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1. Wang D, Chen S, Feng Y, Yang Q, Campbell BH, Tang X, Campbell WB: Reduced expression of 15-lipoxygenase 2 in human head and neck carcinomas. Tumour Biol; 2006;27(5):261-73
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • Nonsteroidal anti-inflammatory drugs (NSAIDs) have demonstrated cancer chemoprevention effects associated with their ability to modulate polyunsaturated fatty acid metabolism.
  • In the present study, we report a significant reduction of 15-lipoxygenase 2 (15-LOX-2) in seven carcinoma cell lines of the human head and neck when compared with normal primary cultured keratinocytes, and 18 primary head and neck squamous cell carcinomas (HNSCC) when compared with matched normal mucosa.
  • 15-LOX-2 is mainly expressed in the mature cells of the benign squamous epithelium, but not in the basal layer cells of benign epithelium, suggesting a role of 15-LOX-2 in cell differentiation.
  • When the effects of NSAIDs were examined on cell proliferation and regulation of 15-LOX-2 in the carcinoma cells, NS398 treatment resulted in significant growth inhibition associated with upregulation of 15-LOX-2 and its major metabolite 15-S-HETE.
  • Finally, restoration of 15-LOX-2 expression into these carcinoma cells significantly inhibited cell proliferation.
  • [MeSH-minor] Carcinoma, Squamous Cell. Cell Proliferation. Cells, Cultured. Gene Expression Regulation, Enzymologic. Humans. Keratinocytes / enzymology. Nitrobenzenes / pharmacology. Sulfonamides / pharmacology. Tumor Cells, Cultured

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  • [Copyright] Copyright (c) 2006 S. Karger AG, Basel.
  • (PMID = 16874012.001).
  • [ISSN] 1010-4283
  • [Journal-full-title] Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine
  • [ISO-abbreviation] Tumour Biol.
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-37981
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Nitrobenzenes; 0 / Sulfonamides; 123653-11-2 / N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; EC 1.13.11.33 / ALOX15B protein, human; EC 1.13.11.33 / Arachidonate 15-Lipoxygenase
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2. Kalthur G, Kumar P, Devi U, Ali S, Upadhya R, Pillai S, Rao A: Susceptibility of peripheral lymphocytes of brain tumour patients to in vitro radiation-induced DNA damage, a preliminary study. Clin Exp Med; 2008 Sep;8(3):147-50
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  • [Title] Susceptibility of peripheral lymphocytes of brain tumour patients to in vitro radiation-induced DNA damage, a preliminary study.
  • OBJECTIVE: The present investigation aimed to study the susceptibility of lymphocytes collected from brain tumour patients to radiation-induced DNA damage under in vitro conditions.
  • METHODS: The peripheral lymphocytes collected from brain tumour patients were exposed to 2-Gy gamma radiation.
  • RESULTS: Lymphocytes of patients with benign and malignant tumour had a significantly higher (p < 0.001) baseline DNA damage compared to lymphocytes from normal subjects.
  • A significant increase (p < 0.001) in DNA damage was observed immediately after irradiation of lymphocytes from healthy subjects and brain tumour patients.
  • DISCUSSION: In conclusion, the lymphocytes of brain tumour patients possess a higher level of basal DNA damage and exhibit a higher susceptibility to a clastogenic agent like radiation.

