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56. Ko CW, Cuthbert RJ, Orsi NM, Brooke DA, Perry SL, Markham AF, Coletta PL, Hull MA: Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice. J Pathol; 2008 Apr;214(5):603-9
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  • [Title] Lack of interleukin-4 receptor alpha chain-dependent signalling promotes azoxymethane-induced colorectal aberrant crypt focus formation in Balb/c mice.
  • Interleukin (IL)-4 receptor (IL-4R) alpha chain-dependent signalling by IL-4 and IL-13 promotes tumour growth and metastasis in mouse models of colorectal cancer.
  • However, the role of IL-4R alpha-dependent signalling during the early, pre-malignant stages of colorectal carcinogenesis has not been investigated.
  • Therefore, we investigated the effect of deletion of the IL-4R alpha gene on azoxymethane-induced colorectal aberrant crypt focus (ACF) multiplicity and size in Balb/c mice.
  • IL-4R alpha(-/-) mice developed significantly more ACFs [median 8, inter-quartile range (IQR) 4-11.5; n = 9] than wild-type (WT) animals (median 4, IQR 1-6; n = 9; p = 0.04, Mann-Whitney U-test).
  • There were significantly higher levels of IL-4 in serum from azoxymethane- and sham-treated IL-4R alpha(-/-) mice than WT animals, but no difference in serum IL-13 levels.
  • We found that mucosal TGFbeta mRNA levels and intestinal epithelial cell TGFbeta immunoreactivity were significantly higher in IL-4R alpha(-/-) mice than in WT animals.
  • In summary, IL-4R alpha-dependent signalling has a protective, anti-neoplastic role during the post-initiation phase of azoxymethane-induced colorectal carcinogenesis in Balb/c mice.
  • Our data should prompt thorough investigation of the role of IL-4R alpha-dependent signalling during human colorectal carcinogenesis, particularly as antagonism of IL-4R signalling represents a therapeutic strategy for asthma and other allergic diseases.
  • [MeSH-major] Colorectal Neoplasms / immunology. Precancerous Conditions / immunology. Receptors, Cell Surface / immunology
  • [MeSH-minor] Animals. Azoxymethane. Carcinogens. Cell Transformation, Neoplastic / immunology. Cell Transformation, Neoplastic / pathology. Disease Models, Animal. Female. Interleukin-13 / blood. Interleukin-4 / blood. Intestinal Mucosa / immunology. Intestinal Mucosa / pathology. Mice. Mice, Inbred BALB C. Mice, Knockout. Signal Transduction / immunology. Transforming Growth Factor beta1 / metabolism. Tumor Necrosis Factor-alpha / blood

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  • [Copyright] Copyright (c) 2008 Pathological Society of Great Britain and Ireland
  • (PMID = 18220315.001).
  • [ISSN] 0022-3417
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G116/146; United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carcinogens; 0 / Il4ra protein, mouse; 0 / Interleukin-13; 0 / Receptors, Cell Surface; 0 / Transforming Growth Factor beta1; 0 / Tumor Necrosis Factor-alpha; 207137-56-2 / Interleukin-4; MO0N1J0SEN / Azoxymethane
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57. Iida H, Honda M, Kawai HF, Yamashita T, Shirota Y, Wang BC, Miao H, Kaneko S: Ephrin-A1 expression contributes to the malignant characteristics of {alpha}-fetoprotein producing hepatocellular carcinoma. Gut; 2005 Jun;54(6):843-51
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  • [Title] Ephrin-A1 expression contributes to the malignant characteristics of {alpha}-fetoprotein producing hepatocellular carcinoma.
  • BACKGROUND AND AIMS: alpha-Fetoprotein (AFP), a tumour marker for hepatocellular carcinoma (HCC), is associated with poor prognosis.
  • Using cDNA microarray analysis, we previously found that ephrin-A1, an angiogenic factor, is the most differentially overexpressed gene in AFP producing hepatoma cell lines.
  • METHODS: We examined ephrin-A1 expression and its effect on cell proliferation and gene expression in five AFP producing hepatoma cell lines, three AFP negative hepatoma cell lines, and 20 human HCC specimens.
  • Thus ephrin-A1 affects hepatoma cell growth. cDNA microarray analysis showed that ephrin-A1 induced expression of genes related to the cell cycle (p21), angiogenesis (angiopoietin 1 and thrombospondin 1), and cell-cell interactions (Rho, integrin, and matrix metalloproteinases) in cultured hepatoma cells.
  • CONCLUSION: These findings suggest that the poor prognosis of patients with AFP producing HCC is partially caused by ephrin-A1 expression, which induces expression of genes related to tumour cell growth, angiogenesis, invasion, and metastasis.
  • [MeSH-major] Carcinoma, Hepatocellular / metabolism. Ephrin-A1 / metabolism. Liver Neoplasms / metabolism. alpha-Fetoproteins / metabolism
  • [MeSH-minor] Cell Cycle Proteins / metabolism. Cell Line, Tumor. Cell Proliferation. Cyclin-Dependent Kinase Inhibitor p21. Cyclin-Dependent Kinases / metabolism. DNA, Complementary / analysis. Dose-Response Relationship, Drug. Gene Expression. Humans. Immunohistochemistry / methods. Oligonucleotide Array Sequence Analysis. Oligonucleotides, Antisense / pharmacology. Prognosis. RNA, Messenger / metabolism

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  • (PMID = 15888795.001).
  • [ISSN] 0017-5749
  • [Journal-full-title] Gut
  • [ISO-abbreviation] Gut
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / CDKN1A protein, human; 0 / Cell Cycle Proteins; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / DNA, Complementary; 0 / Ephrin-A1; 0 / Oligonucleotides, Antisense; 0 / RNA, Messenger; 0 / alpha-Fetoproteins; EC 2.7.11.22 / Cyclin-Dependent Kinases
  • [Other-IDs] NLM/ PMC1774523
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58. Koehn H, Magan N, Isaacs RJ, Stowell KM: Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin. Anticancer Drugs; 2007 Apr;18(4):419-25
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  • [Title] Differential regulation of DNA repair protein Rad51 in human tumour cell lines exposed to doxorubicin.
  • Radiotherapy and chemotherapy often induce DNA double-strand breaks in both normal and malignant cells.
  • The proteins involved in the repair of such lesions are central to cancer prognosis and treatment, as they can be overexpressed in many cancers, accelerating malignant transformation and increasing repair capacity, potentially leading to cellular resistance.
  • If malignant cells can be selectively targeted repair proteins could also be candidates for targeted therapy.
  • In this study, two keyplayers in eukaryotic DNA double-strand break repair, Rad51 and DNA-dependent protein kinase catalytic subunit, were analysed in noncancerous human breast cells (MCF12A) and the breast cancer cell lines (MDA MB 231 and MCF7) in response to treatment with doxorubicin.
  • A cell cycle-independent increase in Rad51 protein levels (a recombinase involved in homologous recombination repair) was observed 24 and 48 h after treatment in MDA MB 231 and MCF12A when exposed to low levels of doxorubicin, whereas MCF7 cells displayed a continuous decrease in Rad51 protein with increasing drug concentration.
  • Topoisomerase II-alpha protein, the primary target of doxorubicin, was upregulated at low concentrations of doxorubicin in all cell lines tested.
  • Here we show that Rad51 protein levels can be differentially regulated in normal and malignant breast cell lines in response to doxorubicin, independent of cell cycle state.
  • [MeSH-minor] Blotting, Western. Breast Neoplasms / drug therapy. Breast Neoplasms / pathology. Cell Cycle / drug effects. Cell Line, Tumor. Cell Survival / drug effects. DNA Damage. Dose-Response Relationship, Drug. Female. Flow Cytometry. Genes, p53 / genetics. Humans. Receptors, Estrogen / genetics. Receptors, Estrogen / physiology. Transforming Growth Factor beta / genetics. Transforming Growth Factor beta / physiology

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  • (PMID = 17351394.001).
  • [ISSN] 0959-4973
  • [Journal-full-title] Anti-cancer drugs
  • [ISO-abbreviation] Anticancer Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Receptors, Estrogen; 0 / Transforming Growth Factor beta; 80168379AG / Doxorubicin; EC 2.7.7.- / Rad51 Recombinase
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59. Huang L, Verstrepen L, Heyninck K, Wullaert A, Revets H, De Baetselier P, Beyaert R: ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells. Oncogene; 2008 Oct 16;27(47):6131-40
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  • [Title] ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells.
  • The epidermal growth factor receptor (EGFR) is frequently overexpressed in various tumours of epidermal origin and is held responsible for tumourigenicity and tumour persistence.
  • Increased nuclear factor (NF)-kappaB activity has been suggested to be involved in the malignant behaviour of EGFR-overexpressing cells.
  • Moreover, EGF-induced NF-kappaB activation could be inhibited by overexpression of ABINs, which were previously identified as intracellular inhibitors of tumour necrosis factor, interleukin-1 and lipopolysaccharide-induced NF-kappaB activation.
  • Adenoviral gene transfer of ABINs reduced constitutive NF-kappaB activity as well as the proliferation of EGFR-overexpressing A431 and DU145 human carcinoma cells.
  • Altogether, these results demonstrate an important role for an ABIN-sensitive non-classical NF-kappaB signalling pathway in the proliferation of EGFR-overexpressing tumour cells, and indicate a potential use for ABIN gene therapy in the treatment of cancer.
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation. Cyclin D1 / genetics. Epidermal Growth Factor / pharmacology. Genetic Therapy. Humans. I-kappa B Proteins / metabolism. NF-kappa B p52 Subunit / metabolism. Phosphorylation. Protein Structure, Tertiary. RNA Interference. Signal Transduction

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  • (PMID = 18622428.001).
  • [ISSN] 1476-5594
  • [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 / Adaptor Proteins, Signal Transducing; 0 / DNA-Binding Proteins; 0 / I-kappa B Proteins; 0 / NF-kappa B; 0 / NF-kappa B p52 Subunit; 0 / TNIP1 protein, human; 0 / TNIP2 protein, human; 136601-57-5 / Cyclin D1; 139874-52-5 / NF-kappaB inhibitor alpha; 62229-50-9 / Epidermal Growth Factor; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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60. Monteagudo C, Martin JM, Jorda E, Llombart-Bosch A: CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors. J Clin Pathol; 2007 Jun;60(6):596-9
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  • [Title] CXCR3 chemokine receptor immunoreactivity in primary cutaneous malignant melanoma: correlation with clinicopathological prognostic factors.
  • BACKGROUND: A role for CXCR3, the receptor for chemokines Mig, IP-10 and interferon-inducible T cell alpha-chemoattractant, in tumour cell migration during melanoma progression has been proposed.
  • AIMS: To analyse CXCR3 expression in primary cutaneous malignant melanomas and its comparison with clinicopathological and prognostic factors.
  • Melanomas were categorised by age, sex, primary site, tumour thickness, growth phase, ulceration, lymphocytic infiltration, recurrence, lymph node and distant metastasis, and survival.
  • In univariate analysis, a significant association of CXCR3-positive tumour cell immunostaining with tumour thickness >1 mm (p = 0.003), absence of lymphocytic infiltration (p = 0.04) and the presence of distant metastasis (p = 0.048) was found.
  • Multivariate analysis found tumour thickness as the only independent factor with considerable association with distant metastases.
  • CONCLUSIONS: Our findings of a positive correlation of CXCR3 tumour cell immunoreactivity in human primary cutaneous melanoma with tumour thickness >1 mm and absence of intratumoral lymphocytic infiltration support the biological implication of CXCR3 in the tumour progression of cutaneous malignant melanoma.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Melanoma / metabolism. Receptors, Chemokine / metabolism. Skin Neoplasms / metabolism

