squamous cell carcinomas of the lung.
  • BACKGROUND: Non-small cell lung cancer (NSCLC) represents the majority (85%) of lung cancers and is comprised mainly of adenocarcinomas and squamous cell carcinomas (SCCs).
  • The sequential pathogenesis of lung adenocarcinomas and SCCs occurs through dissimilar phases as the former tumors typically arise in the lung periphery whereas the latter normally arise near the central airway.
  • METHODOLOGY/PRINCIPAL FINDINGS: We assessed the expression of SOX2, an embryonic stem cell transcriptional factor that also plays important roles in the proliferation of basal tracheal cells and whose expression is restricted to the main and central airways and bronchioles of the developing and adult mouse lung, in NSCLC by various methodologies.
  • Here, we found that SOX2 mRNA levels, from various published datasets, were significantly elevated in lung SCCs compared to adenocarcinomas (all p<0.001).
  • Moreover, a previously characterized OCT4/SOX2/NANOG signature effectively separated lung SCCs from adenocarcinomas in two independent publicly available datasets which correlated with increased SOX2 mRNA in SCCs.
  • Immunohistochemical analysis of various histological lung tissue specimens demonstrated marked nuclear SOX2 protein expression in all normal bronchial epithelia, alveolar bronchiolization structures and premalignant lesions in SCC development (hyperplasia, dysplasia and carcinoma in situ) and absence of expression in all normal alveoli and atypical adenomatous hyperplasias.
  • Moreover, SOX2 protein expression was greatly higher in lung SCCs compared to adenocarcinomas following analyses in two independent large TMA sets (TMA set I, n = 287; TMA set II, n = 511 both p<0.001).
  • Furthermore, amplification of SOX2 DNA was detected in 20% of lung SCCs tested (n = 40) and in none of the adenocarcinomas (n = 17).
  • CONCLUSIONS/SIGNIFICANCE: Our findings highlight a cell-lineage gene expression pattern for the stem cell transcriptional factor SOX2 in the pathogenesis of lung SCCs and suggest a differential activation of stem cell-related pathways between squamous cell carcinomas and adenocarcinomas of the lung.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Proc Natl Acad Sci U S A. 2001 Nov 20;98(24):13790-5 [11707567.001]
  • [Cites] Nat Genet. 2009 Nov;41(11):1238-42 [19801978.001]
  • [Cites] Neoplasia. 2004 Jan-Feb;6(1):1-6 [15068665.001]
  • [Cites] Cancer Res. 1996 May 1;56(9):2224-8 [8616876.001]
  • [Cites] Development. 1997 Dec;124(23):4867-78 [9428423.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Sep 29;95(20):11891-6 [9751761.001]
  • [Cites] Genes Dev. 1998 Oct 15;12(20):3156-61 [9784490.001]
  • [Cites] Cell. 2005 Sep 23;122(6):947-56 [16153702.001]
  • [Cites] Nat Rev Mol Cell Biol. 2005 Nov;6(11):872-84 [16227977.001]
  • [Cites] Nature. 2006 Jan 19;439(7074):353-7 [16273092.001]
  • [Cites] Annu Rev Pathol. 2006;1:331-48 [18039118.001]
  • [Cites] Dev Biol. 2008 May 1;317(1):296-309 [18374910.001]
  • [Cites] Oncogene. 2008 Jun 5;27(25):3635-40 [18212743.001]
  • [Cites] N Engl J Med. 2008 Sep 25;359(13):1367-80 [18815398.001]
  • [Cites] Clin Cancer Res. 2008 Oct 1;14(19):6014-22 [18829480.001]
  • [Cites] Cancer Prev Res (Phila). 2008 Aug;1(3):192-200 [19138956.001]
  • [Cites] Development. 2009 Jun;136(11):1899-907 [19403656.001]
  • [Cites] CA Cancer J Clin. 2009 Jul-Aug;59(4):225-49 [19474385.001]
  • [Cites] Nucleic Acids Res. 2003 Feb 15;31(4):e15 [12582260.001]
  • (PMID = 20161759.001).
  • [ISSN] 1932-6203
  • [Journal-full-title] PloS one
  • [ISO-abbreviation] PLoS ONE
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P50 CA070907; United States / NCI NIH HHS / CA / CA-16672; United States / NCI NIH HHS / CA / P50CA70907
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Homeodomain Proteins; 0 / NANOG protein, human; 0 / Octamer Transcription Factor-3; 0 / POU5F1 protein, human; 0 / SOX2 protein, human; 0 / SOXB1 Transcription Factors
  • [Other-IDs] NLM/ PMC2817751
  •  go-up   go-down


25. Yang YM, Jhanwar-Uniyal M, Schwartz J, Conaway CC, Halicka HD, Traganos F, Chung FL: N-acetylcysteine conjugate of phenethyl isothiocyanate enhances apoptosis in growth-stimulated human lung cells. Cancer Res; 2005 Sep 15;65(18):8538-47
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] N-acetylcysteine conjugate of phenethyl isothiocyanate enhances apoptosis in growth-stimulated human lung cells.
  • We previously showed that dietary treatment with the N-acetylcysteine conjugate of phenethyl isothiocyanate (PEITC-NAC) inhibited benzo(a)pyrene-induced lung tumorigenesis in A/J mice, and that tumor inhibition was associated with induction of activator protein-1 (AP-1) activity and stimulation of apoptosis in the lungs of mice.
  • In the present study, we show that PEITC-NAC also induces apoptosis and AP-1 activity in human lung adenocarcinoma A549 cells, and that activation of AP-1 is important in PEITC-NAC induced apoptosis in these cells.
  • When wild-type c-jun cDNA was transfected into A549 cells, PEITC-NAC-mediated apoptosis was greatly increased in the c-jun-transfected cells compared with the control vector-transfected cells, based on cell morphology and analysis of DNA fragmentation.
  • Furthermore, cells that were pretreated with 100 nmol/L 12-O-tetradecanoyl phorbol-13-acetate, and then treated with 25 micromol/L PEITC-NAC, underwent enhanced apoptosis compared with cells that were treated with PEITC-NAC alone; cells treated with 12-O-tetradecanoyl phorbol-13-acetate alone showed active cell growth without apoptosis.
  • These findings suggest that growth-stimulated cells with an elevated basal AP-1 activity, i.e., A549 cells transfected with wild-type c-jun or treated with a tumor promoter, were more sensitive to PEITC-NAC-mediated apoptosis.
  • The observation that PEITC-NAC induces apoptosis predominantly in growth-promoted cells, such as neoplastic cells, suggests a selective mechanism by which PEITC-NAC inhibits lung carcinogenesis.
  • [MeSH-major] Adenocarcinoma / drug therapy. Apoptosis / drug effects. Cysteine / analogs & derivatives. Lung Neoplasms / drug therapy. Thiocarbamates / pharmacology
  • [MeSH-minor] Animals. Cell Line, Tumor. Dose-Response Relationship, Drug. Enzyme Activation. Humans. JNK Mitogen-Activated Protein Kinases / biosynthesis. JNK Mitogen-Activated Protein Kinases / genetics. JNK Mitogen-Activated Protein Kinases / metabolism. Lung / drug effects. Mice. Mice, Inbred A. Tetradecanoylphorbol Acetate. Transcription Factor AP-1 / physiology. Transfection. Tumor Suppressor Protein p53 / biosynthesis. Tumor Suppressor Protein p53 / genetics

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. 12-O-TETRADECANOYLPHORBOL-13-ACETATE .
  • Hazardous Substances Data Bank. CYSTEINE .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16166335.001).
  • [ISSN] 0008-5472
  • [Journal-full-title] Cancer research
  • [ISO-abbreviation] Cancer Res.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / 1R03CA110057-01; United States / NCI NIH HHS / CA / CA46535
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / N-acetyl-S-(N-2-phenethylthiocarbamoyl)-L-cysteine; 0 / TP53 protein, human; 0 / Thiocarbamates; 0 / Transcription Factor AP-1; 0 / Tumor Suppressor Protein p53; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; K848JZ4886 / Cysteine; NI40JAQ945 / Tetradecanoylphorbol Acetate
  •  go-up   go-down


26. Deng J, Fujimoto J, Ye XF, Men TY, Van Pelt CS, Chen YL, Lin XF, Kadara H, Tao Q, Lotan D, Lotan R: Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis. Cancer Prev Res (Phila); 2010 Apr;3(4):424-37
Guide to Pharmacology. gene/protein/disease-specific - Class C Orphans - overview and references .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Knockout of the tumor suppressor gene Gprc5a in mice leads to NF-kappaB activation in airway epithelium and promotes lung inflammation and tumorigenesis.
  • Mouse models can be useful for increasing the understanding of lung tumorigenesis and assessing the potential of chemopreventive agents.
  • We explored the role of inflammation in lung tumor development in mice with knockout of the tumor suppressor Gprc5a.
  • Examination of normal lung tissue and tumors from 51 Gprc5a(+/+) (adenoma incidence, 9.8%; adenocarcinoma, 0%) and 38 Gprc5a(-/-) mice (adenoma, 63%; adenocarcinoma, 21%) revealed macrophage infiltration into lungs of 45% of the Gprc5a(-/-) mice and 8% of Gprc5a(+/+) mice and the direct association of macrophages with 42% of adenomas and 88% of adenocarcinomas in the knockout mice.
  • Studies with epithelial cells cultured from tracheas of Gprc5a(-/-) and Gprc5a(+/+) mice revealed that Gprc5a loss is associated with increased cell proliferation, resistance to cell death in suspension, and increased basal, tumor necrosis factor alpha-induced, and lipopolysaccharide-induced NF-kappaB activation, which were reversed partially in Gprc5a(-/-) adenocarcinoma cells by reexpression of Gprc5a.
  • Thus, Gprc5a loss enhances NF-kappaB activation in lung epithelial cells, leading to increased autocrine and paracrine interactions, cell autonomy, and enhanced inflammation, which may synergize in the creation of a tumor-promoting microenvironment.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Pneumonia.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] (c) 2010 AACR.
  • [CommentIn] Cancer Prev Res (Phila). 2010 Apr;3(4):403-5 [20354166.001]
  • (PMID = 20354164.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / P30 CA016672; United States / NCI NIH HHS / CA / P30 CA16672
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / NF-kappa B; 0 / RNA, Messenger; 0 / RNA, Small Interfering; 0 / Receptors, G-Protein-Coupled
  •  go-up   go-down


27. Forest V, Campos L, Péoc'h M, Guyotat D, Vergnon JM: [Development of an experimental model for the study of the effects of cryotherapy on lung tumours]. Pathol Biol (Paris); 2005 May;53(4):199-203
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] [Development of an experimental model for the study of the effects of cryotherapy on lung tumours].
  • Adenocarcinomas are today the most frequent lung cancers.
  • MATERIALS AND METHODS: A xenograft system was used: cells from the A549 cell line were injected subcutaneously into SCID mice.
  • The histological study showed that these tumours faithfully reproduced the morphological features of adenocarcinoma, and developed an intratumoral neovascularization.
  • RESULTS: The basal expression of cleaved caspase-3 in untreated tumours (23%) increased after cryotherapy.
  • [MeSH-major] Adenocarcinoma / therapy. Cryotherapy. Lung Neoplasms / therapy. Neoadjuvant Therapy. Neoplasms, Experimental / therapy
  • [MeSH-minor] Animals. Cell Line, Tumor / transplantation. Humans. Male. Mice. Mice, SCID. Neoplasm Transplantation. Xenograft Model Antitumor Assays

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15850952.001).
  • [ISSN] 0369-8114
  • [Journal-full-title] Pathologie-biologie
  • [ISO-abbreviation] Pathol. Biol.
  • [Language] fre
  • [Publication-type] English Abstract; Evaluation Studies; Journal Article
  • [Publication-country] France
  •  go-up   go-down