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  • [Cites] Mol Biotechnol. 2004 Mar;26(3):249-61 [15004294.001]
  • [Cites] Clin Cancer Res. 2005 Jul 1;11(13):4802-9 [16000577.001]
  • [Cites] Semin Radiat Oncol. 1994 Apr;4(2):68-80 [10717093.001]
  • [Cites] Carcinogenesis. 1999 May;20(5):811-5 [10334198.001]
  • [Cites] Clin Chim Acta. 2000 Dec;302(1-2):205-11 [11074076.001]
  • [Cites] Clin Chim Acta. 2000 Jun;296(1-2):203-12 [10807983.001]
  • [Cites] Mutat Res. 2007 Apr 1;617(1-2):104-10 [17303195.001]
  • [Cites] Acta Biochim Pol. 2003;50(1):181-90 [12673358.001]
  • [Cites] Cancer Res. 1996 Apr 1;56(7):1484-6 [8603389.001]
  • [Cites] Exp Cell Res. 1988 Mar;175(1):184-91 [3345800.001]
  • [Cites] Eur J Cancer. 1992;28A(11):1783-91 [1389511.001]
  • [Cites] Clin Chim Acta. 2003 Jul 1;333(1):97-9 [12809743.001]
  • [Cites] Recenti Prog Med. 1991 Jan;82(1):39-44 [2028076.001]
  • [Cites] Radiat Res. 1998 Nov;150(5 Suppl):S42-51 [9806608.001]
  • [Cites] Radiat Res. 1991 Mar;125(3):326-30 [2000457.001]
  • [Cites] Int J Cancer. 2001 Mar 20;95(2):86-91 [11241317.001]
  • [Cites] Int J Radiat Biol. 2002 Jul;78(7):611-6 [12079540.001]
  • [Cites] Clin Chim Acta. 2006 Jun;368(1-2):199-200 [16516879.001]
  • [Cites] Int J Oncol. 2000 Aug;17(2):399-404 [10891553.001]
  • [Cites] Radiother Oncol. 1994 Apr;31(1):1-13 [8041894.001]
  • (PMID = 18791687.001).
  • [ISSN] 1591-8890
  • [Journal-full-title] Clinical and experimental medicine
  • [ISO-abbreviation] Clin. Exp. Med.
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article
  • [Publication-country] Italy
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3. Delgrange E, Sassolas G, Perrin G, Jan M, Trouillas J: Clinical and histological correlations in prolactinomas, with special reference to bromocriptine resistance. Acta Neurochir (Wien); 2005 Jul;147(7):751-7; discussion 757-8
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  • BACKGROUND: Prolactinomas usually exhibit a benign course and can be safely and effectively managed by dopamine agonists (DA).
  • The aim of the present study was to determine whether histological features and markers of cell proliferation correlated to the clinical behaviour of prolactinomas and with DA resistance.
  • The prolactinomas were categorized on the basis of tumour size (48 macroadenomas), invasion of the cavernous sinus (n = 31), and resistance to bromocriptine (BRC) therapy (n = 14).
  • Seven additional parameters were studied, these being age, sex, basal prolactin (PRL) levels, the Ki-67 and PCNA labelling indices (LI), mitotic count, and cellular atypia.
  • Tumour size and invasion were related to cellular atypia and the Ki-67 LI.
  • Six out of the 12 invasive BRC-resistant macroprolactinomas, including the PRL secreting carcinoma, exhibited histological features of aggressiveness (a mitotic count >/=3 [i.e. in the fourth quartile] and/or a high Ki-67 LI and cellular atypia).
  • These findings justify the long-term follow up of these tumours, and the use of surgery and/or radiotherapy if there is concern about the control of tumour growth.
  • [MeSH-minor] Adult. Aged. Drug Resistance. Female. Humans. Hypophysectomy. Ki-67 Antigen / analysis. Magnetic Resonance Imaging. Male. Middle Aged. Mitotic Index. Neoplasm Invasiveness / pathology. Neoplasm Staging. Pituitary Gland / pathology. Retrospective Studies. Sex Factors

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  • (PMID = 15971099.001).
  • [ISSN] 0942-0940
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Dopamine Agonists; 0 / Ki-67 Antigen; 3A64E3G5ZO / Bromocriptine
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4. Harwood CA, Proby CM: Human papillomaviruses and non-melanoma skin cancer. Curr Opin Infect Dis; 2002 Apr;15(2):101-14
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  • Epidemiological and experimental studies have overwhelmingly confirmed human papillomaviruses as important causal agents in anogenital carcinogenesis.
  • Epidemiological human papillomavirus DNA detection studies have shown associations with non-melanoma skin cancer, but have also emphasized the ubiquity of epidermodysplasia verruciformis human papillomavirus types in normal skin, hair follicles and benign hyperproliferative disorders, as have seroepidemiological approaches.