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  • (PMID = 16522748.001).
  • [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 / CXCR3 protein, human; 0 / Neoplasm Proteins; 0 / Receptors, CXCR3; 0 / Receptors, Chemokine
  • [Other-IDs] NLM/ PMC1955073
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66. Katori H, Nozawa A, Tsukuda M: Markers of malignant transformation of sinonasal inverted papilloma. Eur J Surg Oncol; 2005 Oct;31(8):905-11
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  • [Title] Markers of malignant transformation of sinonasal inverted papilloma.
  • AIM: To measure HPV status, epidermal growth factor receptor (EGFR) and transforming growth factor-alpha (TGF-alpha) expression and Ki-67 index in exophytic papilloma (EP), inverted papilloma (IP) with dysplasia, IP with carcinoma and invasive squamous cell carcinoma (SCC).
  • The nasal tissues were stained with monoclonal antibodies to EGFR, TGF-alpha and Ki-67.
  • RESULTS: Significant increase of EGFR and TGF-alpha was observed in IP with severe dysplasia, IP with carcinoma and invasive SCC compared to IP with mild dysplasia and control nasal mucosa.
  • Among IP, HPV 6/11-positive was present in 42% tumour and HPV 16/18-positive was present in 31% of tumours.
  • CONCLUSION: Pre-cancerous lesions of IP exhibited elevated levels of EGFR and TGF-alpha and these expression may be associated with early events in IP carcinogenesis.
  • HPV infection may be an early event in a multistep process of malignant formation of IP.
  • [MeSH-major] Biomarkers, Tumor / analysis. Cell Transformation, Neoplastic / pathology. Nose Neoplasms / pathology. Papilloma, Inverted / pathology. Paranasal Sinus Neoplasms / pathology
  • [MeSH-minor] Antibodies, Monoclonal. Carcinoma / pathology. Carcinoma, Squamous Cell / pathology. Female. Humans. In Situ Hybridization. Ki-67 Antigen / analysis. Male. Middle Aged. Nasal Mucosa / pathology. Neoplasm Invasiveness. Papilloma / pathology. Papillomaviridae / classification. Papillomaviridae / isolation & purification. Precancerous Conditions / pathology. Receptor, Epidermal Growth Factor / analysis. Transforming Growth Factor alpha / analysis

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  • (PMID = 16005600.001).
  • [ISSN] 0748-7983
  • [Journal-full-title] European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology
  • [ISO-abbreviation] Eur J Surg Oncol
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal; 0 / Biomarkers, Tumor; 0 / Ki-67 Antigen; 0 / Transforming Growth Factor alpha; EC 2.7.10.1 / Receptor, Epidermal Growth Factor
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67. Przybyło M, Lityńska A, Pocheć E: Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation. Biochimie; 2005 Feb;87(2):133-42
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  • [Title] Different adhesion and migration properties of human HCV29 non-malignant urothelial and T24 bladder cancer cells: role of glycosylation.
  • In tumour cells, alterations in cellular glycosylation may play a key role in their metastatic behaviour.
  • This study used cell lines having very different behaviour in vivo: HCV29 non-malignant transitional epithelium and T24 bladder transitional cell carcinoma.
  • The functional role of carbohydrates was studied by treating these cells with swainsonine, an inhibitor of Golgi alpha-mannosidase II, and in vitro adhesion and migration assays.
  • Swainsonine treatment reduced the rate of T24 cell migration by 20%.
  • We concluded that beta1-6 branched tri- and tetraantennary complex-type glycans have an important function in adhesion and migration in the studied cell lines.
  • [MeSH-major] Cell Movement. Epithelial Cells / metabolism. Polysaccharides / biosynthesis. Ureter / metabolism. Urinary Bladder Neoplasms / metabolism
  • [MeSH-minor] Cell Adhesion / drug effects. Cell Line, Tumor. Enzyme Inhibitors / pharmacology. Female. Glycosylation / drug effects. Humans. Male. Species Specificity. Swainsonine / pharmacology

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  • (PMID = 15760705.001).
  • [ISSN] 0300-9084
  • [Journal-full-title] Biochimie
  • [ISO-abbreviation] Biochimie
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Polysaccharides; RSY4RK37KQ / Swainsonine
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68. Tajima N, Schönherr K, Niedling S, Kaatz M, Kanno H, Schönherr R, Heinemann SH: Ca2+-activated K+ channels in human melanoma cells are up-regulated by hypoxia involving hypoxia-inducible factor-1alpha and the von Hippel-Lindau protein. J Physiol; 2006 Mar 1;571(Pt 2):349-59
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  • Under chronic hypoxia, tumour cells undergo adaptive changes involving hypoxia-inducible factors (HIFs).
  • This increase involves the HIF system as confirmed by overexpression of HIF-1alpha or the von Hippel-Lindau tumour suppressor gene.
  • Hypoxia increased cell proliferation, but the K(Ca) channel blockers apamin and charybdotoxin slowed down cell growth, particularly under hypoxic conditions.
  • Similar results were obtained for the cell line IGR39 and for acutely isolated cells from a biopsy of a melanoma metastasis.
  • Thus, up-regulation of K(Ca) channels may be a novel mechanism by which HIFs can contribute to the malignant phenotype of human tumour cells.
  • [MeSH-major] Hypoxia-Inducible Factor 1, alpha Subunit / physiology. Intermediate-Conductance Calcium-Activated Potassium Channels / metabolism. Melanoma / metabolism. Potassium Channels, Calcium-Activated / metabolism. Small-Conductance Calcium-Activated Potassium Channels / metabolism. Von Hippel-Lindau Tumor Suppressor Protein / physiology
  • [MeSH-minor] Apamin / pharmacology. Cell Hypoxia. Cell Line, Tumor. Cell Proliferation / drug effects. Humans. Transfection. Tumor Cells, Cultured. Up-Regulation

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  • (PMID = 16396931.001).
  • [ISSN] 0022-3751
  • [Journal-full-title] The Journal of physiology
  • [ISO-abbreviation] J. Physiol. (Lond.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 0 / Intermediate-Conductance Calcium-Activated Potassium Channels; 0 / Potassium Channels, Calcium-Activated; 0 / Small-Conductance Calcium-Activated Potassium Channels; 24345-16-2 / Apamin; EC 6.3.2.19 / Von Hippel-Lindau Tumor Suppressor Protein
  • [Other-IDs] NLM/ PMC1796787
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69. Woodward JK, Rennie IG, Elshaw SR, Burn JL, Sisley K: Invasive and noninvasive uveal melanomas have different adhesive properties. Eye (Lond); 2005 Mar;19(3):342-8
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  • METHODS: Cells from an invasive and noninvasive uveal melanoma cell line and hepatic and dermal microvascular endothelial cells were assessed by flow cytometry for adhesion molecule expression.
  • Tumour cell adhesion to ECM substrates (collagens I and IV, fibronectin, laminin, and vitronectin) and endothelial cells was also investigated using a commercially available assay or a fluorescence-based in vitro assay, respectively.
  • The significance of results comparing cell lines was determined using a Student's t-test, whereby P-values of less than 0.05 were taken as significant.
  • The invasive cell line also expressed higher levels of other integrins than the noninvasive line.
  • CONCLUSIONS: Successful attachment to and migration through the ECM, basement membrane, and endothelium are vital processes involved in malignant progression.
  • [MeSH-minor] Cell Adhesion. Cell Adhesion Molecules / metabolism. Endothelial Cells / pathology. Endothelium, Vascular / pathology. Extracellular Matrix / pathology. Extracellular Matrix Proteins / metabolism. Humans. Integrin alpha Chains / metabolism. Neoplasm Invasiveness. Neoplasm Proteins / metabolism. Tumor Cells, Cultured