28. Yazgan S, Gürsoy S, Yaldiz S, Basok O: Outcome of surgery for lung cancer in young and elderly patients. Surg Today; 2005;35(10):823-7
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Outcome of surgery for lung cancer in young and elderly patients.
  • PURPOSE: It has been suggested that lung cancer follows a more aggressive course and has a poorer prognosis in young patients than in elderly patients.
  • We conducted this study to determine whether the basal characteristics and survival of young patients undergoing surgical resection of lung cancer differ from those of elderly patients.
  • METHODS: Eighty patients who underwent surgery for lung cancer at our hospital between 1989 and 2004 were divided into two groups according to age.
  • The patients' medical records were reviewed with respect to age, gender, histological diagnosis, coexisting diseases, smoking history, postoperative staging, type of operation, and postoperative morbidity, mortality, and survival results.
  • However, the 5-year survival rates for patients who underwent surgery for non-small cell lung cancer did not differ between groups 1 and 2, at 33.3% versus 21.3%, respectively (P = 0.09).
  • CONCLUSIONS: The incidence of adenocarcinoma was higher in the young patients, whose prognosis was slightly better than that of the elderly patients.
  • [MeSH-major] Carcinoma, Non-Small-Cell Lung / mortality. Carcinoma, Non-Small-Cell Lung / surgery. Carcinoma, Small Cell / mortality. Carcinoma, Small Cell / surgery. Lung Neoplasms / mortality. Lung Neoplasms / surgery

  • Genetic Alliance. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16175462.001).
  • [ISSN] 0941-1291
  • [Journal-full-title] Surgery today
  • [ISO-abbreviation] Surg. Today
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Japan
  •  go-up   go-down


29. Leinonen T, Pirinen R, Böhm J, Johansson R, Rinne A, Weber E, Kosma VM: Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer. J Clin Pathol; 2007 May;60(5):515-9
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] Biological and prognostic role of acid cysteine proteinase inhibitor (ACPI, cystatin A) in non-small-cell lung cancer.
  • AIM: To analyse the expression and prognostic role of ACPI in non-small-cell lung cancer (NSCLC).
  • METHOD: Histological samples from 199 patients with resected NSCLC were stained immunohistochemically for the expression of ACPI in normal and preneoplastic bronchial epithelium, and in various types of lung carcinomas.
  • RESULTS: A normal bronchial epithelium showed positive staining for ACPI in the basal cells, whereas the upper two-thirds of the dysplastic epithelium was ACPI positive.
  • High staining for ACPI was found in 74% (91/123) of squamous-cell carcinomas, whereas 16% (8/49) of adenocarcinomas and 30% of (8/27) large-cell carcinomas showed the high expression of ACPI (p<0.001).
  • Among squamous-cell carcinomas, low expression of ACPI was correlated with poor tumour differentiation (p=0.032).
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Cystatins / metabolism. Cysteine Proteinase Inhibitors / metabolism. Lung Neoplasms / metabolism
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adult. Aged. Carcinoma, Large Cell / metabolism. Carcinoma, Large Cell / pathology. Carcinoma, Squamous Cell / metabolism. Carcinoma, Squamous Cell / pathology. Follow-Up Studies. Humans. Immunoenzyme Techniques. Middle Aged. Neoplasm Staging. Precancerous Conditions / metabolism. Prognosis. Survival Analysis

  • Genetic Alliance. consumer health - Lung Cancer.
  • Genetic Alliance. consumer health - Non-small cell lung cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Clin Cancer Res. 2000 Mar;6(3):1052-62 [10741734.001]
  • [Cites] Pathol Res Pract. 1980 Dec;170(1-3):172-9 [18788161.001]
  • [Cites] Prostate. 2001 Sep 15;48(4):274-84 [11536307.001]
  • [Cites] Cancer. 2002 Jun 15;94(12):3141-9 [12115346.001]
  • [Cites] Cancer Lett. 2002 Dec 10;187(1-2):185-90 [12359367.001]
  • [Cites] Cell Mol Life Sci. 2002 Sep;59(9):1503-12 [12440772.001]
  • [Cites] Prostate. 2003 Mar 1;54(4):290-8 [12539227.001]
  • [Cites] Biochem Soc Symp. 2003;(70):179-99 [14587292.001]
  • [Cites] Acta Chem Scand B. 1975;29(7):772-80 [242173.001]
  • [Cites] Acta Histochem. 1978;63(2):183-92 [107702.001]
  • [Cites] Acta Histochem Suppl. 1980;22:325-9 [6789389.001]
  • [Cites] Virchows Arch B Cell Pathol Incl Mol Pathol. 1983;43(2):121-6 [6137100.001]
  • [Cites] Exp Pathol. 1984;26(2):67-70 [6548973.001]
  • [Cites] J Biochem. 1984 Nov;96(5):1437-42 [6441803.001]
  • [Cites] Anat Anz. 1986;161(3):215-30 [2424340.001]
  • [Cites] Acta Histochem. 1987;82(1):5-18 [3122506.001]
  • [Cites] Biol Chem Hoppe Seyler. 1992 Jul;373(7):595-604 [1515089.001]
  • [Cites] Acta Histochem. 1992;93(1):241-8 [1326833.001]
  • [Cites] Biol Chem Hoppe Seyler. 1995 Feb;376(2):71-80 [7794528.001]
  • [Cites] Int J Cancer. 1995 Jul 4;62(1):1-4 [7541394.001]
  • [Cites] Int J Gynecol Pathol. 1995 Jul;14(3):217-22 [8600072.001]
  • [Cites] Eur Arch Otorhinolaryngol. 1997;254 Suppl 1:S150-3 [9065652.001]
  • [Cites] Clin Exp Metastasis. 1997 Jul;15(4):368-81 [9219725.001]
  • [Cites] Adv Exp Med Biol. 1997;421:259-65 [9330706.001]
  • [Cites] Cancer Res. 1998 Feb 1;58(3):432-6 [9458085.001]
  • [Cites] Oncol Rep. 1998 Nov-Dec;5(6):1349-61 [9769367.001]
  • [Cites] Neoplasma. 1998;45(5):318-31 [9921922.001]
  • [Cites] Eur J Hum Genet. 2005 Feb;13(2):208-15 [15483648.001]
  • [Cites] Hum Pathol. 2005 Jan;36(1):44-50 [15712181.001]
  • [Cites] J Clin Pathol. 2001 May;54(5):391-5 [11328840.001]
  • (PMID = 16790691.001).
  • [ISSN] 0021-9746
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cystatins; 0 / Cysteine Proteinase Inhibitors
  • [Other-IDs] NLM/ PMC1994551
  •  go-up   go-down


30. Husain A, Blumenschein G, Esmaeli B: Treatment and outcomes for metastatic sebaceous cell carcinoma of the eyelid. Int J Dermatol; 2008 Mar;47(3):276-9
COS Scholar Universe. author profiles.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Treatment and outcomes for metastatic sebaceous cell carcinoma of the eyelid.
  • OBJECTIVE: To report the management and outcomes in patients with metastatic eyelid sebaceous cell carcinoma.
  • METHODS: The clinical records of four patients with metastatic eyelid sebaceous cell carcinoma treated between January 1999 and August 2006 were reviewed.
  • Metastatic sites included the lung in three patients, regional lymph nodes in two, liver in two, and bone in one.
  • Time from diagnosis of eyelid carcinoma to metastasis ranged from 0 to 62 months.
  • One patient developed lung metastasis 5 years after the diagnosis of eyelid tumor; she was treated with systemic chemotherapy followed by subtotal lung resection.
  • The follow-up time from diagnosis of metastasis to last contact or death ranged from 1 month to 3 years (median of 21 months).
  • CONCLUSION: Eyelid sebaceous cell carcinoma can result in systemic metastasis and death.
  • [MeSH-major] Adenocarcinoma, Sebaceous / secondary. Bone Neoplasms / secondary. Eyelid Neoplasms / pathology. Liver Neoplasms / secondary. Lung Neoplasms / secondary. Parotid Neoplasms / secondary. Sebaceous Gland Neoplasms / pathology
  • [MeSH-minor] Aged. Aged, 80 and over. Carcinoma, Basal Cell / diagnosis. Chalazion / diagnosis. Diagnostic Errors. Female. Humans. Lymphatic Metastasis / radiotherapy. Middle Aged. Retrospective Studies

  • MedlinePlus Health Information. consumer health - Bone Cancer.
  • MedlinePlus Health Information. consumer health - Liver Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18289332.001).
  • [ISSN] 1365-4632
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  •  go-up   go-down


31. Serap D, Ozlem S, Melike Y, Alper D, Aynur A, Ata Türker A, Ardıç S: Acanthosis nigricans in a patient with lung cancer: a case report. Case Rep Med; 2010;2010

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Acanthosis nigricans in a patient with lung cancer: a case report.
  • With this report, we aim to present a rare case of concomitant lung cancer and acanthosis nigricans.
  • Thoracic computed tomography demonstrated a hypodense mass lesion with a dimension of 5 x 5.5 cm at the center of basal segment bronchi of the left pulmonary lobe.
  • The result of the histopathologic examination of the endobronchial tissue biopsy was reported as non-small cell (adenocarcinoma) lung cancer.
  • Result of the histopathologic analysis of the punch biopsy of the skin lesions was reported as acanthosis nigricans .There are no pathognomonic dermatological findings for lung cancer.
  • In conclusion, there are skin lesions that accompany lung cancer and we believe that these should be considered for differential diagnosis.

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Gynecol Oncol. 2002 Feb;84(2):332-4 [11812096.001]
  • [Cites] Diabetes Care. 2002 Jun;25(6):1009-14 [12032107.001]
  • [Cites] Dermatol Clin. 2002 Jul;20(3):523-32 [12170885.001]
  • [Cites] J Dermatol Surg Oncol. 1980 Nov;6(11):923-7 [6257767.001]
  • [Cites] Thorax. 1988 May;43(5):414-5 [2848329.001]
  • [Cites] Dermatologica. 1988;176(3):133-7 [3378650.001]
  • [Cites] J Am Acad Dermatol. 1991 Aug;25(2 Pt 2):361-5 [1894773.001]
  • [Cites] Nihon Kyobu Shikkan Gakkai Zasshi. 1992 Nov;30(11):1991-5 [1484439.001]
  • [Cites] J Am Acad Dermatol. 1994 Jul;31(1):1-19; quiz 20-2 [8021347.001]
  • [Cites] Cancer. 1962 Mar-Apr;15:364-82 [13882755.001]
  • [Cites] Curr Opin Oncol. 1999 Mar;11(2):139-44 [10188080.001]
  • [Cites] Int J Dermatol. 2005 Jan;44(1):45-7 [15663660.001]
  • [Cites] Ann Thorac Cardiovasc Surg. 2009 Dec;15(6):397-400 [20081750.001]
  • [Cites] Pol Arch Med Wewn. 2009 Mar;119(3):180-3 [19514649.001]
  • [Cites] J Am Acad Dermatol. 2000 Feb;42(2 Pt 2):357-62 [10640933.001]
  • [Cites] Diabetes Care. 2004 Jun;27(6):1412-6 [15161797.001]
  • [Cites] J Am Acad Dermatol. 2003 Sep;49(3):541-3 [12963928.001]
  • (PMID = 20811563.001).
  • [ISSN] 1687-9635
  • [Journal-full-title] Case reports in medicine
  • [ISO-abbreviation] Case Rep Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  •  go-up   go-down


32. Wang CC, Tsai MF, Hong TM, Chang GC, Chen CY, Yang WM, Chen JJ, Yang PC: The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion. Oncogene; 2005 Jun 9;24(25):4081-93
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] The transcriptional factor YY1 upregulates the novel invasion suppressor HLJ1 expression and inhibits cancer cell invasion.
  • By using microarray and an invasion/metastasis lung cell line model, we identified the DnaJ-like heat shock protein 40, HLJ1, and found that the expression of HLJ1 correlates negatively with cancer cell invasion ability.
  • Overexpression of HLJ1 can suppress cancer cell invasion in vitro.
  • A serial deletion of the 1.2 kb at the 5'-flanking region of the human HLJ1 gene was subcloned into a vector containing reporter gene and transfected into human lung adenocarcinoma cell line CL1-0, followed by luciferase activity assay.
  • The results indicated that the region from -232 to +176 could drive the basal transcriptional activity of the HLJ1 gene.
  • Co-transfection of the YY1 and HLJ1 basal promoter regions, site-directed mutagenesis, and electrophoretic mobility shift assay confirmed that YY1 could upregulate HLJ1 basal promoter activity.
  • Furthermore, we also demonstrated that overexpression of YY1 in CL1-0 cells can increase HLJ1 expression and reduce cell invasive capability.
  • The reduction of cancer cell invasive ability is, at least in part, through upregulation of E-cadherin expression.
  • [MeSH-major] DNA-Binding Proteins / metabolism. Heat-Shock Proteins / genetics. Lung Neoplasms / genetics. Transcription Factors / metabolism
  • [MeSH-minor] 5' Untranslated Regions / genetics. Adenocarcinoma. Base Sequence. Cell Line, Tumor. Erythroid-Specific DNA-Binding Factors. Gene Expression Regulation, Neoplastic. HSP40 Heat-Shock Proteins. Humans. Molecular Sequence Data. Neoplasm Invasiveness. Neoplasm Metastasis / prevention & control. Promoter Regions, Genetic. RNA, Small Interfering / genetics. Repressor Proteins / metabolism. Tumor Suppressor Proteins / genetics. YY1 Transcription Factor