  • Functional investigations have demonstrated mechanistically relevant interactions between the virus and ultraviolet radiation, host cytokines and cellular proteins including p53 and the pro-apoptotic protein Bak.
  • [MeSH-minor] Carcinoma, Basal Cell / etiology. Carcinoma, Basal Cell / pathology. Carcinoma, Basal Cell / virology. Carcinoma, Squamous Cell / etiology. Carcinoma, Squamous Cell / pathology. Carcinoma, Squamous Cell / virology. Epidermodysplasia Verruciformis / etiology. Epidermodysplasia Verruciformis / pathology. Epidermodysplasia Verruciformis / virology. Humans. Papillomavirus Infections / pathology

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  • (PMID = 11964909.001).
  • [ISSN] 0951-7375
  • [Journal-full-title] Current opinion in infectious diseases
  • [ISO-abbreviation] Curr. Opin. Infect. Dis.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Number-of-references] 113
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5. Hagemann T, Robinson SC, Schulz M, Trümper L, Balkwill FR, Binder C: Enhanced invasiveness of breast cancer cell lines upon co-cultivation with macrophages is due to TNF-alpha dependent up-regulation of matrix metalloproteases. Carcinogenesis; 2004 Aug;25(8):1543-9
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  • [Title] Enhanced invasiveness of breast cancer cell lines upon co-cultivation with macrophages is due to TNF-alpha dependent up-regulation of matrix metalloproteases.
  • Apart from the neoplastic cells, malignant tumours consist of the extracellular matrix (ECM) and normal cells, in particular tumour-associated macrophages (TAM).
  • To understand the mechanisms by which TAM can influence tumour cell invasion we co-cultured the human breast cancer cell lines MCF-7, SK-BR-3 and the benign mammary epithelial cell line hTERT-HME1 with macrophages.
  • Co-incubation enhanced invasiveness of the tumour cells, while hTERT-HME1 remained non-invasive.
  • Addition of the broad-spectrum matrix metalloprotease (MMP)-inhibitor FN 439, neutralizing MMP-9 or tumour necrosis factor-alpha (TNF-alpha) antibodies reduced invasiveness to basal levels.
  • As shown by zymography, all cell lines produced low amounts of MMP-2, -3, -7 and -9 under control conditions.
  • Basal MMP production by macrophages was significantly higher.
  • In the co-cultures, mRNAs for MMPs and TNF-alpha were significantly up-regulated in macrophages, while the mRNA concentrations in the tumour cells remained unchanged.
  • In summary, we have found that co-cultivation of tumour cells with macrophages leads to enhanced invasiveness of the malignant cells due to TNF-alpha dependent MMP induction in the macrophages.
  • [MeSH-major] Breast Neoplasms / pathology. Macrophages / metabolism. Matrix Metalloproteinases / biosynthesis. Tumor Necrosis Factor-alpha / biosynthesis. Up-Regulation
  • [MeSH-minor] Cell Line. Cell Line, Tumor. Coculture Techniques. Collagen / pharmacology. Densitometry. Down-Regulation. Drug Combinations. Enzyme-Linked Immunosorbent Assay. Humans. Laminin / pharmacology. Lipopolysaccharides / metabolism. Matrix Metalloproteinase 2 / metabolism. Matrix Metalloproteinase 3 / biosynthesis. Matrix Metalloproteinase 7 / biosynthesis. Matrix Metalloproteinase 9 / metabolism. Neoplasm Invasiveness. Proteoglycans / pharmacology. RNA / metabolism. RNA, Messenger / metabolism. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 15044327.001).