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  • (PMID = 15258612.001).
  • [ISSN] 0950-222X
  • [Journal-full-title] Eye (London, England)
  • [ISO-abbreviation] Eye (Lond)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell Adhesion Molecules; 0 / Extracellular Matrix Proteins; 0 / Integrin alpha Chains; 0 / Neoplasm Proteins
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70. Oremek GM, Sauer-Eppel H, Bruzdziak TH: Value of tumour and inflammatory markers in lung cancer. Anticancer Res; 2007 Jul-Aug;27(4A):1911-5
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  • [Title] Value of tumour and inflammatory markers in lung cancer.
  • The aim of this study was to evaluate the individual diagnostic utility of tumour and inflammatory markers in patients with different pulmonary diseases.
  • The usefulness of neuron-specific enolase (NSE), carcino-embryonic antigen (CEA), serum pro-gastrin releasing peptide (ProGRP) and CYFRA 21-1, as tumour markers, and C-reactive protein (CRP) and tumour necrosis factor-alpha (TNFalpha) as inflammatory markers for diagnosis, treatment and monitoring of patients with different pulmonary afflictions was investigated.
  • Moreover, serum marker levels were analyzed in 139 patients with different pulmonary malignancies: 29 patients with adenocarcinoma, 30 patients with squamous cell carcinoma, 80 patients with small cell lung cancer (SCLC).
  • All tumour markers showed significantly elevated values in malignant diseases.
  • The acute phase response had a wide range in patients with malignant tumours.
  • In conclusion, when serum tumour markers are abnormally elevated in patients with lung cancer, CEA, CYFRA 21-1, NSE and ProGRP are useful clinical markers, good indicators of disease extent and may have important prognostic value.
  • [MeSH-major] Biomarkers, Tumor / blood. Inflammation / blood. Lung Neoplasms / diagnosis
  • [MeSH-minor] Antigens, Neoplasm / blood. Area Under Curve. C-Reactive Protein / analysis. Carcinoembryonic Antigen / blood. Carcinoma, Non-Small-Cell Lung / blood. Carcinoma, Non-Small-Cell Lung / diagnosis. Carcinoma, Small Cell / blood. Carcinoma, Small Cell / diagnosis. Carcinoma, Squamous Cell / blood. Carcinoma, Squamous Cell / diagnosis. Humans. Immunoassay. Keratin-19. Keratins / blood. Lung Diseases / blood. Lung Diseases / diagnosis. Peptide Fragments / blood. Peptides / blood. Phosphopyruvate Hydratase / blood. ROC Curve. Recombinant Proteins / blood. Sensitivity and Specificity. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 17649794.001).
  • [ISSN] 0250-7005
  • [Journal-full-title] Anticancer research
  • [ISO-abbreviation] Anticancer Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Greece
  • [Chemical-registry-number] 0 / Antigens, Neoplasm; 0 / Biomarkers, Tumor; 0 / Carcinoembryonic Antigen; 0 / Keratin-19; 0 / Peptide Fragments; 0 / Peptides; 0 / Recombinant Proteins; 0 / Tumor Necrosis Factor-alpha; 0 / antigen CYFRA21.1; 0 / pro-gastrin-releasing peptide (31-98); 68238-35-7 / Keratins; 9007-41-4 / C-Reactive Protein; EC 4.2.1.11 / Phosphopyruvate Hydratase
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71. Lansigan F, Foss FM: Current and emerging treatment strategies for cutaneous T-cell lymphoma. Drugs; 2010 Feb 12;70(3):273-86
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  • [Title] Current and emerging treatment strategies for cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCLs) are a rare group of mature T-cell lymphomas presenting primarily in the skin.
  • Other than an allogeneic stem cell transplant, there are no curative therapies for this disease.
  • These therapies include biological immune enhancers such as interferon alpha and extracorporeal photopheresis that exert their effect by stimulating an immune response to the tumour cells.
  • The fusion toxin denileukin diftitox targets the interleukin-2 receptor expressed on malignant T cells.
  • Forodesine is a novel inhibitor of purine nucleoside phosphorylase and leads to apoptosis of malignant T cells.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Combined Modality Therapy / methods. Lymphoma, T-Cell, Cutaneous / drug therapy. Lymphoma, T-Cell, Cutaneous / therapy. Skin Neoplasms / drug therapy. Skin Neoplasms / therapy
  • [MeSH-minor] Antibodies, Monoclonal / therapeutic use. Clinical Protocols. Drug Administration Routes. Hematopoietic Stem Cell Transplantation / methods. Humans

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  • (PMID = 20166766.001).
  • [ISSN] 1179-1950
  • [Journal-full-title] Drugs
  • [ISO-abbreviation] Drugs
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 0 / Antibodies, Monoclonal
  • [Number-of-references] 90
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72. Lau YS, Sabokbar A, Giele H, Cerundolo V, Hofstetter W, Athanasou NA: Malignant melanoma and bone resorption. Br J Cancer; 2006 May 22;94(10):1496-503
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  • [Title] Malignant melanoma and bone resorption.
  • The cellular and humoral mechanisms accounting for osteolysis in skeletal metastases of malignant melanoma are uncertain.
  • We isolated tumour-associated macrophages (TAMs) from metastatic (lymph node/skin) melanomas and cultured them in the presence and absence of osteoclastogenic cytokines and growth factors.
  • The effect of tumour-derived fibroblasts and melanoma cells on osteoclast formation and resorption was also analysed.
  • Tumour-associated macrophage-osteoclast differentiation also occurred via a RANKL-independent pathway when TAMs were cultured with tumour necrosis factor-alpha and interleukin (IL)-1alpha.
  • Our findings indicate that TAMs in metastatic melanomas can differentiate into osteoclasts and that melanoma fibroblasts and melanoma tumour cells can induce osteoclast formation by RANKL-dependent and RANKL-independent mechanisms, respectively.
  • [MeSH-minor] Aged. Aged, 80 and over. Antineoplastic Agents / pharmacology. Carrier Proteins / metabolism. Cell Differentiation. Cells, Cultured. Culture Media, Conditioned / pharmacology. Female. Fibroblasts. Glycoproteins / pharmacology. Humans. Interleukin-1 / pharmacology. Lymphatic Metastasis. Male. Membrane Glycoproteins / metabolism. Middle Aged. Osteolysis / pathology. Osteoprotegerin. RANK Ligand. Receptor Activator of Nuclear Factor-kappa B. Receptors, Cytoplasmic and Nuclear. Receptors, Tumor Necrosis Factor. Reverse Transcriptase Polymerase Chain Reaction. Tumor Necrosis Factor-alpha / pharmacology

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  • (PMID = 16641914.001).
  • [ISSN] 0007-0920
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Carrier Proteins; 0 / Culture Media, Conditioned; 0 / Glycoproteins; 0 / Interleukin-1; 0 / Membrane Glycoproteins; 0 / Osteoprotegerin; 0 / RANK Ligand; 0 / Receptor Activator of Nuclear Factor-kappa B; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Receptors, Tumor Necrosis Factor; 0 / TNFRSF11A protein, human; 0 / TNFRSF11B protein, human; 0 / TNFSF11 protein, human; 0 / Tumor Necrosis Factor-alpha
  • [Other-IDs] NLM/ PMC2361270
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73. Kang KB, Zhu C, Yong SK, Gao Q, Wong MC: Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy. Mol Cancer; 2009;8:66
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  • [Title] Enhanced sensitivity of celecoxib in human glioblastoma cells: Induction of DNA damage leading to p53-dependent G1 cell cycle arrest and autophagy.
  • BACKGROUND: Selective cyclooxygenase (COX)-2 inhibitors elicit anti-proliferative responses in various tumours, however the underlying anti-tumour mechanisms are unclear.
  • Mutational inactivation of the tumour suppressor p53 gene is frequent in malignant gliomas.
  • The role of p53 mutation in the anti-tumour responses of the selective COX-2 inhibitor celecoxib in human glioblastoma cells is unknown.
  • Inhibition of p53 was achieved in U87MG cells transfected with E6 oncoprotein (U87MG-E6) and treated with pifithrin-alpha, a reversible inhibitor of p53 (U87MG-PFT).
  • We investigated whether the anti-glioblastoma responses of celecoxib were p53-dependent, and whether celecoxib induced DNA damage leading to p53-dependent G1 cell cycle arrest, followed by autophagy or apoptosis.
  • RESULTS: Our findings demonstrated that celecoxib concentration-dependently reduced glioblastoma cell viability, following 24 and 72 hours of treatment.
  • Celecoxib induced G1-phase cell cycle arrest, accompanied with p21 activation in U87MG cells.
  • Cell cycle progression of U87MG-E6 and U87MG-PFT cells was not affected by celecoxib.
  • In parallel, celecoxib induced G1 cell cycle arrest in LN229 cells, but not in U373MG cells.
  • Celecoxib inhibits glioblastoma cell viability by induction of DNA damage, leading to p53-dependent G1 cell cycle arrest and p53-dependent autophagy, but not apoptosis.
  • [MeSH-major] Autophagy / drug effects. DNA Damage. G1 Phase / drug effects. Pyrazoles / pharmacology. Sulfonamides / pharmacology. Tumor Suppressor Protein p53 / metabolism
  • [MeSH-minor] Analysis of Variance. Benzothiazoles / pharmacology. Blotting, Western. Celecoxib. Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Comet Assay. Cyclin-Dependent Kinase Inhibitor p21 / genetics. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Cyclooxygenase Inhibitors / pharmacology. Dose-Response Relationship, Drug. G0 Phase / drug effects. Humans. Immunohistochemistry. Reverse Transcriptase Polymerase Chain Reaction. Toluene / analogs & derivatives. Toluene / pharmacology

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  • (PMID = 19706164.001).
  • [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 / Benzothiazoles; 0 / CDKN1A protein, human; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Cyclooxygenase Inhibitors; 0 / Pyrazoles; 0 / Sulfonamides; 0 / Tumor Suppressor Protein p53; 0 / pifithrin; 3FPU23BG52 / Toluene; JCX84Q7J1L / Celecoxib
  • [Other-IDs] NLM/ PMC2741461
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7
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4. Bircan S, Ensari A, Ozturk S, Erdogan N, Dundar I, Ortac F: Immunohistochemical analysis of c-myc, c-jun and estrogen receptor in normal, hyperplastic and neoplastic endometrium. Pathol Oncol Res; 2005;11(1):32-9
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  • [Title] Immunohistochemical analysis of c-myc, c-jun and estrogen receptor in normal, hyperplastic and neoplastic endometrium.
  • To evaluate the role of c-jun and c-myc proto-oncogenes in normal, hyperplastic and neoplastic endometrium in relation to estrogen receptor (ER) status and to investigate whether these genes can be related to other histopathological features of endometrial carcinoma, 32 endometrial carcinomas, 38 endometrial hyperplasias and 22 cyclic endometria (10 proliferative and 12 secretory) were evaluated histologically.
  • Endometrial carcinoma cases were subtyped according to the International Society of Gynecological Pathologists.
  • Immunohistochemical examination was performed using antibodies to ER-alpha, c-myc and c-jun with streptavidin-biotin-peroxidase technique.
  • The mean percentage of ER-alpha positive cells changed cyclically during the menstrual cycle, and it was the highest (96%) and the lowest (31.6%) in proliferative and carcinomatous endometrium, respectively.
  • There was a statistically significant difference between proliferative and secretory phases and proliferative and carcinomatous endometrium in relation to ER-alpha staining (p<0.05).
  • There was also a statistically significant difference with respect to ERalpha reactivity between secretory phase and each hyperplastic group, as well as between the carcinoma group and each hyperplastic group (p<0.05).
  • Although not significant, the mean percentage of c-myc expressing cells in the carcinoma group was higher (15.3%) than that of proliferative phase and hyperplastic groups.
  • The mean percentage of c-jun positive cells in proliferative endometrium was slightly higher than in secretory endometrium, and it was the highest in atypical hyperplastic endometrium (28.3%), but there was no statistically significant difference between the groups.
  • In carcinoma cases, a positive correlation was observed between c-jun positivity and tumor grade (p=0.027, r=0.3908), but such a correlation with c-myc was not found.
  • A positive correlation was detected between ER-alpha and c-myc expression (p=0.038, r=0.3686).
  • A progressive loss of ER seems to be correlated with increasing malignant transformation.
  • C-myc expression might play a role in the development of endometrial carcinoma via ER.
  • The association between c-jun and ER appears to be lost in endometrial carcinoma.
  • The relationship between c-myc, c-jun and ER appears to be altered in endometrial carcinoma compared to that of menstrual endometrium.
  • [MeSH-major] Endometrial Hyperplasia / metabolism. Endometrial Neoplasms / metabolism. Endometrium / metabolism. Estrogen Receptor alpha / metabolism. Proto-Oncogene Proteins c-jun / metabolism. Proto-Oncogene Proteins c-myc / metabolism
  • [MeSH-minor] Adult. Aged. Aged, 80 and over. Biomarkers, Tumor / metabolism. Cell Proliferation. Female. Humans. Immunoenzyme Techniques. Menstrual Cycle / metabolism. Middle Aged. Prognosis