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 15782117.001).
  • [ISSN] 0950-9232
  • [Journal-full-title] Oncogene
  • [ISO-abbreviation] Oncogene
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / 5' Untranslated Regions; 0 / DNA-Binding Proteins; 0 / DNAJB4 protein, human; 0 / Erythroid-Specific DNA-Binding Factors; 0 / HSP40 Heat-Shock Proteins; 0 / Heat-Shock Proteins; 0 / RNA, Small Interfering; 0 / Repressor Proteins; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins; 0 / YY1 Transcription Factor; 0 / YY1 protein, human
  •  go-up   go-down


33. Yin J, Vogel U, Ma Y, Guo L, Wang H, Qi R: Polymorphism of the DNA repair gene ERCC2 Lys751Gln and risk of lung cancer in a northeastern Chinese population. Cancer Genet Cytogenet; 2006 Aug;169(1):27-32
Hazardous Substances Data Bank. L-Lysine .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Polymorphism of the DNA repair gene ERCC2 Lys751Gln and risk of lung cancer in a northeastern Chinese population.
  • The ERCC2 gene (excision repair cross-complementing rodent repair deficiency, complementation group 2 [xeroderma pigmentosum D]) (previously XPD), encoding a DNA repair protein, is involved in nucleotide excision repair and basal transcription.
  • To test the effect of the polymorphism ERCC2 Lys751Gln on the risk of lung cancer in a northeastern Chinese population, a hospital-based case-control study was designed consisting of 147 newly diagnosed and previously untreated subjects with lung cancer and 145 cancer-free control subjects matched on age (+/-3 years), gender, and ethnicity.
  • The C-allele of ERCC2 Lys751Gln was significantly overrepresented among lung cancer cases (C versus A: adjusted odds ratio OR(adj) = 2.61, 95% CI = 1.12-6.05, P = 0.03).
  • The carriers of AC genotype were at 2.78-fold (OR(adj) = 2.78, 95% CI = 1.12-6.93) higher risk of lung cancer than carriers of the AA genotype.
  • Subdivided by tumor type, carriers of AC genotype had a 4.65-fold higher risk of squamous cell carcinoma of lung compared with carriers of AA genotype (OR(adj) = 4.65, 95% CI = 1.67-12.98, P = 0.003); similar, but not statistically significant estimates were found for adenocarcinoma of lung.
  • In conclusion, our results suggest that ERCC2 Lys751Gln(C) allele is a potential risk marker for lung cancer in this northeastern Chinese population.
  • [MeSH-major] DNA Repair / genetics. Glycine / genetics. Lung Neoplasms / genetics. Lysine / genetics. Polymorphism, Genetic. Xeroderma Pigmentosum Group D Protein / genetics

  • Genetic Alliance. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • Hazardous Substances Data Bank. GLYCINE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16875933.001).
  • [ISSN] 0165-4608
  • [Journal-full-title] Cancer genetics and cytogenetics
  • [ISO-abbreviation] Cancer Genet. Cytogenet.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA Primers; EC 3.6.4.12 / Xeroderma Pigmentosum Group D Protein; EC 5.99.- / ERCC2 protein, human; K3Z4F929H6 / Lysine; TE7660XO1C / Glycine
  •  go-up   go-down


34. Ragolia L, Palaia T, Hall CE, Klein J, Büyük A: Diminished lipocalin-type prostaglandin D(2) synthase expression in human lung tumors. Lung Cancer; 2010 Oct;70(1):103-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Diminished lipocalin-type prostaglandin D(2) synthase expression in human lung tumors.
  • Previously, we demonstrated that lipocalin-type prostaglandin D(2) synthase (L-PGDS) induces apoptosis and prevents cell cycle progression in several cell types.
  • In this study we determined the expression of L-PGDS in a variety of human lung tumor types.
  • In addition, we demonstrated that exogenously added L-PGDS could suppress the hyperproliferation and PDGF-stimulated migration of A549 cells, a cultured carcinomic human alveolar basal epithelial cell line.
  • We conclude that L-PGDS may play a key role in modulating lung cancer growth and may offer a novel diagnostic and therapeutic approach for treatment.
  • [MeSH-major] Intramolecular Oxidoreductases / biosynthesis. Lipocalins / biosynthesis. Lung Neoplasms / enzymology
  • [MeSH-minor] Adenocarcinoma, Bronchiolo-Alveolar / enzymology. Adenocarcinoma, Bronchiolo-Alveolar / genetics. Adenocarcinoma, Bronchiolo-Alveolar / pathology. Apoptosis / drug effects. Apoptosis / physiology. Carcinoma, Non-Small-Cell Lung / enzymology. Carcinoma, Non-Small-Cell Lung / genetics. Carcinoma, Non-Small-Cell Lung / pathology. Cell Growth Processes / drug effects. Cell Growth Processes / physiology. Cell Line, Tumor. Cell Movement / drug effects. Cell Movement / physiology. Disease Progression. Gene Expression Regulation, Enzymologic. Gene Expression Regulation, Neoplastic. Humans. Platelet-Derived Growth Factor / pharmacology. Reverse Transcriptase Polymerase Chain Reaction

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright 2010 Elsevier Ireland Ltd. All rights reserved.
  • (PMID = 20144489.001).
  • [ISSN] 1872-8332
  • [Journal-full-title] Lung cancer (Amsterdam, Netherlands)
  • [ISO-abbreviation] Lung Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Lipocalins; 0 / Platelet-Derived Growth Factor; EC 5.3.- / Intramolecular Oxidoreductases; EC 5.3.99.2 / prostaglandin R2 D-isomerase
  •  go-up   go-down


35. Szczepański P, Niedzielska G, Szczepańska B: [Simultaneous detection of three histopathologically different kinds of cancer]. Otolaryngol Pol; 2005;59(6):915-8
MedlinePlus Health Information. consumer health - Nasal Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • RESULTS: After histopathological examination carcinoma flat epithelium of the nose, carcinoma basal cell of the left cheek and adenocarcinoma aciniform partially solid of the right lung were diagnosed.
  • The complete removal of carcinoma basal cell of the left check and carcinoma flat epithelium of the nose together with plastic surgery of nasal wing with rhinochilo flap were done.
  • Also lobe of lung lower was removed.
  • [MeSH-major] Adenocarcinoma / pathology. Carcinoma, Basal Cell / pathology. Lung Neoplasms / pathology. Nose Neoplasms / pathology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16521465.001).
  • [ISSN] 0030-6657
  • [Journal-full-title] Otolaryngologia polska = The Polish otolaryngology
  • [ISO-abbreviation] Otolaryngol Pol
  • [Language] pol
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Poland
  •  go-up   go-down


36. Uke M, Rekhi B, Ajit D, Jambhekar NA: The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears. Cytopathology; 2010 Feb;21(1):56-63
MedlinePlus Health Information. consumer health - Lung Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The use of p63 as an effective immunomarker in the diagnosis of pulmonary squamous cell carcinomas on de-stained bronchial lavage cytological smears.
  • OBJECTIVES: A diagnosis in pulmonary onco-cytopathology primarily necessitates distinguishing small cell carcinoma (SCLC) from non-small cell carcinoma (NSCLC), which includes squamous cell carcinoma and adenocarcinoma.
  • Lately, p63 antibody has been used for distinguishing squamous cell carcinoma from SCLC and adenocarcinoma.
  • RESULTS: Out of 100 cases, 21 were cytologically diagnosed as squamous cell carcinoma.
  • Twenty of these showed 2+ or 3+ p63 positivity, whereas one, which was adenocarcinoma on histology, showed 1+ staining.
  • Of seven cases cytologically diagnosed as adenocarcinoma, six showed no p63 staining, whereas one, which was squamous cell carcinoma on histology, showed 1+ staining.
  • The former three were found to be SCLC on histology while the latter was squamous cell carcinoma.
  • The former eight were adenocarcinoma on histology and the latter two were squamous cell carcinoma.
  • The 10 cases that showed 1+ p63 staining were adenocarcinomas (n = 5), squamous cell carcinoma (n = 4) and NSCLC, not otherwise specified (n = 1).
  • Positive staining was seen in normal basal cells, which acted as an internal control.
  • Overall sensitivity of p63 for squamous cell carcinoma was 100% and specificity was 90.4%.
  • CONCLUSIONS: p63 immunostaining on processed cytology smears can be used to help identify squamous cell carcinoma.
  • Its diffuse expression was specific for squamous cell carcinoma while focal staining was also seen in adenocarcinoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Squamous Cell / pathology. Lung Neoplasms / pathology. Trans-Activators / metabolism. Tumor Suppressor Proteins / metabolism
  • [MeSH-minor] Adenocarcinoma / diagnosis. Adult. Aged. Aged, 80 and over. Bronchoalveolar Lavage / methods. Bronchoalveolar Lavage Fluid / cytology. Carcinoma, Non-Small-Cell Lung / diagnosis. Diagnosis, Differential. Female. Humans. Male. Middle Aged. Transcription Factors

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19744186.001).
  • [ISSN] 1365-2303
  • [Journal-full-title] Cytopathology : official journal of the British Society for Clinical Cytology
  • [ISO-abbreviation] Cytopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / TP63 protein, human; 0 / Trans-Activators; 0 / Transcription Factors; 0 / Tumor Suppressor Proteins
  •  go-up   go-down


37. Sato H, Yazawa T, Suzuki T, Shimoyamada H, Okudela K, Ikeda M, Hamada K, Yamada-Okabe H, Yao M, Kubota Y, Takahashi T, Kamma H, Kitamura H: Growth regulation via insulin-like growth factor binding protein-4 and -2 in association with mutant K-ras in lung epithelia. Am J Pathol; 2006 Nov;169(5):1550-66

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Growth regulation via insulin-like growth factor binding protein-4 and -2 in association with mutant K-ras in lung epithelia.
  • We investigated altered mRNA expression on K-Ras activation in human peripheral lung epithelial cells (HPL1A) using oligonucleotide microarrays.
  • Mutated K-Ras stably expressed in HPL1A accelerated cell growth and induced the expression of insulin-like growth factor (IGF)-binding protein (IGFBP)-4 and IGFBP-2, which modulate cell growth via IGF.
  • Other lung epithelial cell lines (NHBE and HPL1D) revealed the same phenomena as HPL1A by mutated K-ras transgene.
  • Lung cancer cell growth was also accelerated by mutated K-ras gene transduction, whereas IGFBP-4/2 induction was weaker compared with mutated K-Ras-expressing lung epithelial cells.
  • To understand the differences in IGFBP-4/2 inducibility via K-Ras-activated signaling between nonneoplastic lung epithelia and lung carcinoma, we addressed the mechanisms of IGFBP-4/2 transcriptional activation.
  • Furthermore, IGFBP-4 and IGFBP-2 promoters were often hypermethylated in lung carcinoma, yielding low basal expression/weak induction of IGFBP-4/2.
  • These findings suggest that continuous K-Ras activation accelerates cell growth and evokes a feedback system through IGFBP-4/2 to prevent excessive growth.
  • Moreover, this growth regulation is disrupted in lung cancers because of promoter hypermethylation of IGFBP-4/2 genes.
  • [MeSH-major] Cell Growth Processes. Epithelial Cells / cytology. Genes, ras / genetics. Insulin-Like Growth Factor Binding Protein 2 / metabolism. Insulin-Like Growth Factor Binding Protein 4 / metabolism. Lung / cytology. Point Mutation / genetics
  • [MeSH-minor] Adenocarcinoma / pathology. DNA Methylation. Early Growth Response Protein 1 / metabolism. Gene Expression. Gene Expression Regulation. Humans. Mitogen-Activated Protein Kinases / metabolism. Phosphorylation. Promoter Regions, Genetic / genetics. Protein Binding. RNA, Messenger / genetics. RNA, Messenger / metabolism. Sequence Deletion. Transfection. Tumor Cells, Cultured