  • [ISSN] 0143-3334
  • [Journal-full-title] Carcinogenesis
  • [ISO-abbreviation] Carcinogenesis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Drug Combinations; 0 / Laminin; 0 / Lipopolysaccharides; 0 / Proteoglycans; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; 119978-18-6 / matrigel; 63231-63-0 / RNA; 9007-34-5 / Collagen; EC 3.4.24.- / Matrix Metalloproteinases; EC 3.4.24.17 / Matrix Metalloproteinase 3; EC 3.4.24.23 / Matrix Metalloproteinase 7; EC 3.4.24.24 / Matrix Metalloproteinase 2; EC 3.4.24.35 / Matrix Metalloproteinase 9
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6. Karen JK, Gareau DS, Dusza SW, Tudisco M, Rajadhyaksha M, Nehal KS: Detection of basal cell carcinomas in Mohs excisions with fluorescence confocal mosaicing microscopy. Br J Dermatol; 2009 Jun;160(6):1242-50
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  • [Title] Detection of basal cell carcinomas in Mohs excisions with fluorescence confocal mosaicing microscopy.
  • Contrast agents such as acridine orange in fluorescence and acetic acid in reflectance have been used in ex vivo imaging to enhance nuclear contrast.
  • OBJECTIVES: To evaluate the sensitivity and specificity of ex vivo real-time imaging with fluorescence confocal mosaicing microscopy, using acridine orange, for the detection of residual basal cell carcinoma (BCC) in Mohs fresh tissue excisions.
  • Very good correlation was observed between confocal mosaics and matched Mohs frozen sections for benign and malignant skin structures, overall tumour burden and location, and identification of all major histological subtypes of BCC.
  • [MeSH-major] Carcinoma, Basal Cell / pathology. Mohs Surgery / methods. Skin Neoplasms / pathology

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  • [Cites] Surgery. 2000 Dec;128(6):1088-1100; discussion 1100-1 [11114647.001]
  • [Cites] J Microsc. 2009 Jan;233(1):149-59 [19196421.001]
  • [Cites] Arch Dermatol. 2004 Jun;140(6):736-42 [15210467.001]
  • [Cites] Arch Otolaryngol Head Neck Surg. 2004 Aug;130(8):923-8 [15313861.001]
  • [Cites] J Cell Biol. 1985 Apr;100(4):1309-23 [3920227.001]
  • [Cites] Dermatol Surg. 2004 Dec;30(12 Pt 1):1470-8 [15606734.001]
  • [Cites] J Biomed Opt. 2005 May-Jun;10(3):034009 [16229653.001]
  • [Cites] Br J Dermatol. 2006 Feb;154(2):305-9 [16433801.001]
  • [Cites] Opt Lett. 2006 Apr 1;31(7):942-4 [16599219.001]
  • [Cites] J Am Acad Dermatol. 2006 Sep;55(3):408-12 [16908344.001]
  • [Cites] Opt Lett. 2006 Sep 15;31(18):2756-8 [16936882.001]
  • [Cites] J Biomed Opt. 2007 Jan-Feb;12(1):014005 [17343480.001]
  • [Cites] Appl Opt. 2007 Apr 1;46(10):1843-51 [17356629.001]
  • [Cites] J Biomed Opt. 2007 May-Jun;12(3):034004 [17614712.001]
  • [Cites] J Biomed Opt. 2007 May-Jun;12(3):034027 [17614735.001]
  • [Cites] Lasers Surg Med. 2007 Oct;39(9):696-705 [17960751.001]
  • [Cites] J Biomed Opt. 2007 Sep-Oct;12(5):051901 [17994884.001]
  • [Cites] J Invest Dermatol. 2008 May;128(5):1248-55 [17989735.001]
  • [Cites] J Biomed Opt. 2008 Mar-Apr;13(2):024013 [18465976.001]
  • [Cites] Br J Dermatol. 2008 Jul;159(1):152-61 [18460029.001]
  • [Cites] J Biomed Opt. 2008 Jul-Aug;13(4):044016 [19021344.001]
  • [Cites] J Biomed Opt. 2008 Sep-Oct;13(5):054001 [19021381.001]
  • [Cites] J Invest Dermatol. 2001 Nov;117(5):1137-43 [11710924.001]
  • (PMID = 19416248.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / P30 CA008748; United States / NIBIB NIH HHS / EB / R01 EB002715; United States / NIBIB NIH HHS / EB / R01 EB002715-05; United States / NIBIB NIH HHS / EB / R01EB002715
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Other-IDs] NLM/ NIHMS95359; NLM/ PMC2693082
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