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  • (PMID = 15800680.001).
  • [ISSN] 1219-4956
  • [Journal-full-title] Pathology oncology research : POR
  • [ISO-abbreviation] Pathol. Oncol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Estrogen Receptor alpha; 0 / Proto-Oncogene Proteins c-jun; 0 / Proto-Oncogene Proteins c-myc
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75. Kang KP, Kim DH, Jung YJ, Lee AS, Lee S, Lee SY, Jang KY, Sung MJ, Park SK, Kim W: Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation. Nephrol Dial Transplant; 2009 Oct;24(10):3012-20
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  • [Title] Alpha-lipoic acid attenuates cisplatin-induced acute kidney injury in mice by suppressing renal inflammation.
  • BACKGROUND: Cisplatin is a chemotherapeutic agent used in treatment of malignant tumours.
  • Alpha-lipoic acid (alpha-LA) has anti-inflammatory effects that inhibit both adhesion molecule expression in human endothelial cells and monocyte adhesion by suppressing the nuclear factor-kappaB (NF-kappaB) signalling pathway.
  • The goals of this study were to investigate the anti-inflammatory effects of alpha-LA during cisplatin-induced renal injury and to examine the mechanisms of protection.
  • METHODS: C57BL/6 mice were given cisplatin (20 mg/kg) with or without alpha-LA treatment (100 mg/kg for 3 days).
  • Renal function, histological changes, adhesion molecule expression and inflammatory cell infiltration were examined.
  • The effect of alpha-LA on NF-kappaB activity was evaluated by examining nuclear translocation and phosphorylation of NF-kappaB p65 subunits in kidney tissue.
  • RESULTS: Cisplatin-induced decreases in renal function, measured by blood urea nitrogen, serum creatinine level and renal tubular injury scores, were attenuated by alpha-LA treatment. alpha-LA decreased the tissue levels of tumour necrosis factor-alpha, the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1), and suppressed the infiltration of CD11b-positive macrophages. alpha-LA also attenuated the cisplatin-induced increases in the phosphorylation and nuclear translocation of NF- kappaB p65 subunits in kidney tissue.
  • CONCLUSIONS: These results suggest that alpha-LA treatment ameliorates cisplatin-induced acute kidney injury by reducing inflammatory adhesion molecule expression and NF-kappaB activity.

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  • (PMID = 19474282.001).
  • [ISSN] 1460-2385
  • [Journal-full-title] Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
  • [ISO-abbreviation] Nephrol. Dial. Transplant.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 73Y7P0K73Y / Thioctic Acid; Q20Q21Q62J / Cisplatin
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76. Setyono-Han B, Stürzebecher J, Schmalix WA, Muehlenweg B, Sieuwerts AM, Timmermans M, Magdolen V, Schmitt M, Klijn JG, Foekens JA: Suppression of rat breast cancer metastasis and reduction of primary tumour growth by the small synthetic urokinase inhibitor WX-UK1. Thromb Haemost; 2005 Apr;93(4):779-86
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Suppression of rat breast cancer metastasis and reduction of primary tumour growth by the small synthetic urokinase inhibitor WX-UK1.
  • The serine protease uPA (urokinase-type plasminogen activator) and its receptor uPAR (CD87) are often elevated in malignant tumours, hence, inhibition of this tumour-associated plasminogen activation system provides an attractive target for therapeutic strategies.
  • The anti-tumour and anti-metastatic (number of lung foci and weight of the axillary lymph nodes) properties were studied by subcutaneous administration of WX-UK1 to Brown Norwegian (BN) rats carrying orthotopically transplanted BN472 rat breast tumours.
  • WX-UK1 selectively inhibited tumour-related proteases from rats and humans such as uPA, plasmin, or thrombin in the sub or low micromolar range.
  • Chronical administration of the L-enantiomer of WXUK1 impaired primary tumour growth and metastasis of BN472 rat breast cancer in a dose-dependent manner.
  • In conclusion, our results provide evidence that WX-UK1 as a single agent inhibits breast tumour growth and metastasis in vivo, and thus is a promising candidate drug to treat human cancer.
  • [MeSH-minor] Animals. Antineoplastic Agents / pharmacology. Antineoplastic Agents / therapeutic use. Cell Line, Tumor. Cell Proliferation / drug effects. Drug Evaluation, Preclinical. Female. Gene Expression Regulation, Neoplastic. Neoplasm Transplantation. Phenylalanine / analogs & derivatives. Phenylalanine / therapeutic use. Plasminogen Activator Inhibitor 1 / genetics. RNA, Neoplasm / analysis. Rats. Rats, Inbred BN. Receptors, Cell Surface / genetics. Receptors, Urokinase Plasminogen Activator

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  • (PMID = 15841327.001).
  • [ISSN] 0340-6245
  • [Journal-full-title] Thrombosis and haemostasis
  • [ISO-abbreviation] Thromb. Haemost.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / PLAUR protein, human; 0 / Plasminogen Activator Inhibitor 1; 0 / Plaur protein, rat; 0 / RNA, Neoplasm; 0 / Receptors, Cell Surface; 0 / Receptors, Urokinase Plasminogen Activator; 47E5O17Y3R / Phenylalanine; EC 3.4.21.73 / Urokinase-Type Plasminogen Activator; UJ925Q0P3B / WX-UK1
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77. Eyden B: The myofibroblast: a study of normal, reactive and neoplastic tissues, with an emphasis on ultrastructure. part 2 - tumours and tumour-like lesions. J Submicrosc Cytol Pathol; 2005 Nov;37(3-4):231-96
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] The myofibroblast: a study of normal, reactive and neoplastic tissues, with an emphasis on ultrastructure. part 2 - tumours and tumour-like lesions.
  • This paper describes the ultrastructure of the commoner myofibroblastic tumours and tumour-like lesions.
  • The objective is to complement mainstream pathology texts, which have concentrated on the clinical and light microscopy features of these lesions and which have arguably but understandably somewhat neglected electron microscopy as an ancillary diagnostic tool and a technique for investigating tumour cell biology.
  • Ultrastructural features are described of nodular fasciitis, the myofibromatoses (including Dupuytren's disease), inflammatory myofibroblastic tumour, post-operative spindle cell nodule, fibroma of tendon sheath, fibrous pseudotumour, benign fibrous histiocytoma, atypical fibroxanthoma, dermatofibrosarcoma protuberans, myofibrosarcoma (myofibroblastic sarcoma), malignant fibrous histiocytoma (pleomorphic myofibrosarcoma), epithelioid sarcoma and spindle-cell carcinoma.
  • The fibronexus is emphasised as an important marker for the most confident diagnosis of myofibrosarcoma.
  • Some pathologists accept a light microscope definition, which includes alpha-smooth-muscle actin positivity, h-caldesmon negativity and, in some cases, desmin positivity.
  • Myofibroblastoma and angiomyofibroblastoma are examples of tumours argued on the basis of ultrastructural findings (sometimes in combination with desmin staining) to be primitively differentiated smooth-muscle cell rather than myofibroblastic proliferations.

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  • (PMID = 16612972.001).
  • [ISSN] 1122-9497
  • [Journal-full-title] Journal of submicroscopic cytology and pathology
  • [ISO-abbreviation] J. Submicrosc. Cytol. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Italy
  • [Number-of-references] 344
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78. Vasiljeva O, Korovin M, Gajda M, Brodoefel H, Bojic L, Krüger A, Schurigt U, Sevenich L, Turk B, Peters C, Reinheckel T: Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice. Oncogene; 2008 Jul 10;27(30):4191-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Reduced tumour cell proliferation and delayed development of high-grade mammary carcinomas in cathepsin B-deficient mice.
  • Expression levels of the papain-like cysteine protease cathepsin B (Ctsb) have been positively correlated with mammary tumour progression and metastasis; however, its roles in the hallmark processes of malignant growth remain poorly defined.
  • Using Ctsb-deficient mice we investigated tumour cell differentiation, proliferation and apoptosis in the Tg(MMTV-PyMT) mouse mammary cancer model.
  • Mice lacking Ctsb exhibited reduced cell proliferation in mammary carcinomas and their lung metastases.
  • Notably, intravenous injection of primarily isolated, Ctsb-expressing tumour cells into congenic Ctsb-deficient mice revealed impaired cell proliferation in the resulting experimental lung metastases, providing evidence for the involvement of Ctsb in paracrine regulation of cancer cell proliferation.
  • No Ctsb genotype-dependent difference in tumour cell death was observed in vivo or by treatment of isolated PyMT cancer cells with tumour necrosis factor-alpha.
  • [MeSH-major] Carcinoma / genetics. Cathepsin B / genetics. Cell Proliferation. Immunity, Innate / genetics. Mammary Neoplasms, Animal / genetics. Tumor Burden / genetics
  • [MeSH-minor] Animals. Cell Death / genetics. Disease Progression. Female. Lung Neoplasms / genetics. Lung Neoplasms / secondary. Mice. Mice, Knockout. Neoplasm Transplantation. Time Factors. Tumor Cells, Cultured


79. Boyd M, Sorensen A, McCluskey AG, Mairs RJ: Radiation quality-dependent bystander effects elicited by targeted radionuclides. J Pharm Pharmacol; 2008 Aug;60(8):951-8
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  • The efficacy of radiotherapy may be partly dependent on indirect effects, which can sterilise malignant cells that are not directly irradiated.
  • We determined bystander responses generated by the uptake of radioiodinated iododeoxyuridine ([*I]IUdR) and radiohaloanalogues of meta-iodobenzylguanidine ([*I]MIBG) by noradrenaline transporter (NAT) gene-transfected tumour cells.
  • Multicellular spheroids that consisted of 5% of NAT-expressing cells, capable of the active uptake of radiopharmaceutical, were sterilised by treatment with 20 kBqmL(-1) of the alpha-emitter meta-[211At]astatobenzylguanidine ([211At]MABG).
  • Similarly, in nude mice, retardation of the growth of tumour xenografts containing 5% NAT-positivity was observed after treatment with [131I]MIBG.
  • Cells exposed to media from [131I]MIBG- or [131I]IUdR-treated cells demonstrated a dose-response relationship with respect to clonogenic cell death.
  • It is concluded that radiopharmaceutical-induced bystander effects may depend on LET of the decay particles but are independent of site of intracellular concentration of radionuclide.
  • [MeSH-minor] Animals. Cell Death / radiation effects. Cell Line, Tumor. Culture Media, Conditioned / metabolism. Dose-Response Relationship, Radiation. Humans. Iodine Radioisotopes. Mice. Mice, Nude. Norepinephrine Plasma Membrane Transport Proteins / genetics. Norepinephrine Plasma Membrane Transport Proteins / metabolism. Radiation Dosage. Spheroids, Cellular. Transfection. Xenograft Model Antitumor Assays