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Cancer Res. 1997 Nov 1;57(21):4898-904 [9354455.001]
  • [Cites] J Biol Chem. 1999 May 21;274(21):15030-40 [10329706.001]
  • [Cites] Nat Biotechnol. 1996 Dec;14(13):1675-80 [9634850.001]
  • [Cites] Genes Dev. 1999 Nov 15;13(22):2905-27 [10579998.001]
  • [Cites] Endocr Rev. 1999 Dec;20(6):761-87 [10605625.001]
  • [Cites] DNA Seq. 2000;10(6):429-32 [10826704.001]
  • [Cites] Oncogene. 2000 Jun 8;19(25):2930-42 [10871844.001]
  • [Cites] Endocr Relat Cancer. 2001 Sep;8(3):161-73 [11566607.001]
  • [Cites] Cancer Res. 2001 Oct 15;61(20):7647-53 [11606407.001]
  • [Cites] J Cell Sci. 2002 Jun 15;115(Pt 12):2591-601 [12045229.001]
  • [Cites] Am J Pathol. 2002 Jul;161(1):291-300 [12107114.001]
  • [Cites] Int J Oncol. 2003 Mar;22(3):469-80 [12579299.001]
  • [Cites] J Cell Physiol. 2003 Aug;196(2):326-33 [12811826.001]
  • [Cites] J Endocrinol. 2003 Aug;178(2):177-93 [12904166.001]
  • [Cites] Endocrinology. 1999 Jun;140(6):2501-8 [10342835.001]
  • [Cites] J Pathol. 1999 Jan;187(2):191-9 [10365094.001]
  • [Cites] Science. 1999 Aug 27;285(5432):1390-3 [10464095.001]
  • [Cites] J Clin Oncol. 2004 Nov 15;22(22):4632-42 [15542813.001]
  • [Cites] Oncogene. 2005 Feb 17;24(8):1423-33 [15608673.001]
  • [Cites] J Biol Chem. 2005 Apr 8;280(14):14212-21 [15689620.001]
  • [Cites] Lung Cancer. 2005 Oct;50(1):1-8 [15950315.001]
  • [Cites] J Cell Biochem. 2006 Apr 1;97(5):984-98 [16288470.001]
  • [Cites] Am J Pathol. 2004 Jan;164(1):91-100 [14695323.001]
  • [Cites] Oncogene. 2004 Apr 1;23(14):2454-64 [14767471.001]
  • [Cites] Eur J Endocrinol. 2004 Aug;151 Suppl 1:S17-22 [15339239.001]
  • [Cites] Cancer Res. 1986 Feb;46(2):985-8 [3940658.001]
  • [Cites] Cancer. 1986 Apr 15;57(8):1555-64 [3004694.001]
  • [Cites] Science. 1987 Nov 6;238(4828):797-9 [3672127.001]
  • [Cites] Cell. 1988 Apr 8;53(1):37-43 [3127059.001]
  • [Cites] Cancer. 1990 Jul 15;66(2):289-94 [2196110.001]
  • [Cites] Cancer Res. 1991 Sep 15;51(18 Suppl):5023s-5044s [1884379.001]
  • [Cites] Mol Endocrinol. 1992 May;6(5):826-36 [1376411.001]
  • [Cites] Nature. 1993 Oct 28;365(6449):781-3 [8413661.001]
  • [Cites] J Biol Chem. 1993 Nov 25;268(33):24892-901 [7693708.001]
  • [Cites] Cancer. 1994 Feb 15;73(4):1163-70 [8313318.001]
  • [Cites] Nature. 1994 Aug 18;370(6490):508-9 [8052306.001]
  • [Cites] Cancer. 1995 Jan 1;75(1 Suppl):191-202 [8000996.001]
  • [Cites] Am J Pathol. 1995 Apr;146(4):876-87 [7717455.001]
  • [Cites] Cancer Res. 1996 May 1;56(9):2224-8 [8616876.001]
  • [Cites] Am J Surg Pathol. 1996 May;20(5):553-62 [8619420.001]
  • [Cites] J Pathol. 1996 Jul;179(3):254-9 [8774479.001]
  • [Cites] Endocrinology. 1997 Jan;138(1):332-43 [8977421.001]
  • [Cites] J Pathol. 1997 Apr;181(4):401-4 [9196437.001]
  • [Cites] Oncogene. 1998 Sep 17;17(11 Reviews):1395-413 [9779987.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Dec 8;95(25):14863-8 [9843981.001]
  • [Cites] Biochim Biophys Acta. 1999 Jan 11;1448(3):349-62 [9990287.001]
  • [Cites] Am J Clin Pathol. 1999 May;111(5):610-22 [10230351.001]
  • [Cites] Virchows Arch. 1997 Dec;431(6):415-24 [9428929.001]
  • (PMID = 17071580.001).
  • [ISSN] 0002-9440
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Early Growth Response Protein 1; 0 / Insulin-Like Growth Factor Binding Protein 2; 0 / Insulin-Like Growth Factor Binding Protein 4; 0 / RNA, Messenger; EC 2.7.11.24 / Mitogen-Activated Protein Kinases
  • [Other-IDs] NLM/ PMC1780191
  •  go-up   go-down


38. Della Peruta M, Giagulli C, Laudanna C, Scarpa A, Sorio C: RHOA and PRKCZ control different aspects of cell motility in pancreatic cancer metastatic clones. Mol Cancer; 2010;9:61
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] RHOA and PRKCZ control different aspects of cell motility in pancreatic cancer metastatic clones.
  • We analyzed the role of RHOA and PRKCZ in the motility attitude of two subclones of the pancreatic adenocarcinoma cell line SUIT-2 (S2), with different in vivo metastatic potential in nude mice: S2-m with a low metastatic potential and highly metastatic S2-CP9 using RHOA and PRKCZ cell-permeable inhibitory peptides.
  • METHODS: Adhesion assays, cell permeable peptides, RHOA activity assay, western blotting RESULTS: When used in combination cell-permeable inhibitory peptides partially inhibited cell adhesion by about 50% in clone S2-CP9.
  • Conversely, S2-m was unable to migrate toward both ends of the wound in basal conditions.
  • CONCLUSION: Herein, we demonstrate a critical role for RHOA and PRKCZ in the regulation of different aspects of cell motility of pancreatic adenocarcinoma and demonstrate the need to inhibit both pathways to obtain a functionally relevant effect in most assays.
  • [MeSH-major] Cell Movement. Lung Neoplasms / enzymology. Lung Neoplasms / secondary. Pancreatic Neoplasms / enzymology. Pancreatic Neoplasms / pathology. Protein Kinase C / metabolism. rhoA GTP-Binding Protein / metabolism
  • [MeSH-minor] Animals. Cell Adhesion / drug effects. Cell Line, Tumor. Cell Membrane Permeability / drug effects. Cell Shape / drug effects. Clone Cells. Mice. Mice, Nude. Peptides / pharmacology. Wound Healing / drug effects

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] IUBMB Life. 2000 Aug;50(2):85-90 [11185963.001]
  • [Cites] Nat Immunol. 2009 Feb;10(2):185-94 [19136961.001]
  • [Cites] Virchows Arch. 2001 Dec;439(6):798-802 [11787853.001]
  • [Cites] Nat Rev Cancer. 2002 Dec;2(12):897-909 [12459728.001]
  • [Cites] Nat Rev Cancer. 2002 Feb;2(2):133-42 [12635176.001]
  • [Cites] J Cell Sci. 1999 Nov;112 ( Pt 22):4067-78 [10547366.001]
  • [Cites] Biochem J. 2000 Mar 15;346 Pt 3:617-22 [10698687.001]
  • [Cites] Mol Cell Biol. 2000 Apr;20(8):2880-9 [10733591.001]
  • [Cites] J Biol Chem. 2000 Apr 14;275(15):10838-44 [10753878.001]
  • [Cites] Curr Opin Cell Biol. 2000 Aug;12(4):400-6 [10873818.001]
  • [Cites] J Biol Chem. 2000 Jun 16;275(24):18311-7 [10748207.001]
  • [Cites] J Cell Physiol. 2003 May;195(2):276-89 [12652654.001]
  • [Cites] Lab Invest. 2003 Aug;83(8):1155-63 [12920244.001]
  • [Cites] Mol Cell Biol. 2003 Oct;23(19):6809-22 [12972601.001]
  • [Cites] Immunity. 2004 Jan;20(1):25-35 [14738762.001]
  • [Cites] Virchows Arch. 2004 Mar;444(3):269-77 [14677066.001]
  • [Cites] Traffic. 2004 Jul;5(7):470-7 [15180824.001]
  • [Cites] Exp Cell Res. 2004 Nov 15;301(1):43-9 [15501444.001]
  • [Cites] J Natl Cancer Inst. 1966 Apr;36(4):641-5 [4160686.001]
  • [Cites] N Engl J Med. 1992 Feb 13;326(7):455-65 [1732772.001]
  • [Cites] J Biol Chem. 1998 Apr 17;273(16):9656-66 [9545299.001]
  • [Cites] Biochemistry. 1998 Apr 14;37(15):5249-57 [9548756.001]
  • [Cites] J Biol Chem. 1998 Nov 13;273(46):30306-15 [9804792.001]
  • [Cites] Cell Motil Cytoskeleton. 1999;43(4):269-87 [10423269.001]
  • [Cites] Virchows Arch. 2005 Mar;446(3):239-45 [15688169.001]
  • [Cites] Curr Biol. 2006 Aug 8;16(15):1531-7 [16887350.001]
  • [Cites] IUBMB Life. 2007 Feb;59(2):60-7 [17454296.001]
  • [Cites] J Immunol. 2008 Mar 1;180(5):2815-23 [18292502.001]
  • [Cites] Clin Exp Metastasis. 2000;18(7):561-71 [11688961.001]
  • (PMID = 20236512.001).
  • [ISSN] 1476-4598
  • [Journal-full-title] Molecular cancer
  • [ISO-abbreviation] Mol. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Peptides; EC 2.7.11.1 / protein kinase C zeta; EC 2.7.11.13 / Protein Kinase C; EC 3.6.5.2 / rhoA GTP-Binding Protein
  • [Other-IDs] NLM/ PMC2846889
  •  go-up   go-down


39. Koshimizu TA, Fujiwara Y, Sakai N, Shibata K, Tsuchiya H: Oxytocin stimulates expression of a noncoding RNA tumor marker in a human neuroblastoma cell line. Life Sci; 2010 Mar 13;86(11-12):455-60
Hazardous Substances Data Bank. CALCIUM, ELEMENTAL .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Oxytocin stimulates expression of a noncoding RNA tumor marker in a human neuroblastoma cell line.
  • AIMS: A noncoding RNA, metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), is upregulated in several malignant tumors.
  • The aim of this study is to clarify how MALAT1 gene expression is altered by extracellular signals in the SK-N-SH neuroblastoma cell line and to define its proximal promoter in order to study the mechanism of MALAT1 gene expression.
  • Although the expression of immediate early genes returned to basal levels after 3h, MALAT1 transcript levels peaked 6-24h after stimulation.
  • SIGNIFICANCE: The expression of the tumor marker MALAT1 ncRNA is sensitive to cell surface receptor activation by oxytocin in a neuroblastoma cell line.
  • [MeSH-minor] Brain Neoplasms / metabolism. Calcium / metabolism. Cell Line, Tumor. Cyclic AMP Response Element-Binding Protein / biosynthesis. Cyclic AMP Response Element-Binding Protein / genetics. Humans. Informatics. Neuroblastoma / metabolism. Oligonucleotide Array Sequence Analysis. Receptors, Oxytocin / agonists. Reverse Transcriptase Polymerase Chain Reaction

