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  <item rdf:about="http://hdl.handle.net/2268/147655">
    <title>DENDRITIC CELLS IN BARRETT’S ESOPHAGUS CARCINOGENESIS: AN INADEQUATE  MICROENVIRONMENT FOR ANTITUMOR IMMUNITY?</title>
    <link>http://hdl.handle.net/2268/147655</link>
    <description>Title: DENDRITIC CELLS IN BARRETT’S ESOPHAGUS CARCINOGENESIS: AN INADEQUATE  MICROENVIRONMENT FOR ANTITUMOR IMMUNITY?
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Somja, Joan; Demoulin, Stéphanie; RONCARATI, Patrick; Herfs, Michael; BLETARD, Noëlla; Delvenne, Philippe; Hubert, Pascale</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/147505">
    <title>Confrontation anatomo-clinique. Cancer thyroidin après irradiation: revue de la littérature à propos d'un cas</title>
    <link>http://hdl.handle.net/2268/147505</link>
    <description>Title: Confrontation anatomo-clinique. Cancer thyroidin après irradiation: revue de la littérature à propos d'un cas
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Leonard, Philippe; Delvenne, Philippe; Collignon, Jacques; Ghaye, Benoît; Merchie, G.; Deneufbourg, Jean-Marie; Boniver, Jacques</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/147260">
    <title>Comparing duration of response and duration of clinical benefit between fulvestrant treatment groups in the CONFIRM trial: application of new methodology.</title>
    <link>http://hdl.handle.net/2268/147260</link>
    <description>Title: Comparing duration of response and duration of clinical benefit between fulvestrant treatment groups in the CONFIRM trial: application of new methodology.
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Garnett, Sally Anne; Martin, Miguel; JERUSALEM, Guy; Petruzelka, Lubos; Torres, Roberto; Bondarenko, Igor N.; Khasanov, Rustem; Verhoeven, Didier; Pedrini, Jose L.; Smirnova, Iva; Lichinitser, Mikhail R.; Pendergrass, Kelly; Lindemann, Justin P. O.; Di Leo, Angelo
&lt;br/&gt;
&lt;br/&gt;Abstract: Comparisons of duration of response (DoR) and duration of clinical benefit (DoCB) within clinical trials are prone to biases. To address these biases, we used new methodology to prospectively analyze expected DoR and expected DoCB. Objective response rate and clinical benefit rate were calculated for fulvestrant 500 and 250 mg, and used to calculate expected DoR and expected DoCB for each dose group. The ratios for expected DoR and expected DoCB (expected DoR500/expected DoR250 and expected DoCB500/expected DoCB250) were then calculated, thereby allowing statistical comparisons of these endpoints between each arm of the COmparisoN of Faslodex In Recurrent or Metastatic breast cancer (CONFIRM) trial. Expected DoRs for fulvestrant 500 and 250 mg were 3.2 and 3.6 months, respectively. The expected DoR ratio between fulvestrant 500 and 250 mg was not statistically significant (0.89; 95 % CI, 0.48-1.67, P = 0.724). The expected DoCBs for fulvestrant 500 and 250 mg were 9.8 and 7.2 months, respectively. The expected DoCB ratio showed that the expected DoCB for fulvestrant 500 mg was significantly improved compared with the expected DoCB for fulvestrant 250 mg (1.36; 95 % CI, 1.07-1.73, P = 0.013). Analysis of the expected DoR and expected DoCB showed fulvestrant 500 mg significantly increased expected DoCB compared with fulvestrant 250 mg in the CONFIRM trial.</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/146351">
    <title>Preliminary results of [18F]FPRGD2 PET/CT imaging of integrin αvβ3 levels in patients with locally advanced rectal carcinoma</title>
    <link>http://hdl.handle.net/2268/146351</link>
    <description>Title: Preliminary results of [18F]FPRGD2 PET/CT imaging of integrin αvβ3 levels in patients with locally advanced rectal carcinoma
&lt;br/&gt;