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  • (PMID = 18644188.001).
  • [ISSN] 0022-3573
  • [Journal-full-title] The Journal of pharmacy and pharmacology
  • [ISO-abbreviation] J. Pharm. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Culture Media, Conditioned; 0 / Iodine Radioisotopes; 0 / Norepinephrine Plasma Membrane Transport Proteins; 0 / Radiopharmaceuticals; 35MRW7B4AD / 3-Iodobenzylguanidine; LGP81V5245 / Idoxuridine
  • [Number-of-references] 70
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80. Patrikainen L, Porvari K, Kurkela R, Hirvikoski P, Soini Y, Vihko P: Expression profiling of PC-3 cell line variants and comparison of MIC-1 transcript levels in benign and malignant prostate. Eur J Clin Invest; 2007 Feb;37(2):126-33
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  • [Title] Expression profiling of PC-3 cell line variants and comparison of MIC-1 transcript levels in benign and malignant prostate.
  • BACKGROUND: The mechanisms behind prostate cancer progression are largely unknown, but macrophage inhibitory cytokine 1 (MIC-1) has been suggested to be involved in tumour dissemination in vivo due to its reductive effect on cell adhesion.
  • MATERIALS AND METHODS: We used two PC-3 prostate cancer epithelial cell line variants as tools to screen for gene expression differences during prostate cancer progression by cDNA microarray analysis.
  • Selected genes were further analysed by Northern blot analysis using mRNA isolated from prostatic cell lines and tissues.
  • MIC-1 expression was studied by in situ hybridization in archival patient specimens containing benign and malignant prostatic tissue.
  • RESULTS: Gene expression of human collagen type VI, basement membrane heparan sulphate proteoglycan, integrin alpha 1, and fibronectin I were remarkably decreased in suspension-adapted PC-3 (saPC-3) cells, indicating a gene expression profile of reduced cell adhesion.
  • [MeSH-major] Cytokines / metabolism. Prostatic Neoplasms / diagnosis
  • [MeSH-minor] Blotting, Northern. Cell Adhesion / physiology. Cell Line, Tumor. Epithelial Cells / metabolism. Gene Expression. Growth Differentiation Factor 15. Humans. Male. RNA, Messenger / metabolism

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  • (PMID = 17217378.001).
  • [ISSN] 0014-2972
  • [Journal-full-title] European journal of clinical investigation
  • [ISO-abbreviation] Eur. J. Clin. Invest.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cytokines; 0 / GDF15 protein, human; 0 / Growth Differentiation Factor 15; 0 / RNA, Messenger
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81. Franz M, Wolheim A, Richter P, Umbreit C, Dahse R, Driemel O, Hyckel P, Virtanen I, Kosmehl H, Berndt A: Stromal laminin chain distribution in normal, hyperplastic and malignant oral mucosa: relation to myofibroblast occurrence and vessel formation. J Oral Pathol Med; 2010 Apr;39(4):290-8
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  • [Title] Stromal laminin chain distribution in normal, hyperplastic and malignant oral mucosa: relation to myofibroblast occurrence and vessel formation.
  • BACKGROUND: The contribution of stromal laminin chain expression to malignant potential, tumour stroma reorganization and vessel formation in oral squamous cell carcinoma (OSCC) is not fully understood.
  • METHODS: Frozen tissue of OSCC (9x G1, 24x G2, 8x G3) and normal (2x)/hyperplastic (11x) oral mucosa was subjected to laminin chain and alpha-smooth muscle actin (ASMA) immunohistochemistry.
  • Results were correlated to tumour grade.
  • A vascular basement membrane reorganization concerning alpha3 and gamma2 chain laminins during tumour angioneogenesis is suggested.
  • [MeSH-minor] Actins / analysis. Antigens, CD31 / analysis. Basement Membrane / pathology. Cell Transformation, Neoplastic / pathology. Connective Tissue / blood supply. Connective Tissue / pathology. Endothelial Cells / pathology. Endothelium, Vascular / pathology. Fluorescent Antibody Technique. Humans. Hyperplasia. Up-Regulation

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  • (PMID = 19889153.001).
  • [ISSN] 1600-0714
  • [Journal-full-title] Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology
  • [ISO-abbreviation] J. Oral Pathol. Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Denmark
  • [Chemical-registry-number] 0 / Actins; 0 / Antigens, CD31; 0 / LAMA4 protein, human; 0 / LAMC2 protein, human; 0 / Laminin; 0 / laminin alpha 2; 0 / laminin alpha5; 170834-93-2 / laminin alpha 3
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82. Tomasetti M, Andera L, Alleva R, Borghi B, Neuzil J, Procopio A: Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis. FEBS Lett; 2006 Apr 3;580(8):1925-31
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  • [Title] Alpha-tocopheryl succinate induces DR4 and DR5 expression by a p53-dependent route: implication for sensitisation of resistant cancer cells to TRAIL apoptosis.
  • We evaluated the ability of alpha-tocopheryl succinate (alpha-TOS) to sensitise TRAIL-resistant malignant mesothelioma (MM) cells to TRAIL-induced apoptosis.
  • We show that alpha-TOS activates expression of DR4/DR5 in a p53-dependent manner and re-establishes sensitivity of resistant MM cells to TRAIL-mediated apoptosis, as documented in p53wt MM cells but not in their p53null counterparts.
  • MM cells selected for TRAIL resistance expressed low cell surface levels of DR4 and DR5.
  • Treatment with sub-lethal doses of alpha-TOS restored expression of DR4 and DR5.
  • The ability of alpha-TOS to modulate expression of pro-apoptotic genes may play a role in sensitisation of tumour cells to immunological stimuli.
  • [MeSH-major] Apoptosis / drug effects. Apoptosis Regulatory Proteins / pharmacology. Drug Resistance, Neoplasm / drug effects. Membrane Glycoproteins / pharmacology. Receptors, Tumor Necrosis Factor / metabolism. Tumor Necrosis Factor-alpha / pharmacology. Tumor Suppressor Protein p53 / metabolism. Vitamin E / analogs & derivatives
  • [MeSH-minor] Cytoplasm / metabolism. Humans. Neoplasms / metabolism. Neoplasms / pathology. Receptors, Cell Surface / metabolism. Receptors, TNF-Related Apoptosis-Inducing Ligand. Recombinant Proteins / metabolism. TNF-Related Apoptosis-Inducing Ligand. Tocopherols. Tumor Cells, Cultured

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  • (PMID = 16529749.001).
  • [ISSN] 0014-5793
  • [Journal-full-title] FEBS letters
  • [ISO-abbreviation] FEBS Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Cell Surface; 0 / Receptors, TNF-Related Apoptosis-Inducing Ligand; 0 / Receptors, Tumor Necrosis Factor; 0 / Recombinant Proteins; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFRSF10A protein, human; 0 / TNFRSF10B protein, human; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; 0 / Tumor Suppressor Protein p53; 1406-18-4 / Vitamin E; 1406-66-2 / Tocopherols
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83. Eyden B, Banerjee SS, Shenjere P, Fisher C: The myofibroblast and its tumours. J Clin Pathol; 2009 Mar;62(3):236-49
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  • Tumours and tumour-like lesions of myofibroblasts may present diagnostic difficulty because of their rarity and because of uncertainties in identifying the myofibroblast.
  • The objectives of this review are to provide a definition of the myofibroblast and an account of its biology for facilitating an understanding of the cell and of myofibroblastic lesions; and to describe, in the context of common diagnostic problems, the features of benign and malignant myofibroblastic lesions.
  • The main characteristics of the myofibroblast include a spindled or stellate morphology; immunostaining for alpha-smooth muscle actin and the extra domain A variant of cellular fibronectin; and an ultrastructure of rough endoplasmic reticulum, peripheral contractile filaments and the cell-to-matrix junction known as the fibronexus.
  • [MeSH-minor] Diagnosis, Differential. Fasciitis / pathology. Humans

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  • (PMID = 18930983.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Number-of-references] 203
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84. Kuljaca S, Liu T, Tee AE, Haber M, Norris MD, Dwarte T, Marshall GM: Enhancing the anti-angiogenic action of histone deacetylase inhibitors. Mol Cancer; 2007;6:68
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  • BACKGROUND: Histone deacetylase inhibitors (HDACIs) have many effects on cancer cells, such as growth inhibition, induction of cell death, differentiation, and anti-angiogenesis, all with a wide therapeutic index.
  • RESULTS: Trichostatin A (TSA) and alpha-interferon (IFNalpha) were the most effective combination across a range of different cancer cell lines, while normal non-malignant cells did not respond in the same manner to the combination therapy.
  • Moreover, inhibition of p21WAF1 expression in a p21WAF1-expressing breast cancer cell line by a specific siRNA increased the cytotoxic effects of TSA and IFNalpha.
  • In vitro assays of endothelial cell function showed that TSA and IFNalpha decreased endothelial cell migration, invasion, and capillary tubule formation, without affecting endothelial cell viability.
  • Combination TSA and IFNalpha therapy markedly reduced tumour angiogenesis in neuroblastoma-bearing transgenic mice.
  • [MeSH-minor] Animals. Anoxia. Cell Movement. Cyclin-Dependent Kinase Inhibitor p21 / metabolism. Drug Synergism. Humans. Hydroxamic Acids / pharmacology. Interferon-alpha / metabolism. Mice. Models, Biological. Neoplasm Invasiveness. Neoplasm Transplantation