  • Genetic Alliance. consumer health - Neuroblastoma.
  • National BioResource Project. culture/stock collections - NBRP resources .
  • Hazardous Substances Data Bank. Oxytocin .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Copyright] Copyright (c) 2010 Elsevier Inc. All rights reserved.
  • (PMID = 20149803.001).
  • [ISSN] 1879-0631
  • [Journal-full-title] Life sciences
  • [ISO-abbreviation] Life Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cyclic AMP Response Element-Binding Protein; 0 / RNA, Neoplasm; 0 / Receptors, Oxytocin; 50-56-6 / Oxytocin; SY7Q814VUP / Calcium
  •  go-up   go-down


40. Xue LY, Zou SM, Zheng S, Xie YQ, Wen P, Liu XY, Lin DM, Lü N: [Expression of fascin and CK14 in different histological types of cancer and its differential diagnostic significance]. Zhonghua Zhong Liu Za Zhi; 2010 Nov;32(11):838-44
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.
  • OBJECTIVE: To investigate and analyze the expression of fascin and CK14 in multiple histological types of cancer and to explore the potential value of the two proteins as markers in diagnosis and differential diagnosis of various cancer types.
  • METHODS: Tissue microarray containing esophageal squamous cell carcinoma (SCC), lung SCC, larynx SCC, uterine cervical SCC, SCC of external genital organs, lung adenocarcinoma, gastric adenocarcinoma, colorectal adenocarcinoma, heptocellular carcinoma, pancreatic ductal adenocarcinoma, breast infiltrating ductal carcinoma, thyroid papillary carcinoma, uterine endometrioid adenocarcinoma, ovarian serous adenocarcinoma and renal clear cell carcinoma, 30 cases each, as well as corresponding normal controls was constructed.
  • RESULTS: In normal esophagus, bronchus, larynx, uterine cervix and skin, fascin was mainly expressed in the basal cells or reserve cells, but the expression was diffuse in esophageal SCC, lung SCC, larynx SCC, uterine cervical SCC and SCC of external genital organs, with a positive rate of 90.0%, 90.0%, 96.7%, 78.6% and 89.7%, respectively.
  • In lung adenocarcinoma, gastric adenocarcinoma, colorectal adenocarcinoma, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, breast infiltrating dutal adenocarcinoma, thyroid papillary carcinoma, uterine endometrioid adenocarcinoma, ovarian serous adenocarcinoma and renal clear cell carcinoma, the positive rates were 38.0%, 23.3%, 14.3%, 10.3%, 73.3%, 13.3%, 6.7%, 60.0%, 66.7% and 10.0%, respectively.
  • CK14 was mainly expressed in the basal cells, reserve cells or myoepithelia of normal tissues.
  • The positive rates of CK14 were 76.7%, 36.7%, 83.3%, 60.7% and 96.3% in esophageal SCC, lung SCC, larynx SCC, uterine cervical SCC and SCC of external genital organs, respectively.
  • It was weak and focal in lung adenocarcinoma, gastric adenocarcinoma, colorectal adenocarcinoma, hepatocellular carcinoma, pancreatic ductal adenocarcinoma, breast infiltrating dutal adenocarcinoma, thyroid papillary carcinoma, uterine endometrioid adenocarcinoma, ovarian serous adenocarcinoma, and renal clear cell carcinoma, with a positive rate of 13.3%, 13.3%, 20.7%, 41.4%, 46.7%, 6.7%, 40.0%, 13.3%, 20.0% and 6.7%, respectively.
  • Combination of fascin and CK14 should be a valuable marker in diagnosis and differential diagnosis of carcinoma.
  • [MeSH-major] Adenocarcinoma / metabolism. Carcinoma, Squamous Cell / metabolism. Carrier Proteins / metabolism. Keratin-14 / metabolism. Laryngeal Neoplasms / metabolism. Microfilament Proteins / metabolism
  • [MeSH-minor] Breast Neoplasms / metabolism. Breast Neoplasms / pathology. Carcinoma, Hepatocellular / metabolism. Carcinoma, Hepatocellular / pathology. Colorectal Neoplasms / metabolism. Colorectal Neoplasms / pathology. Cystadenocarcinoma, Serous / metabolism. Cystadenocarcinoma, Serous / pathology. Diagnosis, Differential. Esophageal Neoplasms / metabolism. Esophageal Neoplasms / pathology. Female. Humans. Liver Neoplasms / metabolism. Liver Neoplasms / pathology. Lung Neoplasms / metabolism. Lung Neoplasms / pathology. Male. Ovarian Neoplasms / metabolism. Ovarian Neoplasms / pathology. Stomach Neoplasms / metabolism. Stomach Neoplasms / pathology. Uterine Cervical Neoplasms / metabolism. Uterine Cervical Neoplasms / pathology

  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21223690.001).
  • [ISSN] 0253-3766
  • [Journal-full-title] Zhonghua zhong liu za zhi [Chinese journal of oncology]
  • [ISO-abbreviation] Zhonghua Zhong Liu Za Zhi
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Keratin-14; 0 / Microfilament Proteins; 146808-54-0 / fascin
  •  go-up   go-down


41. Wang GF, Lai MD, Yang RR, Chen PH, Su YY, Lv BJ, Sun LP, Huang Q, Chen SZ: Histological types and significance of bronchial epithelial dysplasia. Mod Pathol; 2006 Mar;19(3):429-37
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.
  • Pulmonary epithelium is known to undergo a preneoplastic process prior to the development of lung carcinoma.
  • Squamous dysplasia and atypical adenomatous hyperplasia have been identified and classified as preinvasive lesions of squamous cell carcinoma and peripheral pulmonary adenocarcinoma, respectively.
  • However, these commonly recognized preinvasive lesions do not completely explain the development of all histological types of lung carcinoma.
  • By examining 114 resection lung specimens, we concluded that there are four histological patterns of bronchial epithelial dysplasia based on morphological features (basal cell dysplasia, columnar cell dysplasia, bronchial epithelial dysplasia with transitional differentiation, and squamous dysplasia).
  • Basal cell dysplasia was focally positive for cytokeratin (CK) 17 and 10/13; columnar cell dysplasia was generally positive for CK7, 8, and 18; bronchial epithelial dysplasia with transitional differentiation had a heterogeneous immunoprofile, while squamous dysplasia was positive for CK10/13 and focally positive for CK17.
  • By Crosstabs McNemar test, the Mann-Whitney U-test (for two independent groups), the Kruskal-Wallis one-way nonparametric ANOVA (for >2 independent groups) and Spearman correlation analysis, the degree and extent of bronchial epithelial dysplasia was shown to be positively correlated with the incidence of bronchogenic carcinoma and multifocal primary lung carcinoma (P<0.05).
  • (1) bronchial epithelium can develop various patterns of dysplasia with abnormal/ambiguous cell differentiation and abnormal expressions of p53 and Ki-67.
  • Thus, these bronchial epithelial dysplastic lesions may represent a preneoplastic process. (2) The degree of bronchial epithelial dysplasia may significantly predispose individuals to bronchogenic carcinoma and multifocal primary lung carcinoma.
  • [MeSH-major] Lung Neoplasms / pathology. Precancerous Conditions / pathology
  • [MeSH-minor] Adult. Aged. Bronchial Neoplasms / metabolism. Bronchial Neoplasms / pathology. Carcinoma, Bronchogenic / metabolism. Carcinoma, Bronchogenic / pathology. Cell Differentiation. Epithelial Cells / chemistry. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Keratins / analysis. Ki-67 Antigen / analysis. Male. Middle Aged. Respiratory Mucosa / chemistry. Respiratory Mucosa / pathology. Tumor Suppressor Protein p53 / analysis

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16415791.001).
  • [ISSN] 0893-3952
  • [Journal-full-title] Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc
  • [ISO-abbreviation] Mod. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ki-67 Antigen; 0 / Tumor Suppressor Protein p53; 68238-35-7 / Keratins
  •  go-up   go-down


42. Cappello F, Di Stefano A, David S, Rappa F, Anzalone R, La Rocca G, D'Anna SE, Magno F, Donner CF, Balbi B, Zummo G: Hsp60 and Hsp10 down-regulation predicts bronchial epithelial carcinogenesis in smokers with chronic obstructive pulmonary disease. Cancer; 2006 Nov 15;107(10):2417-24
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: The relation between smoking, chronic obstructive pulmonary disease (COPD), and lung cancer (LC) is an open field of investigation.
  • A higher frequency of adenocarcinoma has been reported in patients with COPD.
  • Heat shock proteins (Hsps) are implicated in tumoral cell growth and differentiation.
  • The aim of the present study was to investigate the expression of Hsp60 and Hsp10 in bronchial biopsies from smokers with COPD and in 10 lung cancer patients and to evaluate the association between Hsps expression and carcinogenetic steps of LC.
  • METHOD: An immunohistochemical study was performed for Hsp60 and Hsp10 in bronchial biopsies from 35 COPD (postbronchodilator forced expiratory volume in 1 second [FEV(1)]: 53 +/- 19% [mean +/- SD]) patients with a history of smoking (53 +/- 34 pack/years) and in 10 patients with adenocarcinoma or adenosquamous carcinoma (ASC).
  • RESULTS.: In smokers with COPD, 10 out of 35 patients had a normal bronchial epithelium (NBE), 12 showed basal cell hyperplasia (BCH), 5 squamous metaplasia (SM), and 8 dysplasia (Dy).
  • [MeSH-major] Carcinoma, Bronchogenic / diagnosis. Chaperonin 10 / metabolism. Chaperonin 60 / metabolism. Lung Neoplasms / diagnosis. Pulmonary Disease, Chronic Obstructive / complications. Smoking / adverse effects
  • [MeSH-minor] Adenocarcinoma / complications. Adenocarcinoma / diagnosis. Adenocarcinoma / pathology. Aged. Blotting, Western. Carcinoma, Adenosquamous / complications. Carcinoma, Adenosquamous / diagnosis. Carcinoma, Adenosquamous / pathology. Disease Progression. Down-Regulation. Humans. Middle Aged. Prognosis. Respiratory Mucosa / pathology


43. Watson S, Serrate C, Vignot S: [Sonic Hedgehog signaling pathway: from embryology to molecular targeted therapies]. Bull Cancer; 2010 Dec;97(12):1477-83
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • During the past few years its implication in carcinogenesis has become clear and today it is acknowledged that this pathway plays a role in the malignant transformation of multiple cell types, either owing to the mutation of some of its components or to its erratic activation.
  • New molecular targeted therapies that inhibit the pathway have shown their unquestionable efficiency in several tumours -among which basal cell carcinoma, medulloblastoma, or pancreatic adenocarcinoma.
  • [MeSH-minor] Anilides / therapeutic use. Animals. Carcinoma, Basal Cell / drug therapy. Carcinoma, Basal Cell / genetics. Cerebellar Neoplasms / genetics. Embryonic Induction / physiology. Humans. Lung Neoplasms / genetics. Medulloblastoma / genetics. Mutation / physiology. Neoplastic Stem Cells / physiology. Pancreatic Neoplasms / genetics. Patient Selection. Pyridines / therapeutic use. Receptors, Cell Surface / physiology. Signal Transduction / drug effects. Signal Transduction / physiology. Skin Neoplasms / drug therapy. Skin Neoplasms / genetics. Small Cell Lung Carcinoma / genetics

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 21220225.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Anilides; 0 / Hedgehog Proteins; 0 / HhAntag691; 0 / Pyridines; 0 / Receptors, Cell Surface; 0 / patched receptors
  •  go-up   go-down