&lt;br/&gt;Author, co-author: WITHOFS, Nadia; MARTINIVE, Philippe; SCAGNOL, Irène; THONON, David; Giacomelli, Fabrice; Mievis, Frédéric; COUCKE, Philippe; CATALDO, Didier; Sanjiv, Gambhir; HUSTINX, Roland</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/146350">
    <title>FDG PET/CT for radiotherapy treatment planning. Comparison of functional volume delineation algorithms</title>
    <link>http://hdl.handle.net/2268/146350</link>
    <description>Title: FDG PET/CT for radiotherapy treatment planning. Comparison of functional volume delineation algorithms
&lt;br/&gt;
&lt;br/&gt;Author, co-author: WITHOFS, Nadia; Bernard, Claire; VAN DER REST, Catherine; MARTINIVE, Philippe; HATT, Mathieu; Dimitris, Visvikis; COUCKE, Philippe; HUSTINX, Roland</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/145257">
    <title>Transposition en réseau des trajets cliniques d’un Service de Radiothérapie dans le modèle de Reason pour la prévention et la gestion des évènements indésirables</title>
    <link>http://hdl.handle.net/2268/145257</link>
    <description>Title: Transposition en réseau des trajets cliniques d’un Service de Radiothérapie dans le modèle de Reason pour la prévention et la gestion des évènements indésirables
&lt;br/&gt;
&lt;br/&gt;Author, co-author: DELGAUDINE, Marie; LENAERTS, Eric; RENARD, André; PRINCEN, Fabienne; COUCKE, Philippe</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144749">
    <title>Dendritic cells in Barrett's esophagus carcinogenesis: an inadequate microenvironment for antitumor immunity?</title>
    <link>http://hdl.handle.net/2268/144749</link>
    <description>Title: Dendritic cells in Barrett's esophagus carcinogenesis: an inadequate microenvironment for antitumor immunity?
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Somja, Joan; Demoulin, Stéphanie; RONCARATI, Patrick; Herfs, Michael; BLETARD, Noëlla; Delvenne, Philippe; Hubert, Pascale</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144747">
    <title>Dendritic cells in Barrett's carcinogenesis: an inadequate environment for antitumor immunity?</title>
    <link>http://hdl.handle.net/2268/144747</link>
    <description>Title: Dendritic cells in Barrett's carcinogenesis: an inadequate environment for antitumor immunity?
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Somja, Joan; Demoulin, Stéphanie; RONCARATI, Patrick; Herfs, Michael; BLETARD, Noëlla; Delvenne, Philippe; Hubert, Pascale</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144508">
    <title>Disruption of COX-2 modulates gene expression and the cardiac injury response to doxorubicin</title>
    <link>http://hdl.handle.net/2268/144508</link>
    <description>Title: Disruption of COX-2 modulates gene expression and the cardiac injury response to doxorubicin
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Neilan, Tomas; Doherty, Glen; Chen, Gang; Deflandre, Catherine; McAllister, Hester; Butler, Ryan; McClelland, Sarah; Kay, Elaine; Ballou, Leslie; Fitzgerald
&lt;br/&gt;
&lt;br/&gt;Abstract: To determine the role of cyclooxygenase (COX)-2 in anthracycline-induced cardiac toxicity, we administered doxorubicin (Dox) to mice with genetic disruption of COX-2 (COX-2−/−). After treatment with Dox, COX-2−/− mice had increased cardiac dysfunction and cardiac cell apoptosis compared with Dox-treated wild-type mice. The expression of the death-associated protein kinase-related apoptosis-inducing protein kinase-2 was also increased in Dox-treated COX-2−/− animals. The altered gene expression, cardiac injury, and dysfunction after Dox treatment in COX-2−/− mice was attenuated by a stable prostacyclin analog, iloprost. Wild-type mice treated with Dox developed cardiac fibrosis that was absent in COX-2−/− mice and unaffected by iloprost. These results suggest that genetic disruption of COX-2 increases the cardiac dysfunction after treatment with Dox by an increase in cardiac cell apoptosis. This Dox-induced cardiotoxicity in COX-2−/− mice was attenuated by a prostacyclin analog, suggesting a protective role for prostaglandins in this setting.</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144477">