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  • (PMID = 17958916.001).
  • [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 / Angiogenesis Inhibitors; 0 / CDKN1A protein, human; 0 / Cdkn1a protein, mouse; 0 / Cyclin-Dependent Kinase Inhibitor p21; 0 / Enzyme Inhibitors; 0 / Histone Deacetylase Inhibitors; 0 / Hydroxamic Acids; 0 / Interferon-alpha; 3X2S926L3Z / trichostatin A
  • [Other-IDs] NLM/ PMC2173905
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85. Dohi O, Ohtani H, Hatori M, Sato E, Hosaka M, Nagura H, Itoi E, Kokubun S: Histogenesis-specific expression of fibroblast activation protein and dipeptidylpeptidase-IV in human bone and soft tissue tumours. Histopathology; 2009 Oct;55(4):432-40
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  • The aim was to identify cell types that express FAP and DPP-IV in human bone and soft tissue tumours, and to determine whether there are any correlations between the expression of FAP and DPP-IV and the malignant potential of tumours.
  • METHODS AND RESULTS: This study analysed in situ expression in 25 malignant and 13 benign human bone and soft tissue tumours.
  • Immunohistochemistry using pre-fixed frozen sections revealed that FAP was positive in low-grade myofibroblastic sarcoma, the fibroblastic component of osteosarcomas, and malignant fibrous histiocytomas, but negative in Ewing's sarcomas and rhabdomyosarcomas.
  • Giant cells expressed DPP-IV in giant cell tumours.
  • CONCLUSIONS: Our data suggest that FAP and DPP-IV are consistently expressed in bone and soft tissue tumour cells that are histogenetically related to activated fibroblasts and/or myofibroblasts, irrespective of their malignancy.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Bone Neoplasms / metabolism. Bone Neoplasms / pathology. Dipeptidyl Peptidase 4 / metabolism. Gelatinases / metabolism. Membrane Proteins / metabolism. Serine Endopeptidases / metabolism. Soft Tissue Neoplasms / metabolism. Soft Tissue Neoplasms / pathology
  • [MeSH-minor] Fibroblasts / metabolism. Fibroblasts / pathology. Histiocytoma, Malignant Fibrous / metabolism. Histiocytoma, Malignant Fibrous / pathology. Humans. Macrophages / metabolism. Macrophages / pathology. Monocytes / metabolism. Monocytes / pathology. Osteosarcoma / metabolism. Osteosarcoma / pathology. Rhabdomyosarcoma / metabolism. Rhabdomyosarcoma / pathology. Sarcoma, Ewing / metabolism. Sarcoma, Ewing / pathology

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  • (PMID = 19817894.001).
  • [ISSN] 1365-2559
  • [Journal-full-title] Histopathology
  • [ISO-abbreviation] Histopathology
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Membrane Proteins; EC 3.4.14.5 / Dipeptidyl Peptidase 4; EC 3.4.21.- / Serine Endopeptidases; EC 3.4.21.- / fibroblast activation protein alpha; EC 3.4.24.- / Gelatinases
  • [Other-IDs] NLM/ PMC2784039
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86. Redpath M, Marques CM, Dibden C, Waddon A, Lalla R, Macneil S: Ibuprofen and hydrogel-released ibuprofen in the reduction of inflammation-induced migration in melanoma cells. Br J Dermatol; 2009 Jul;161(1):25-33
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  • OBJECTIVES: The aims of this study were: (i) to examine the effects of ibuprofen on the major proinflammatory cytokine tumour necrosis factor (TNF)-alpha induction of migration of C8161 and HBL human melanoma cells;.
  • METHODS: Melanoma cells were exposed to 300 U mL(-1) TNF-alpha for a 24-h period prior to making a scratch wound to which ibuprofen or ibuprofen-loaded hydrogels were then added.
  • The effects of relevant concentrations of ibuprofen on cell viability and apoptosis were examined.
  • RESULTS: Ibuprofen at 10(-3) mol L(-1) significantly reduced TNF-alpha-stimulated migration of both cell types to that of nonstimulated cells (P < 0.001).
  • TNF-alpha-unstimulated cell migration was not significantly affected.
  • CONCLUSIONS: These results demonstrate that TNF-alpha upregulated malignant melanoma migration in vitro and that this could be reduced by ibuprofen both in solution and delivered from a hydrogel.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Apoptosis / drug effects. Cell Movement / drug effects. Ibuprofen / pharmacology. Melanoma / pathology. Skin Neoplasms / pathology. Tumor Necrosis Factor-alpha / pharmacology
  • [MeSH-minor] Delayed-Action Preparations / pharmacology. Humans. Hydrogel / pharmacology. Inflammation / drug therapy. Tumor Cells, Cultured

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  • (PMID = 19438858.001).
  • [ISSN] 1365-2133
  • [Journal-full-title] The British journal of dermatology
  • [ISO-abbreviation] Br. J. Dermatol.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0401428; United Kingdom / Medical Research Council / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Delayed-Action Preparations; 0 / Tumor Necrosis Factor-alpha; 25852-47-5 / Hydrogel; WK2XYI10QM / Ibuprofen
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87. Lazer G, Idelchuk Y, Schapira V, Pikarsky E, Katzav S: The haematopoietic specific signal transducer Vav1 is aberrantly expressed in lung cancer and plays a role in tumourigenesis. J Pathol; 2009 Sep;219(1):25-34
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  • Physiological expression of Vav1 is restricted to the haematopoietic system, where its best-known function is as a GDP/GTP nucleotide exchange factor for Rho/RacGTPases, an activity strictly controlled by tyrosine phosphorylation downstream of cell surface receptors.
  • Here we find Vav1 expression in 42% of 78 lung cancer cell lines analysed.
  • Moreover, immunohistochemical analysis of primary human lung cancer tissue samples revealed Vav1 expression in 26/59 malignant samples, including adenocarcinoma, squamous cell carcinoma and bronchioloalveolar carcinoma.
  • Stronger Vav1 staining was associated with larger tumour size. siRNA-mediated knockdown of Vav1 in lung cancer cells reduced proliferation in agar and tumour growth in nude mice, while control siRNA had no effect, suggesting that Vav1 plays a critical role in the tumorigenicity of lung cancer cells.
  • [MeSH-major] Carcinoma / metabolism. Gene Expression Regulation, Neoplastic. Hematopoiesis / genetics. Lung Neoplasms / metabolism. Proto-Oncogene Proteins c-vav / metabolism. Signal Transduction / genetics
  • [MeSH-minor] Animals. Cell Line, Tumor. Female. Gene Expression. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Humans. Immunohistochemistry / methods. Mice. Mice, Nude. RNA Interference. RNA, Small Interfering / pharmacology. Reverse Transcriptase Polymerase Chain Reaction / methods. Transforming Growth Factor alpha / genetics. rac GTP-Binding Proteins / genetics

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  • (PMID = 19533802.001).
  • [ISSN] 1096-9896
  • [Journal-full-title] The Journal of pathology
  • [ISO-abbreviation] J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Proto-Oncogene Proteins c-vav; 0 / RNA, Small Interfering; 0 / Transforming Growth Factor alpha; 0 / VAV1 protein, human; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; EC 3.6.5.2 / rac GTP-Binding Proteins
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88. Kasper G, Vogel A, Klaman I, Gröne J, Petersen I, Weber B, Castaños-Vélez E, Staub E, Mennerich D: The human LAPTM4b transcript is upregulated in various types of solid tumours and seems to play a dual functional role during tumour progression. Cancer Lett; 2005 Jun 16;224(1):93-103
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  • [Title] The human LAPTM4b transcript is upregulated in various types of solid tumours and seems to play a dual functional role during tumour progression.
  • LAPTM4b (lysosome associated protein transmembrane 4 beta) was recently identified as a gene overexpressed in human hepatocellular carcinoma and belongs to the mammalian LAPTM family.
  • By analysing genome-wide expression profiles of microdissected solid tumour samples by the means of Affymetrix GenChip hybridisation, we found LAPTM4b to be upregulated in 88% (23/26) of lung and in 67% (18/27) of colon carcinoma patients.
  • Other members of the LAPTM family were not overexpressed in the investigated tumour samples according to GeneChip hybridisation data.
  • Due to sequence analysis of bilaterian LAPTM proteins we suggests the presence of four transmembrane helices per protein, which are probably packed together by hydrophobic forces that are excerted by several evolutionary conserved aromatic residues within the alpha-helices.
  • We discuss an active role for LAPTM4b during disease progression of malignant cells and conclude that its putative dual functional involvement in tumour cell proliferation as well as in multidrug-resistance may represent LAPTM4b as a target suitable for development of novel therapeutic agents.
  • [MeSH-minor] Amino Acid Sequence. Blotting, Northern. Cell Proliferation. Cell Transformation, Neoplastic. Disease Progression. Female. Humans. Male. Molecular Sequence Data. Oligonucleotide Array Sequence Analysis. Reverse Transcriptase Polymerase Chain Reaction. Tissue Distribution. Up-Regulation

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  • (PMID = 15911104.001).
  • [ISSN] 0304-3835
  • [Journal-full-title] Cancer letters
  • [ISO-abbreviation] Cancer Lett.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / LAPTM4B protein, human; 0 / Membrane Proteins; 0 / Oncogene Proteins
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89. Escher N, Spies-Weisshart B, Kaatz M, Melle C, Bleul A, Driesch D, Wollina U, von Eggeling F: Identification of HNP3 as a tumour marker in CD4+ and CD4- lymphocytes of patients with cutaneous T-cell lymphoma. Eur J Cancer; 2006 Jan;42(2):249-55
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  • [Title] Identification of HNP3 as a tumour marker in CD4+ and CD4- lymphocytes of patients with cutaneous T-cell lymphoma.
  • Cutaneous T-cell lymphomas (CTCL) are characterized by malignant proliferation of skin homing T-cells.
  • Lymphocytes were separated in CD4+ and CD4- fractions by magnetic cell sorting (MACS).
  • For the generated combined rule base for the CD4- cell fraction, both the sensitivity and specificity for the prediction of CTCL reached 96%, while for the CD4+ fraction they were 92% and 84%, respectively, for sensitivity and specificity.
  • The most significant peak at 3489Da could be identified as HNP3, an alpha-defensin, by immunocapturing.
  • These results open up both the possibility for the use of this protein signature, especially HNP3, to more effectively monitor and screen CTCL, and the avenue to identify the other relevant peaks for a better understanding of the development of this tumour.
  • [MeSH-major] Biomarkers, Tumor / metabolism. CD4-Positive T-Lymphocytes / metabolism. Lymphoma, T-Cell, Cutaneous / diagnosis. Skin Neoplasms / diagnosis. alpha-Defensins / metabolism