44. Eriksson SE, Prast-Nielsen S, Flaberg E, Szekely L, Arnér ES: High levels of thioredoxin reductase 1 modulate drug-specific cytotoxic efficacy. Free Radic Biol Med; 2009 Dec 1;47(11):1661-71
Hazardous Substances Data Bank. 1-CHLORO-2,4-DINITROBENZENE .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Here we analyzed the effects of TrxR1 targeting in the human A549 lung carcinoma cell line, having a very high basal TrxR1 expression.
  • Knocking down TrxR1 by approx 90% using siRNA gave only a slight effect on cell growth, irrespective of concurrent glutathione depletion (> or = 98% decrease), and no increase in cell death or distorted cell cycle phase distributions.
  • [MeSH-major] Adenocarcinoma / drug therapy. Lung Neoplasms / drug therapy. Thioredoxin Reductase 1 / metabolism
  • [MeSH-minor] Apoptosis / drug effects. Apoptosis / genetics. Auranofin / pharmacology. Cell Cycle / drug effects. Cell Cycle / genetics. Cell Growth Processes / drug effects. Cell Growth Processes / genetics. Cell Line, Tumor. Cisplatin / pharmacology. Dinitrochlorobenzene / pharmacology. Drug Resistance, Neoplasm / drug effects. Drug Resistance, Neoplasm / genetics. Humans. Naphthoquinones / pharmacology. RNA, Small Interfering / genetics. Vitamin K 3 / pharmacology

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • Hazardous Substances Data Bank. CIS-DIAMINEDICHLOROPLATINUM .
  • Hazardous Substances Data Bank. AURANOFIN .
  • Hazardous Substances Data Bank. MENADIONE .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19766715.001).
  • [ISSN] 1873-4596
  • [Journal-full-title] Free radical biology & medicine
  • [ISO-abbreviation] Free Radic. Biol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Naphthoquinones; 0 / RNA, Small Interfering; 3H04W2810V / Auranofin; 723JX6CXY5 / Vitamin K 3; EC 1.8.1.9 / Thioredoxin Reductase 1; GE3IBT7BMN / Dinitrochlorobenzene; Q20Q21Q62J / Cisplatin; W6Q80SK9L6 / juglone
  •  go-up   go-down


45. Gade P, Singh AK, Roy SK, Reddy SP, Kalvakolanu DV: Down-regulation of the transcriptional mediator subunit Med1 contributes to the loss of expression of metastasis-associated dapk1 in human cancers and cancer cells. Int J Cancer; 2009 Oct 1;125(7):1566-74
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • We have recently shown that CCAAT/Enhancer binding protein-beta (C/EBP-beta) is required for the basal and interferon gamma (IFN-gamma)-induced expression of dapk1 in many cell types.
  • C/EBP-beta interacts with the transcriptional Mediator, a multisubunit complex that couples enhancer bound transcription factors to the basal transcriptional machinery in an IFN-gamma dependent manner for regulating dapk1 expression.
  • We compared the relative occupancy of these factors at the dapk1 promoter at CRE/ATF sites in normal and cancer cell lines.
  • A significantly lower binding of these factors to the CRE/ATF site of dapk1 promoter occurred in human cancer cell lines than in normal cells.
  • We show that loss of Med1 expression correlates with a corresponding loss of dapk1 expression in a number of primary human lung carcinomas.
  • Med1 levels were significantly lower in cancer cell lines than in normal controls.
  • Our studies reveal a critical parameter limiting dapk1 expression in cancer cell lines.

  • MedlinePlus Health Information. consumer health - Lung Cancer.
  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Mol Cell. 1999 Nov;4(5):735-43 [10619021.001]
  • [Cites] J Biol Chem. 2002 Nov 22;277(47):45611-8 [12235159.001]
  • [Cites] Mol Cell Biol. 2000 Dec;20(24):9192-202 [11094071.001]
  • [Cites] Leukemia. 2001 Jan;15(1):89-94 [11243405.001]
  • [Cites] Mol Cell Biol. 2001 Mar;21(5):1621-32 [11238899.001]
  • [Cites] Curr Opin Cell Biol. 2001 Jun;13(3):274-80 [11343897.001]
  • [Cites] Breast Cancer Res Treat. 2001 Jun;67(3):245-53 [11561770.001]
  • [Cites] Eur J Cancer. 2000 Dec;36(18):2294-300 [11094302.001]
  • [Cites] Nat Cell Biol. 2002 Jan;4(1):51-8 [11740493.001]
  • [Cites] J Biol Chem. 2002 Feb 1;277(5):3585-92 [11724781.001]
  • [Cites] Nature. 2003 Jan 16;421(6920):290-4 [12529648.001]
  • [Cites] Int J Oncol. 2003 Mar;22(3):601-8 [12579314.001]
  • [Cites] Clin Cancer Res. 2003 Apr;9(4):1370-5 [12684406.001]
  • [Cites] Cancer Res. 2003 Nov 15;63(22):7694-8 [14633692.001]
  • [Cites] Eur J Cancer. 2004 Jan;40(1):21-7 [14687785.001]
  • [Cites] Mol Cell Biol. 2004 Jul;24(13):5989-99 [15199152.001]
  • [Cites] Mol Cancer. 2003 May 13;2:24 [12773202.001]
  • [Cites] Mol Cell Biol. 1993 Jul;13(7):3964-74 [8321203.001]
  • [Cites] Genes Dev. 1994 Nov 15;8(22):2781-91 [7958933.001]
  • [Cites] Genes Dev. 1995 Jan 1;9(1):15-30 [7828849.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Jan 9;93(1):465-9 [8552662.001]
  • [Cites] Mol Cell Biol. 1997 Apr;17(4):2038-47 [9121452.001]
  • [Cites] EMBO J. 1997 Mar 3;16(5):998-1008 [9118961.001]
  • [Cites] Oncogene. 1997 Jul 24;15(4):403-7 [9242376.001]
  • [Cites] Nature. 1997 Nov 13;390(6656):180-4 [9367156.001]
  • [Cites] J Biol Chem. 1998 Oct 30;273(44):28545-8 [9786841.001]
  • [Cites] Oncogene. 2005 Feb 17;24(8):1461-6 [15608685.001]
  • [Cites] Nat Cell Biol. 2005 Mar;7(3):311-8 [15723054.001]
  • [Cites] J Interferon Cytokine Res. 2005 Dec;25(12):757-69 [16375604.001]
  • [Cites] J Biol Chem. 2006 Jan 6;281(1):80-9 [16263706.001]
  • [Cites] Annu Rev Biochem. 2006;75:189-210 [16756490.001]
  • [Cites] Oncogene. 2006 Nov 16;25(54):7138-47 [16732315.001]
  • [Cites] Oncogene. 2007 Feb 1;26(5):781-7 [16862175.001]
  • [Cites] Biochem J. 2007 Mar 15;402(3):559-66 [17083329.001]
  • [Cites] Cell. 2007 Jun 1;129(5):879-90 [17540169.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6204-11 [17616677.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6212-20 [17616678.001]
  • [Cites] Am J Pathol. 2007 Oct;171(4):1352-68 [17823279.001]
  • [Cites] Oncol Rep. 2007 Dec;18(6):1427-34 [17982626.001]
  • [Cites] Br J Haematol. 2007 Dec;139(5):744-52 [17961188.001]
  • [Cites] Mol Cell Biol. 2008 Apr;28(8):2528-48 [18250155.001]
  • [Cites] J Biol Chem. 2008 May 9;283(19):13077-86 [18339625.001]
  • [Cites] Mol Cell Biol. 2008 Jun;28(12):4204-14 [18391023.001]
  • [Cites] Mol Cell. 2008 Nov 21;32(4):519-28 [19026782.001]
  • [Cites] Nat Genet. 2000 Mar;24(3):300-3 [10700188.001]
  • [Cites] J Biol Chem. 2000 May 19;275(20):14779-82 [10747854.001]
  • [Cites] Genes Chromosomes Cancer. 2000 Jun;28(2):138-44 [10824998.001]
  • [Cites] Trends Biochem Sci. 2000 Jun;25(6):277-83 [10838567.001]
  • [Cites] Mol Cell. 2000 Apr;5(4):683-93 [10882104.001]
  • [Cites] Nature. 2002 May 30;417(6888):563-7 [12037571.001]
  • [Cites] Oncogene. 2002 May 2;21(19):2961-70 [12082526.001]
  • [Cites] Annu Rev Biochem. 2000;69:729-49 [10966474.001]
  • (PMID = 19521987.001).
  • [ISSN] 1097-0215
  • [Journal-full-title] International journal of cancer
  • [ISO-abbreviation] Int. J. Cancer
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA105005; United States / NIEHS NIH HHS / ES / ES11863; United States / NCI NIH HHS / CA / R01 CA105005; United States / NIEHS NIH HHS / ES / R01 ES011863; United States / NCI NIH HHS / CA / CA78282; United States / NCI NIH HHS / CA / R01 CA078282; United States / NHLBI NIH HHS / HL / HL66109; United States / NHLBI NIH HHS / HL / R01 HL066109; United States / NCI NIH HHS / CA / R01 CA078282-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / MED1 protein, human; 0 / Med1 protein, mouse; 0 / Mediator Complex Subunit 1; 0 / Transcription Factors; 82115-62-6 / Interferon-gamma; EC 2.7.11.1 / DAPK1 protein, human; EC 2.7.11.1 / Dapk1 protein, mouse; EC 2.7.11.1 / Death-Associated Protein Kinases; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinase 3
  • [Other-IDs] NLM/ NIHMS137980; NLM/ PMC4010141
  •  go-up   go-down


46. Young GS, Setayesh K: Spin-echo echo-planar perfusion MR imaging in the differential diagnosis of solitary enhancing brain lesions: distinguishing solitary metastases from primary glioma. AJNR Am J Neuroradiol; 2009 Mar;30(3):575-7
MedlinePlus Health Information. consumer health - Soft Tissue Sarcoma.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Spin-echo echo-planar perfusion MR imaging in the differential diagnosis of solitary enhancing brain lesions: distinguishing solitary metastases from primary glioma.
  • [MeSH-minor] Adenocarcinoma / secondary. Adult. Aged. Astrocytoma / pathology. Breast Neoplasms / pathology. Carcinoma, Basal Cell / secondary. Colorectal Neoplasms / pathology. Diagnosis, Differential. Esophageal Neoplasms / pathology. Female. Humans. Lung Neoplasms / pathology. Male. Melanoma / secondary. Middle Aged. Models, Neurological. Prostatic Neoplasms / pathology. Retrospective Studies. Sensitivity and Specificity. Skin Neoplasms / pathology

  • Genetic Alliance. consumer health - Glioma.
  • MedlinePlus Health Information. consumer health - Brain Tumors.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19095787.001).
  • [ISSN] 1936-959X
  • [Journal-full-title] AJNR. American journal of neuroradiology
  • [ISO-abbreviation] AJNR Am J Neuroradiol
  • [Language] eng
  • [Publication-type] Journal Article; Technical Report
  • [Publication-country] United States
  •  go-up   go-down


47. Morton JP, Lewis BC: Shh signaling and pancreatic cancer: implications for therapy? Cell Cycle; 2007 Jul 1;6(13):1553-7
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Hedgehog signaling has been implicated in the development of several human cancers, including small cell lung carcinomas, medulloblastomas, basal cell carcinomas, and digestive tract tumors.
  • Elevated levels of pathway components are observed in pancreatic ductal adenocarcinoma (PDAC) precursor lesions, and these levels increase further as lesions progress to more advanced stages.