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  • (PMID = 16338134.001).
  • [ISSN] 0959-8049
  • [Journal-full-title] European journal of cancer (Oxford, England : 1990)
  • [ISO-abbreviation] Eur. J. Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Biomarkers, Tumor; 0 / alpha-Defensins; 0 / human neutrophil peptide 3
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90. Salonen J, Leminen A, Stenman UH, Butzow R, Heikinheimo M, Heikinheimo O: Tissue AP-2gamma and Oct-3/4, and serum CA 125 as diagnostic and prognostic markers of malignant ovarian germ cell tumors. Tumour Biol; 2008;29(1):50-6
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  • [Title] Tissue AP-2gamma and Oct-3/4, and serum CA 125 as diagnostic and prognostic markers of malignant ovarian germ cell tumors.
  • Histology, clinical stage and treatment response are used to define the prognosis of malignant ovarian germ cell tumors (MOGCTs).
  • Serum levels of alpha-fetoprotein, human chorionic gonadotropin and CA 125 were determined, and immunohistochemistry for CA 125 as well as the pluripotent stem cell markers AP-2gamma and Oct-3/4 was performed in tumor specimens and the NCC-IT human germinoma cell line.
  • Immunohistochemical evaluation revealed that in most cases the elevated CA 125 levels originated from the tumor tissue.
  • Most dysgerminomas as well as the germinoma cell line were positive for AP-2gamma and Oct-3/4, whereas the majority of yolk sac tumors and immature teratomas were negative.
  • [MeSH-major] Biomarkers, Tumor / metabolism. CA-125 Antigen / blood. Neoplasms, Germ Cell and Embryonal / metabolism. Octamer Transcription Factor-3 / metabolism. Ovarian Neoplasms / metabolism. Transcription Factor AP-2 / metabolism
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Chorionic Gonadotropin / blood. Female. Humans. Middle Aged. Neoplasm Staging. Prognosis. alpha-Fetoproteins / metabolism

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  • [Copyright] (c) 2008 S. Karger AG, Basel
  • (PMID = 18497549.001).
  • [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 / Biomarkers, Tumor; 0 / CA-125 Antigen; 0 / Chorionic Gonadotropin; 0 / Octamer Transcription Factor-3; 0 / Transcription Factor AP-2; 0 / alpha-Fetoproteins
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91. Marini P, Schmid A, Jendrossek V, Faltin H, Daniel PT, Budach W, Belka C: Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis. BMC Cancer; 2005 Jan 14;5:5
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  • [Title] Irradiation specifically sensitises solid tumour cell lines to TRAIL mediated apoptosis.
  • BACKGROUND: TRAIL (tumor necrosis factor related apoptosis inducing ligand) is an apoptosis inducing ligand with high specificity for malignant cell systems.
  • Combined treatment modalities using TRAIL and cytotoxic drugs revealed highly additive effects in different tumour cell lines.
  • Little is known about the efficacy and underlying mechanistic effects of a combined therapy using TRAIL and ionising radiation in solid tumour cell systems.
  • METHODS: Tumour cell systems derived from breast- (MDA MB231), lung--(NCI H460) colorectal--(Colo 205, HCT-15) and head and neck cancer (FaDu, SCC-4) were treated with a combination of TRAIL and irradiation using two different time schedules.
  • RESULTS: The combined treatment of TRAIL with irradiation strongly increased apoptosis induction in all treated tumour cell lines compared to treatment with TRAIL or irradiation alone.
  • Upregulation of TRAIL receptor DR5 after irradiation was observed in four of six tumour cell lines but did not correlate to tumour cell sensitisation to TRAIL.
  • TRAIL did not show toxicity in normal tissue cell systems.
  • In addition, pre-irradiation did not sensitise all nine tested human normal tissue cell cultures to TRAIL.
  • Sequential application of ionising radiation followed by TRAIL is associated with an synergistic induction of cell death in a large panel of solid tumour cell lines.
  • [MeSH-major] Antineoplastic Agents / therapeutic use. Apoptosis. Membrane Glycoproteins / therapeutic use. Neoplasms / therapy. Radiation, Ionizing. Tumor Necrosis Factor-alpha / therapeutic use
  • [MeSH-minor] Apoptosis Regulatory Proteins. Caspase 8. Caspases / metabolism. Cell Line, Tumor. Cells, Cultured. Combined Modality Therapy. Humans. Poly(ADP-ribose) Polymerases / metabolism. Receptors, Tumor Necrosis Factor / metabolism. TNF-Related Apoptosis-Inducing Ligand

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  • (PMID = 15651986.001).
  • [ISSN] 1471-2407
  • [Journal-full-title] BMC cancer
  • [ISO-abbreviation] BMC Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Apoptosis Regulatory Proteins; 0 / Membrane Glycoproteins; 0 / Receptors, Tumor Necrosis Factor; 0 / TNF-Related Apoptosis-Inducing Ligand; 0 / TNFSF10 protein, human; 0 / Tumor Necrosis Factor-alpha; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases; EC 3.4.22.- / CASP8 protein, human; EC 3.4.22.- / Caspase 8; EC 3.4.22.- / Caspases
  • [Other-IDs] NLM/ PMC547906
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92. Orii T, Takeda H, Kawata S, Maeda K, Yamakawa M: Differential immunophenotypic analysis of dendritic cell tumours. J Clin Pathol; 2010 Jun;63(6):497-503
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  • [Title] Differential immunophenotypic analysis of dendritic cell tumours.
  • AIMS: The phenotypic and biological characteristics of dendritic cell (DC) tumours have not been fully elucidated.
  • The aim of this study was to compare the immunophenotypic characteristics of DC-related markers and cell-cycle-associated markers among DC tumours and finally to utilise them for differential diagnosis of DC tumours.
  • METHODS: Tissue sections from 28 patients with DC tumours were immunohistochemically examined using DC-related and cell-cycle-associated markers.
  • RESULTS: The Langerhans cell histiocytosis (LCH) and Langerhans cell sarcoma (LCS) samples were positive for S-100 protein, CD1a, Langerin, fascin, DEC-205 and DC-SIGN.
  • Interdigitating dendritic cell sarcoma (IDCS) was positive for S-100 protein and fascin and negative for Langerin.
  • Follicular dendritic cell sarcoma was distinguished from other DC tumours by the lack of DC-SIGN, Langerin and DCE-205.
  • CONCLUSIONS: These results suggest that Langerin can be used to distinguish LCS from IDCS, and DC-SIGN and DEC-205 can be used to identify DC tumour cells.
  • The frequency of cell-cycle-associated markers can be used for the differential diagnosis of malignant and benign DC tumours.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Dendritic Cell Sarcoma, Interdigitating / diagnosis. Histiocytosis, Langerhans-Cell / diagnosis. Langerhans Cell Sarcoma / diagnosis
  • [MeSH-minor] Adolescent. Adult. Aged. Cell Cycle Proteins / metabolism. Child. Dendritic Cells / immunology. Diagnosis, Differential. Female. Forkhead Transcription Factors / analysis. Histones / metabolism. Humans. Immunophenotyping. Interleukin-3 Receptor alpha Subunit / analysis. Male. Middle Aged. Neoplasm Proteins / metabolism. Tumor Suppressor Protein p53 / metabolism. Young Adult

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  • (PMID = 20439325.001).
  • [ISSN] 1472-4146
  • [Journal-full-title] Journal of clinical pathology
  • [ISO-abbreviation] J. Clin. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Cell Cycle Proteins; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Histones; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Neoplasm Proteins; 0 / Tumor Suppressor Protein p53
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93. Rago V, Romeo F, Giordano F, Ferraro A, Andò S, Carpino A: Identification of ERbeta1 and ERbeta2 in human seminoma, in embryonal carcinoma and in their adjacent intratubular germ cell neoplasia. Reprod Biol Endocrinol; 2009;7:56
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  • [Title] Identification of ERbeta1 and ERbeta2 in human seminoma, in embryonal carcinoma and in their adjacent intratubular germ cell neoplasia.
  • BACKGROUND: Estrogens exert a role on germ cell physiology of normal human testis through the mediation of the estrogen receptor (ER) beta subtypes.
  • Epidemiological studies evidenced an increased incidence of testicular germ cell cancer after elevated pre-natal estrogen exposure but the expression of estrogen receptors in these testicular neoplasms has not been well elucidated.
  • METHODS: Immunohistochemistry and Western blot analysis were used to investigate the expression of three distinct ER isoforms, ERalpha, ERbeta1, and ERbeta2 in paraffin-embedded tissues from seminomas and embryonal carcinomas, which are the most common testicular germ cell tumours.
  • A similar pattern of estrogen receptor immunostaining was also observed in the malignant germ cells of intratubular germ cell neoplasia, adjacent to testicular cancers.
  • Western blot analysis of tumour extracts revealed two immunoreactive bands, a 59 kDa band for ERbeta1 and a 53 kDa band for ERbeta2.
  • CONCLUSION: A variable ERbeta expression was previously reported in testicular germ cell tumours and, particularly, an ERbeta down-regulation was evidenced in seminoma and embryonal carcinoma.
  • Conversely, the current study has clearly identified ERbeta1 and ERbeta2 in the neoplastic cells of seminoma and embryonal carcinoma, as well as in the malignant cells of their common pre-invasive precursor, intratubular germ cell neoplasia.
  • [MeSH-major] Carcinoma, Embryonal / metabolism. Estrogen Receptor beta / metabolism. Neoplasms, Germ Cell and Embryonal / metabolism. Seminoma / metabolism. Testicular Neoplasms / metabolism
  • [MeSH-minor] Adult. Blotting, Western. Down-Regulation / physiology. Estrogen Receptor alpha / metabolism. Humans. Immunohistochemistry. Male. Young Adult

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  • (PMID = 19493328.001).
  • [ISSN] 1477-7827
  • [Journal-full-title] Reproductive biology and endocrinology : RB&E
  • [ISO-abbreviation] Reprod. Biol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Estrogen Receptor alpha; 0 / Estrogen Receptor beta
  • [Other-IDs] NLM/ PMC2700117
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94. Charles J, Chaperot L, Salameire D, Di Domizio J, Aspord C, Gressin R, Jacob MC, Richard MJ, Beani JC, Plumas J, Leccia MT: Plasmacytoid dendritic cells and dermatological disorders: focus on their role in autoimmunity and cancer. Eur J Dermatol; 2010 Jan-Feb;20(1):16-23
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  • The presence of PDC, cells capable of producing large quantities of interferon alpha (IFN-alpha) in response to pathogenic agents or danger signals, seems to be closely related to pathological conditions.
  • PDC have been observed in inflammatory immunoallergic dermatological disorders, in malignant cutaneous tumours and in cutaneous lesions of infectious origin.
  • Their function within a tumour context is not as well known and is controversial.
  • They could have a tolerogenic role towards tumour cells in the absence of an activator but they also have the capacity to become activated in response to Toll-like receptor (TLR) ligands and could therefore be useful for therapeutic purposes.
  • [MeSH-minor] Humans. Interferon-alpha / immunology. Interferon-alpha / secretion