  • Genetic Alliance. consumer health - Pancreatic cancer.
  • MedlinePlus Health Information. consumer health - Pancreatic Cancer.
  • COS Scholar Universe. author profiles.
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17611415.001).
  • [ISSN] 1551-4005
  • [Journal-full-title] Cell cycle (Georgetown, Tex.)
  • [ISO-abbreviation] Cell Cycle
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD95; 0 / Hedgehog Proteins; 0 / SHH protein, human
  • [Number-of-references] 41
  •  go-up   go-down


48. van den Top JG, de Heer N, Klein WR, Ensink JM: Penile and preputial tumours in the horse: a retrospective study of 114 affected horses. Equine Vet J; 2008 Sep;40(6):528-32
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.
  • Data recorded included age, gelding or stallion and breed; type and site of lesion; involvement of regional lymph nodes; histopathology (including grading of squamous cell carcinoma); and results of radiographic examination of the thorax.
  • Squamous cell carcinoma (SCC) was the most prevalent neoplasm followed by papillomas and melanomas.
  • A basal cell carcinoma, neurofibrosarcoma, adenocarcinoma or fibrosarcoma were each found on single horses.
  • Squamous cell carcinomas with poor differentiation had a higher tendency to metastasise than did more differentiated tumours.
  • CONCLUSIONS: Squamous cell carcinoma is the most common urogenital tumour of the male horse and occurs primarily in old horses.
  • Radiology of the thorax to detect lung metastases is of little value.
  • [MeSH-major] Carcinoma, Squamous Cell / veterinary. Horse Diseases / pathology. Penile Neoplasms / veterinary
  • [MeSH-minor] Age Factors. Animals. Breeding. Horses. Lymph Nodes / pathology. Lymph Nodes / surgery. Lymphatic Metastasis / diagnosis. Male. Neoplasm Metastasis / diagnosis. Neoplasm Staging / veterinary. Orchiectomy / veterinary. Papilloma / epidemiology. Papilloma / pathology. Papilloma / surgery. Papilloma / veterinary. Pedigree. Penis / pathology. Penis / surgery. Retrospective Studies. Urethra / pathology. Urethra / surgery

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18487101.001).
  • [ISSN] 0425-1644
  • [Journal-full-title] Equine veterinary journal
  • [ISO-abbreviation] Equine Vet. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  •  go-up   go-down


49. Quinn AM, Penning TM: Comparisons of (+/-)-benzo[a]pyrene-trans-7,8-dihydrodiol activation by human cytochrome P450 and aldo-keto reductase enzymes: effect of redox state and expression levels. Chem Res Toxicol; 2008 May;21(5):1086-94
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.
  • The resting NADPH/NAD (+) ratio was determined in A549 human lung adenocarcinoma cells to be 0.28.
  • Basal mRNA transcript levels of AKR1C1-1C3 exceed those of both basal and 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD)-induced P450 1A1 and 1B1 by up to 90-fold in A549 cells as measured by real-time reverse transcriptase polymerase chain reaction (RT-PCR) methods.
  • Functional assays of both A549 and HBEC-KT cell lysates demonstrated a lack of TCDD-inducible P450 1A1/1B1 activity but robust basal expression of AKR1A1 and AKR1C activities, where the functional assay for P450 detection is 300-fold more sensitive than the functional assay for AKR isoforms.
  • These data suggest that AKR enzymes may effectively compete with P450 1A1/1B1 for PAH trans-dihydrodiol activation in human lung cells.
  • [MeSH-minor] Catalysis. Cell Line, Tumor. Humans. Kinetics. Molecular Structure. NAD / metabolism. Oxidation-Reduction / drug effects

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 18402469.001).
  • [ISSN] 1520-5010
  • [Journal-full-title] Chemical research in toxicology
  • [ISO-abbreviation] Chem. Res. Toxicol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P01 CA092537; United States / NIEHS NIH HHS / ES / P30 ES013508; United States / NCI NIH HHS / CA / R01 CA39504
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dihydroxydihydrobenzopyrenes; 0U46U6E8UK / NAD; 13345-25-0 / benzo(a)pyrene 7,8-dihydrodiol; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.- / Oxidoreductases
  •  go-up   go-down


50. Birkenkamp-Demtröder K, Wagner L, Brandt Sørensen F, Bording Astrup L, Gartner W, Scherübl H, Heine B, Christiansen P, Ørntoft TF: Secretagogin is a novel marker for neuroendocrine differentiation. Neuroendocrinology; 2005;82(2):121-38
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Our previous microarray-based studies identified secretagogin to be highly expressed in normal colon mucosa compared to basal expression in colon adenocarcinomas.
  • Secretagogin was strongly expressed in the cytosol and the nucleus of 19 well-differentiated neuroendocrine carcinoids and carcinoid metastases, as well as in neuroendocrine tumors from the lung, pancreas and adrenal gland.
  • [MeSH-minor] Adenocarcinoma / metabolism. Adenocarcinoma / pathology. Adolescent. Adult. Aged. Aged, 80 and over. Biomarkers, Tumor. Blotting, Western. Carcinoid Tumor / metabolism. Carcinoid Tumor / pathology. Cell Differentiation / physiology. Chromogranin A. Chromogranins / metabolism. Female. Humans. Immunohistochemistry. Lung Neoplasms / secondary. Male. Microscopy, Fluorescence. Middle Aged. Neoplasm Metastasis. Oligonucleotide Array Sequence Analysis. Peptidylprolyl Isomerase / metabolism. Phosphopyruvate Hydratase / metabolism. Secretagogins. Synaptophysin / metabolism. Tacrolimus Binding Proteins / metabolism

  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16449819.001).
  • [ISSN] 0028-3835
  • [Journal-full-title] Neuroendocrinology
  • [ISO-abbreviation] Neuroendocrinology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Calcium-Binding Proteins; 0 / Chromogranin A; 0 / Chromogranins; 0 / SCGN protein, human; 0 / Secretagogins; 0 / Synaptophysin; EC 4.2.1.11 / Phosphopyruvate Hydratase; EC 5.2.1.- / Tacrolimus Binding Proteins; EC 5.2.1.8 / FKBP10 protein, human; EC 5.2.1.8 / Peptidylprolyl Isomerase
  •  go-up   go-down


51. Wooten-Blanks LG, Song P, Senkal CE, Ogretmen B: Mechanisms of ceramide-mediated repression of the human telomerase reverse transcriptase promoter via deacetylation of Sp3 by histone deacetylase 1. FASEB J; 2007 Oct;21(12):3386-97
NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The generation of C18-ceramide via the expression of ceramide synthase 1 (CerS1), and not C16-ceramide by CerS5 or CerS6 expression, resulted in repression of the hTERT promoter via deacetylation of Sp3 by histone deacetylase 1 (HDAC1) in A549 human lung adenocarcinoma cells.
  • Expression of the deacetylated Sp3 mutant resulted in repression, whereas its acetylated mutant induced basal hTERT promoter activity in Drosophila S2 cells, which do not express any endogenous Sp3, and in A549 cells.
  • [MeSH-minor] Acetylation. Animals. Base Sequence. Cell Line. Histone Deacetylase 1. Humans. Molecular Sequence Data. Mutation. Signal Transduction / physiology

  • COS Scholar Universe. author profiles.
  • Gene Ontology. gene/protein/disease-specific - Gene Ontology annotations from this paper .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 17548428.001).
  • [ISSN] 1530-6860
  • [Journal-full-title] FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • [ISO-abbreviation] FASEB J.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / CA-88932
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Ceramides; 0 / SP3 protein, human; 148710-94-5 / Sp3 Transcription Factor; EC 2.7.7.49 / TERT protein, human; EC 2.7.7.49 / Telomerase; EC 3.5.1.98 / HDAC1 protein, human; EC 3.5.1.98 / Histone Deacetylase 1; EC 3.5.1.98 / Histone Deacetylases
  •  go-up   go-down


52. Mangal D, Vudathala D, Park JH, Lee SH, Penning TM, Blair IA: Analysis of 7,8-dihydro-8-oxo-2'-deoxyguanosine in cellular DNA during oxidative stress. Chem Res Toxicol; 2009 May;22(5):788-97
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • The LC-MRM/MS method was used to determine that the basal 8-oxo-dGuo level in DNA from human bronchoalveolar H358 cells was 2.2 +/- 0.4 8-oxo-dGuo/10(7) dGuo (mean +/- standard deviation) or 5.5 +/- 1.0 8-oxo-dGuo/10(8) nucleotides.
  • Similar levels were observed in human lung adenocarcinoma A549 cells, mouse hepatoma Hepa-1c1c7 cells, and human HeLa cervical epithelial adenocarcinoma cells.
  • These values are an order of magnitude lower than is typically reported for basal 8-oxo-dGuo levels in DNA as determined by other MS- or chromatography-based assays.
  • In contrast, no 8-oxo-dGuo was observed in H358 cell DNA after treatment with MMS.
  • In keeping with this concept, inhibition of catechol-O-methyl transferase (COMT)-mediated detoxification of B[a]P-7,8-catechol with Ro 410961 caused increased 8-oxo-dGuo formation in the H358 cell DNA.

  • COS Scholar Universe. author profiles.
  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Free Radic Res. 1998 Dec;29(6):601-8 [10098465.001]
  • [Cites] Electrophoresis. 1999 Jul;20(10):2133-8 [10451126.001]
  • [Cites] Free Radic Res. 2002 Jun;36(6):649-59 [12180190.001]
  • [Cites] Carcinogenesis. 2002 Nov;23(11):1911-8 [12419840.001]
  • [Cites] Carcinogenesis. 2002 Dec;23(12):2129-33 [12507938.001]
  • [Cites] Carcinogenesis. 2000 Mar;21(3):361-70 [10688856.001]
  • [Cites] Chem Res Toxicol. 2000 Mar;13(3):135-60 [10725110.001]
  • [Cites] Chem Res Toxicol. 2000 Jul;13(7):541-9 [10898585.001]
  • [Cites] Nutrition. 2001 Feb;17(2):161, 163-5 [11240347.001]
  • [Cites] J Biol Chem. 2001 Feb 23;276(8):40601-4 [11246639.001]
  • [Cites] Nucleic Acids Res. 2001 May 15;29(10):2117-26 [11353081.001]
  • [Cites] Science. 2001 Jun 15;292(5524):2083-6 [11408659.001]
  • [Cites] Biochemistry. 2001 Sep 11;40(36):10901-10 [11535067.001]
  • [Cites] Trends Cardiovasc Med. 2001 Apr-May;11(3-4):148-55 [11686005.001]
  • [Cites] Rapid Commun Mass Spectrom. 2003;17(2):126-34 [12512091.001]
  • [Cites] Biochem Pharmacol. 2003 Apr 1;65(7):1035-41 [12663039.001]
  • [Cites] Free Radic Biol Med. 2003 Apr 15;34(8):1089-99 [12684094.001]
  • [Cites] FASEB J. 2003 Jul;17(10):1195-214 [12832285.001]
  • [Cites] Cell Mol Life Sci. 2003 Oct;60(10):2064-83 [14618256.001]
  • [Cites] Chem Res Toxicol. 2003 Nov;16(11):1470-6 [14615974.001]
  • [Cites] FASEB J. 2005 Jan;19(1):82-4 [15533950.001]
  • [Cites] Mol Carcinog. 2005 Mar;42(3):127-41 [15584022.001]
  • [Cites] Free Radic Biol Med. 2005 Jun 15;38(12):1543-52 [15917183.001]
  • [Cites] Chem Res Toxicol. 2005 Jun;18(6):1026-37 [15962938.001]
  • [Cites] Mutat Res. 2005 Dec 11;591(1-2):60-73 [16081110.001]
  • [Cites] Clin Chim Acta. 2006 Mar;365(1-2):30-49 [16214123.001]
  • [Cites] Toxicology. 2006 Apr 17;221(2-3):172-8 [16457930.001]
  • [Cites] Toxicology. 2006 Apr 17;221(2-3):166-71 [16490296.001]
  • [Cites] Chem Res Toxicol. 2006 May;19(5):719-28 [16696575.001]
  • [Cites] Mutagenesis. 2006 May;21(3):185-90 [16597659.001]
  • [Cites] Antioxid Redox Signal. 2006 May-Jun;8(5-6):1021-31 [16771692.001]
  • [Cites] DNA Repair (Amst). 2006 Jul 13;5(7):761-72 [16621731.001]
  • [Cites] DNA Repair (Amst). 2006 Nov 8;5(11):1337-45 [16861056.001]
  • [Cites] DNA Repair (Amst). 2007 Mar 1;6(3):274-9 [17161978.001]
  • [Cites] J Neurosci Res. 2007 Apr;85(5):919-34 [17279544.001]
  • [Cites] DNA Repair (Amst). 2007 Jun 1;6(6):760-9 [17280880.001]
  • [Cites] Mutat Res. 2007 Jul 1;620(1-2):135-44 [17403525.001]
  • [Cites] Mutat Res. 2007 Jul 1;620(1-2):71-82 [17434188.001]
  • [Cites] J Nutr Biochem. 2007 Sep;18(9):567-79 [17360173.001]
  • [Cites] J Phys Chem B. 2007 Sep 6;111(35):10453-60 [17661513.001]
  • [Cites] Mol Aspects Med. 2007 Jun-Aug;28(3-4):307-22 [17659329.001]
  • [Cites] Mol Biotechnol. 2007 Sep;37(1):48-51 [17914163.001]
  • [Cites] Cancer Epidemiol Biomarkers Prev. 2008 Jan;17(1):3-14 [18199707.001]
  • [Cites] Free Radic Biol Med. 2008 Feb 1;44(3):464-73 [17983606.001]
  • [Cites] J Neurol Sci. 2008 Mar 15;266(1-2):57-62 [17888453.001]
  • [Cites] Eur J Nutr. 2008 May;47 Suppl 2:19-28 [18458832.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 May 13;105(19):6846-51 [18474869.001]
  • [Cites] Chem Res Toxicol. 2008 May;21(5):1039-49 [18489080.001]
  • [Cites] Acc Chem Res. 2008 Aug;41(8):1075-83 [18666785.001]
  • [Cites] Free Radic Biol Med. 2008 Nov 1;45(9):1318-25 [18775490.001]
  • [Cites] J Natl Cancer Inst. 2003 Sep 3;95(17):1263-5 [12953074.001]
  • [Cites] Mutat Res. 2002 Jan 15;513(1-2):37-48 [11719088.001]
  • [Cites] Free Radic Res. 2002 Mar;36(3):239-45 [12071341.001]
  • [Cites] Free Radic Res. 2002 Mar;36(3):307-16 [12071350.001]
  • [Cites] J Biol Chem. 2002 Jul 5;277(27):24799-808 [11978787.001]
  • [Cites] Mutat Res. 2003 Oct 29;531(1-2):177-90 [14637254.001]
  • [Cites] Arch Biochem Biophys. 2004 Mar 1;423(1):57-65 [14989265.001]
  • [Cites] Clin Cancer Res. 2004 May 1;10(9):2977-85 [15131033.001]
  • [Cites] Lancet Oncol. 2004 Oct;5(10):600-6 [15465463.001]
  • [Cites] J Biol Chem. 1988 Feb 5;263(4):1814-20 [3276678.001]
  • [Cites] J Environ Pathol Toxicol Oncol. 1992 May-Jun;11(3):139-43 [1625183.001]
  • [Cites] Proc Natl Acad Sci U S A. 1993 Sep 1;90(17):7915-22 [8367443.001]
  • [Cites] Ann Rheum Dis. 1993 Sep;52(9):659-66 [8239761.001]
  • [Cites] Mol Cell Biol. 1995 Feb;15(2):989-96 [7823963.001]
  • [Cites] Environ Health Perspect. 1994 Dec;102 Suppl 10:33-6 [7705301.001]
  • [Cites] J Bacteriol. 1996 Jul;178(13):3885-92 [8682794.001]
  • [Cites] Science. 1996 Jul 5;273(5271):59-63 [8658196.001]
  • [Cites] Biotechniques. 1997 Mar;22(3):550-3 [9067036.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jan 6;95(1):288-93 [9419368.001]
  • [Cites] Chem Res Toxicol. 1998 Aug;11(8):882-7 [9705749.001]
  • [Cites] FASEB J. 1998 Oct;12(13):1397-400 [9761783.001]
  • [Cites] Nucleic Acids Res. 1998 Nov 15;26(22):5116-22 [9801308.001]
  • [Cites] Free Radic Res. 1998 Dec;29(6):541-50 [10098458.001]
  • (PMID = 19309085.001).
  • [ISSN] 1520-5010
  • [Journal-full-title] Chemical research in toxicology
  • [ISO-abbreviation] Chem. Res. Toxicol.
  • [Language] ENG
  • [Grant] United States / NIEHS NIH HHS / ES / R01 ES015857; United States / NIEHS NIH HHS / ES / U01ES016004; United States / NCI NIH HHS / CA / R01CA130038; United States / NIEHS NIH HHS / ES / R01ES015857; United States / NIEHS NIH HHS / ES / P30 ES013508; United States / NIEHS NIH HHS / ES / U01 ES016004; United States / NIEHS NIH HHS / ES / P30ES013508; United States / NCI NIH HHS / CA / R01 CA130038
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; G9481N71RO / Deoxyguanosine
  • [Other-IDs] NLM/ PMC2684441
  •  go-up   go-down