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  • (PMID = 19850548.001).
  • [ISSN] 1167-1122
  • [Journal-full-title] European journal of dermatology : EJD
  • [ISO-abbreviation] Eur J Dermatol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Interferon-alpha
  • [Number-of-references] 25
  • [Other-IDs] NLM/ HALMS471485; NLM/ PMC2881955
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95. Paraskeva PA, Ridgway PF, Olsen S, Isacke C, Peck DH, Darzi AW: A surgically induced hypoxic environment causes changes in the metastatic behaviour of tumours in vitro. Clin Exp Metastasis; 2006;23(2):149-57
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  • The use of laparoscopic techniques for curative resections of malignant tumours has been under scrutiny.
  • The potential benefits to the patient in the form of earlier recovery and less immune paresis are countered by the reports of increased tumour recurrence.
  • The biological sequelae of the hypoxic laparoscopic environment on tumour cells is unknown.
  • Components of the metastatic cascade were evaluated under in vitro laparoscopic conditions using a human colonic adenocarcinoma cell line (SW1222).
  • Exposure to the laparoscopic gases carbon dioxide and helium for 4 h, comparable to the duration of a laparoscopic colorectal resection, had no effect on cell viability.
  • The changes were reflected at the molecular level by significant down regulation of adhesion molecules known to be involved in tumour progression (E-cadherin, CD44 and beta1 sub-unit).
  • [MeSH-major] Adenocarcinoma / surgery. Cell Hypoxia. Colonic Neoplasms / surgery. Laparoscopy / adverse effects
  • [MeSH-minor] Cadherins / metabolism. Carbon Dioxide / adverse effects. Cell Adhesion. Cell Adhesion Molecules / metabolism. Extracellular Matrix Proteins / metabolism. Helium / adverse effects. Humans. Hypoxia-Inducible Factor 1, alpha Subunit / analysis. Neoplasm Metastasis. Time Factors. Tumor Cells, Cultured

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  • (PMID = 16912913.001).
  • [ISSN] 0262-0898
  • [Journal-full-title] Clinical & experimental metastasis
  • [ISO-abbreviation] Clin. Exp. Metastasis
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cadherins; 0 / Cell Adhesion Molecules; 0 / Extracellular Matrix Proteins; 0 / Hypoxia-Inducible Factor 1, alpha Subunit; 142M471B3J / Carbon Dioxide; 206GF3GB41 / Helium
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96. Nutt JE, Razak AR, O'Toole K, Black F, Quinn AE, Calvert AH, Plummer ER, Lunec J: The role of folate receptor alpha (FRalpha) in the response of malignant pleural mesothelioma to pemetrexed-containing chemotherapy. Br J Cancer; 2010 Feb 2;102(3):553-60
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  • [Title] The role of folate receptor alpha (FRalpha) in the response of malignant pleural mesothelioma to pemetrexed-containing chemotherapy.
  • BACKGROUND: The standard treatment of choice for malignant pleural mesothelioma is chemotherapy with pemetrexed and platinum, but the clinical outcome is poor.
  • This study investigates the response to pemetrexed in a panel of eight mesothelioma cell lines and the clinical outcome for patients treated with pemetrexed in relation to folate receptor alpha (FRalpha).
  • METHODS: Cell lines were treated with pemetrexed to determine the concentration that reduced growth to 50% (GI(50)).
  • RESULTS: A wide range of GI(50) values was obtained for the cell lines, H2452 cells being the most sensitive (GI(50) 22 nM) and RS5 cells having a GI(50) value greater than 10 microM.
  • No FRalpha protein was detected in any cell line, and there was no relationship between sensitivity and expression of folate transporters.
  • FRalpha was detected in 39% of tumour samples, generally in a small percentage of cells.

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  • (PMID = 20051956.001).
  • [ISSN] 1532-1827
  • [Journal-full-title] British journal of cancer
  • [ISO-abbreviation] Br. J. Cancer
  • [Language] ENG
  • [Grant] United Kingdom / Cancer Research UK / /
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Folate Receptors, GPI-Anchored; 0 / Folic Acid Antagonists; 0 / Glutamates; 0 / Receptors, Cell Surface; 04Q9AIZ7NO / Pemetrexed; 5Z93L87A1R / Guanine
  • [Other-IDs] NLM/ PMC2822938
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97. Ardon H, Verbinnen B, Maes W, Beez T, Van Gool S, De Vleeschouwer S: Technical advancement in regulatory T cell isolation and characterization using CD127 expression in patients with malignant glioma treated with autologous dendritic cell vaccination. J Immunol Methods; 2010 Jan 31;352(1-2):169-73
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  • [Title] Technical advancement in regulatory T cell isolation and characterization using CD127 expression in patients with malignant glioma treated with autologous dendritic cell vaccination.
  • We have successfully treated over two hundred high-grade glioma (HGG) patients with immunotherapy consisting of vaccination with autologous dendritic cells (DCs) loaded with autologous tumour lysate.
  • It has been documented that regulatory T cells (Treg) can counteract anti-tumour immune responses.
  • Here, we validated IL-7 receptor alpha subunit (CD127)dim expression as a marker for human Treg within HGG patients, as a less laborious assay for routine use in tumour vaccination trials.
  • [MeSH-major] Biomarkers / metabolism. Cancer Vaccines. Central Nervous System Neoplasms / immunology. Glioma / immunology. Interleukin-7 Receptor alpha Subunit / metabolism. T-Lymphocyte Subsets / metabolism. T-Lymphocytes, Regulatory / metabolism
  • [MeSH-minor] Antigens, CD4 / biosynthesis. Antigens, Neoplasm / immunology. Antigens, Neoplasm / metabolism. Cells, Cultured. Dendritic Cells / immunology. Dendritic Cells / metabolism. Forkhead Transcription Factors / biosynthesis. Humans. Interleukin-2 Receptor alpha Subunit / biosynthesis. Lymphocyte Culture Test, Mixed. Monitoring, Physiologic. Transplantation, Autologous

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  • [Copyright] Copyright 2009 Elsevier B.V. All rights reserved.
  • (PMID = 19874827.001).
  • [ISSN] 1872-7905
  • [Journal-full-title] Journal of immunological methods
  • [ISO-abbreviation] J. Immunol. Methods
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, Neoplasm; 0 / Biomarkers; 0 / Cancer Vaccines; 0 / FOXP3 protein, human; 0 / Forkhead Transcription Factors; 0 / Interleukin-2 Receptor alpha Subunit; 0 / Interleukin-7 Receptor alpha Subunit
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98. Greco S, Elia MG, Muscella A, Romano S, Storelli C, Marsigliante S: Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture. J Endocrinol; 2005 Aug;186(2):291-301
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  • [Title] Bradykinin stimulates cell proliferation through an extracellular-regulated kinase 1 and 2-dependent mechanism in breast cancer cells in primary culture.
  • We here investigated the mitogenic effects and the signalling pathways of BK in primary cultured human epithelial breast cells obtained from a tumour and from the histologically proven non-malignant tissue adjacent to the tumour.
  • BK provoked cell proliferation, increase in cytosolic calcium, activation of protein kinase C (PKC)-alpha, -beta, -delta, -epsilon and -eta and phosphorylation of the extracellular-regulated kinases 1 and 2 (ERK1/2).
  • In conclusion, the mitogenic effects of BK are retained in peritumour and tumour cells; hence, it is likely that BK has an important role in cancer endorsement and progression.
  • [MeSH-minor] Analysis of Variance. Calcium / analysis. Cell Proliferation / drug effects. Enzyme Activation. Female. Humans. Immunoblotting / methods. Intracellular Fluid / chemistry. Oligonucleotide Array Sequence Analysis. Phosphatidylinositol 3-Kinases / metabolism. Receptors, Bradykinin / metabolism. Tumor Cells, Cultured

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  • (PMID = 16079255.001).
  • [ISSN] 0022-0795
  • [Journal-full-title] The Journal of endocrinology
  • [ISO-abbreviation] J. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Mitogens; 0 / Receptors, Bradykinin; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.11.24 / Mitogen-Activated Protein Kinases; S8TIM42R2W / Bradykinin; SY7Q814VUP / Calcium
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99. Woenckhaus J, Steger K, Sturm K, Münstedt K, Franke FE, Fenic I: Prognostic value of PIK3CA and phosphorylated AKT expression in ovarian cancer. Virchows Arch; 2007 Apr;450(4):387-95
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  • Disrupted phosphatidylinositol 3-kinase (PI3K) activity and its effect on the downstream target AKT plays an important role in malignant diseases.
  • Gain and/or amplification of PIK3CA gene, encoding the catalytic subunit of phosphatidylinositol 3-kinase (p110 alpha) and its increased expression are associated with enhanced PI3K activity in ovarian cancer cell lines.
  • The expression of p110 alpha, phosphorylated AKT (pAKT) and the proliferation marker Ki-67 were immunohistochemically investigated.
  • PIK3CA amplification and Ki-67 index were strong predictors for an early tumour-associated death. p110 alpha expression correlated with 3q26.3 gain and Ki-67 index but not with the patient outcome.
  • No relationship could be observed between p110 alpha and pAKT or between pAKT and disease outcome.
  • Our results underline the prognostic significance of PIK3CA in ovarian carcinoma and argue against a simple linear model of PIK3CA gain/amplification followed by PI3K activation and consecutive AKT phosphorylation in ovarian carcinoma.

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  • (PMID = 17377809.001).
  • [ISSN] 0945-6317
  • [Journal-full-title] Virchows Archiv : an international journal of pathology
  • [ISO-abbreviation] Virchows Arch.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Ki-67 Antigen; EC 2.7.1.- / Phosphatidylinositol 3-Kinases; EC 2.7.1.137 / PIK3CA protein, human; EC 2.7.11.1 / Proto-Oncogene Proteins c-akt
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100. Bien E, Balcerska A: Serum soluble interleukin 2 receptor alpha in human cancer of adults and children: a review. Biomarkers; 2008 Feb;13(1):1-26
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Serum soluble interleukin 2 receptor alpha in human cancer of adults and children: a review.
  • In most haematological malignancies, including different types of leukaemias and lymphomas, sIL-2Ralpha has been found to be released directly from the surface of neoplastic cells thus reflecting the tumour bulk, turnover and activity.
  • They include malignant melanoma and carcinomas of the kidney, head and neck, oesophagus and lung.
  • It is suggested that in most malignant solid tumours, elevated levels of sIL-2Ralpha are likely to be the product of normal peripheral mononuclear cells activated in response to the neoplasm's growth or that they are released from activated lymphoid cells infiltrating neoplastic tissues.
  • This latter hypothesis has been proved by discovering the high expression of CD25 on the cell surface of most of these cells.
  • The authors review the published data on clinical applicability of soluble IL-2Ralpha determination in terms of diagnostics, prognosis and treatment monitoring of particular types of malignant disorders both in adults and in children.
  • [MeSH-major] Biomarkers, Tumor / blood. Interleukin-2 Receptor alpha Subunit / blood. Neoplasms / blood

  • MedlinePlus Health Information. consumer health - Cancer in Children.
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  • (PMID = 17906988.001).
  • [ISSN] 1354-750X
  • [Journal-full-title] Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals
  • [ISO-abbreviation] Biomarkers
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Interleukin-2 Receptor alpha Subunit
  • [Number-of-references] 169
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