53. Puebla-Mora AG, Heras A, Cano-Valdez AM, Domínguez-Malagón H: Human telomerase and alpha-methylacyl-coenzyme A racemase in prostatic carcinoma. A comparative immunohistochemical study. Ann Diagn Pathol; 2006 Aug;10(4):205-8
MedlinePlus Health Information. consumer health - Prostate Cancer.

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Human telomerase detected by in situ hybridization has been demonstrated to be a useful tool for the diagnosis of malignancy and has also been tested by reverse transcriptase-polymerase chain reaction in several tumors such as hepatic cell carcinoma, melanoma, colonic carcinoma, gastric carcinoma, biliary carcinoma, breast carcinoma, mesothelioma, lung carcinoma, female tract carcinoma, and prostatic carcinoma.
  • Fifty-five specimens of diverse prostatic lesions were selected for study (43 needle biopsies and 12 transurethral resections); there were 61 malignancies (47 infiltrating carcinomas and 14 high-grade prostatic intraepithelial neoplasias [PIN]) and 29 benign lesions (10 basal cell hyperplasias, 12 nodular hyperplasias, 4 chronic prostatitis, and 3 atrophic glands).
  • [MeSH-major] Adenocarcinoma / enzymology. DNA-Binding Proteins / metabolism. Immunoenzyme Techniques / methods. Prostatic Intraepithelial Neoplasia / enzymology. Prostatic Neoplasms / enzymology. Racemases and Epimerases / metabolism. Telomerase / metabolism

  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 16844561.001).
  • [ISSN] 1092-9134
  • [Journal-full-title] Annals of diagnostic pathology
  • [ISO-abbreviation] Ann Diagn Pathol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / DNA-Binding Proteins; EC 2.7.7.49 / Telomerase; EC 5.1.- / Racemases and Epimerases; EC 5.1.99.4 / alpha-methylacyl-CoA racemase
  •  go-up   go-down


54. Vesely DL: Cardiac and renal hormones: anticancer effects in vitro and in vivo. J Investig Med; 2009 Jan;57(1):22-8
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.
  • BACKGROUND: Four cardiovascular hormones, ie, vessel dilator, long-acting natriuretic peptide, kaliuretic peptide, and atrial natriuretic peptide each at 1 mmol/L, decrease up to 97% of human breast, ovarian, pancreatic, colon, kidney, and prostate adenocarcinoma cells, as well as small cell and squamous cell lung cancer cells within 24 hours.
  • CONCLUSIONS: The cardiac hormones' anticancer mechanism of action(s) include a strong inhibition of mitogen (epidermal growth factor and insulin) activated extracellular signal-regulated kinases (ERK) 1/2 and as well as inhibition of basal extracellular-signal regulated kinase 1/2 and upstream MEK 1/2 phosphorylation.

  • MedlinePlus Health Information. consumer health - Cancer Chemotherapy.
  • COS Scholar Universe. author profiles.
  • NCI CPTC Antibody Characterization Program. NCI CPTC Antibody Characterization Program .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • (PMID = 19092678.001).
  • [ISSN] 1081-5589
  • [Journal-full-title] Journal of investigative medicine : the official publication of the American Federation for Clinical Research
  • [ISO-abbreviation] J. Investig. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Natriuretic Peptides
  • [Number-of-references] 76
  •  go-up   go-down


55. Reynolds PR, Cosio MG, Hoidal JR: Cigarette smoke-induced Egr-1 upregulates proinflammatory cytokines in pulmonary epithelial cells. Am J Respir Cell Mol Biol; 2006 Sep;35(3):314-9
The Lens. Cited by Patents in .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Using immunohistochemistry, we demonstrated that pulmonary adenocarcinoma cells (A-549) and primary epithelial cells lacking basal Egr-1 markedly induce Egr-1 expression after CSE exposure.

  • MedlinePlus Health Information. consumer health - Smoking.
  • COS Scholar Universe. author profiles.
  • KOMP Repository. gene/protein/disease-specific - KOMP Repository (subscription/membership/fee required).
  • Mouse Genome Informatics (MGI). Mouse Genome Informatics (MGI) .
  • [Email] Email this result item
    Email the results to the following email address:   [X] Close
  • [Cites] Respir Physiol. 2001 Oct;128(1):3-11 [11535256.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 Jul 7;95(14):8298-303 [9653181.001]
  • [Cites] Am J Respir Cell Mol Biol. 2001 Nov;25(5):620-7 [11713105.001]
  • [Cites] Chest. 2002 May;121(5 Suppl):116S-120S [12010838.001]
  • [Cites] Nat Rev Immunol. 2002 May;2(5):372-7 [12033743.001]
  • [Cites] Ann N Y Acad Sci. 2003 Dec;1002:197-216 [14751836.001]
  • [Cites] J Biol Chem. 2004 Aug 27;279(35):37124-32 [15197188.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Oct 12;101(41):14895-900 [15469929.001]
  • [Cites] Am J Respir Crit Care Med. 2004 Nov 1;170(9):974-80 [15282203.001]
  • [Cites] Am Rev Respir Dis. 1977 Feb;115(2):285-93 [842942.001]
  • [Cites] Am Rev Respir Dis. 1978 Sep;118(3):617-21 [101105.001]
  • [Cites] J Clin Invest. 1990 Mar;85(3):766-71 [2107209.001]
  • [Cites] Am Rev Respir Dis. 1990 Dec;142(6 Pt 1):1422-8 [2252262.001]
  • [Cites] Cell Regul. 1991 Mar;2(3):251-60 [1859855.001]
  • [Cites] Circ Res. 1992 Dec;71(6):1351-60 [1385005.001]
  • [Cites] Prog Nucleic Acid Res Mol Biol. 1995;50:191-224 [7754034.001]
  • [Cites] Science. 1996 Mar 8;271(5254):1427-31 [8596917.001]
  • [Cites] Science. 1996 Aug 30;273(5279):1219-21 [8703054.001]
  • [Cites] Clin Chest Med. 2000 Mar;21(1):67-86, viii [10763090.001]
  • [Cites] Am J Pathol. 2000 Oct;157(4):1311-20 [11021835.001]
  • [Cites] Am J Physiol Lung Cell Mol Physiol. 2001 Jun;280(6):L1189-95 [11350797.001]
  • [Cites] Am J Pathol. 1999 Mar;154(3):665-70 [10079243.001]
  • [Cites] Trends Neurosci. 1999 Apr;22(4):167-73 [10203854.001]
  • [Cites] J Biol Chem. 1999 May 21;274(21):15030-40 [10329706.001]
  • [Cites] J Appl Physiol (1985). 2005 Feb;98(2):732-8 [15475598.001]
  • [Cites] J Biol Chem. 2005 Sep 16;280(37):32548-54 [16033766.001]
  • [Cites] Eur Respir J. 1996 Oct;9(10):1989-94 [8902455.001]
  • [Cites] Ann Thorac Surg. 1997 Jun;63(6):1669-75 [9205166.001]
  • [Cites] Science. 1997 Sep 26;277(5334):2002-4 [9302297.001]
  • [Cites] Neurochem Int. 1997 Oct;31(4):477-510; discussion 517-6 [9307998.001]
  • [Cites] Circ Res. 1997 Oct;81(4):457-61 [9314825.001]
  • [Cites] Cancer Gene Ther. 1998 Jan-Feb;5(1):3-28 [9476963.001]
  • [Cites] J Clin Invest. 1998 Apr 15;101(8):1699-707 [9541501.001]
  • [Cites] Eur J Pharmacol. 2001 Oct 19;429(1-3):195-207 [11698041.001]
  • (PMID = 16601242.001).
  • [ISSN] 1044-1549
  • [Journal-full-title] American journal of respiratory cell and molecular biology
  • [ISO-abbreviation] Am. J. Respir. Cell Mol. Biol.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL07636; United States / NHLBI NIH HHS / HL / HL72903
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cytokines; 0 / DNA, Antisense; 0 / EGR1 protein, human; 0 / Early Growth Response Protein 1
  • [Other-IDs] NLM/ PMC2643284
  •  go-up   go-down






Advertisement