    <title>Risk Of Malignancies In A Single Center Cohort Of IBD-Patients Treated with Immunosuppressives and Anti-TNF-antibodies</title>
    <link>http://hdl.handle.net/2268/144477</link>
    <description>Title: Risk Of Malignancies In A Single Center Cohort Of IBD-Patients Treated with Immunosuppressives and Anti-TNF-antibodies
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Steinborn, A; Beigel, F; Breiteneicher, S; Van Steen, Kristel; Schnitzler, F; Göke, B; Weidinger, M; Brand, S; Ochsenkühn, T; Seiderer, J</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144476">
    <title>Risk Of Malignancies In A Single Center Cohort Of IBD-Patients Treated with Immunosuppressives and Anti-TNF-antibodies</title>
    <link>http://hdl.handle.net/2268/144476</link>
    <description>Title: Risk Of Malignancies In A Single Center Cohort Of IBD-Patients Treated with Immunosuppressives and Anti-TNF-antibodies
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Steinborn, A; Beigel, F; Breiteneicher, S; Van Steen, Kristel; Schnitzler, F; Göke, B; Weidinger, M; Brand, S; Ochsenkühn, T; Seiderer, J</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144475">
    <title>Rate of Malignancies and Infections in a Large Single Center Cohort of IBD Patients Treated With Thiopurines and Anti-TNF-Antibodies.</title>
    <link>http://hdl.handle.net/2268/144475</link>
    <description>Title: Rate of Malignancies and Infections in a Large Single Center Cohort of IBD Patients Treated With Thiopurines and Anti-TNF-Antibodies.
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Ochsenkühn, T; Steinborn, A; Beigel, F; Mahachie John, Jestinah; Van Steen, Kristel; Schnitzler, S; Tillack, C; Göke, B; Weidinger, M; Brand, S; Seiderer, J</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144474">
    <title>Rate of Malignancies and Infections in a Large Single Center Cohort of IBD Patients Treated With Thiopurines and Anti-TNF-Antibodies.</title>
    <link>http://hdl.handle.net/2268/144474</link>
    <description>Title: Rate of Malignancies and Infections in a Large Single Center Cohort of IBD Patients Treated With Thiopurines and Anti-TNF-Antibodies.
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Ochsenkühn, T; Steinborn, A; Beigel, F; Breiteneicher, S; Mahachie John, Jestinah; Van Steen, Kristel; Schnitzler, F; Tillack, C; Göke, B; Weidinger, M; Brand, S; Seiderer, J</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/144473">
    <title>Rate of Malignancies and Infections in a Large Single Center Cohort of IBD Patients Treated With Thiopurines and Anti-TNF-Antibodies.</title>
    <link>http://hdl.handle.net/2268/144473</link>
    <description>Title: Rate of Malignancies and Infections in a Large Single Center Cohort of IBD Patients Treated With Thiopurines and Anti-TNF-Antibodies.
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Ochsenkühn, T; Steinborn, A; Beigel, F; Breiteneicher, S; Mahachie John, Jestinah; Van Steen, Kristel; Schnitzler, F; Tillack, C; Göke, B; Weidinger, M; Seiderer, S; Seiderer, J</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/143585">
    <title>Elaboration d’un plan de formation continue à partir de l’approche processus dans un service de Radiothérapie</title>
    <link>http://hdl.handle.net/2268/143585</link>
    <description>Title: Elaboration d’un plan de formation continue à partir de l’approche processus dans un service de Radiothérapie
&lt;br/&gt;
&lt;br/&gt;Author, co-author: LENAERTS, Eric; DELGAUDINE, Marie; COUCKE, Philippe</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/143584">
    <title>VEGF111, a new VEGF-A isoform induced by genotoxic agents; resistance to proteolytic</title>
    <link>http://hdl.handle.net/2268/143584</link>
    <description>Title: VEGF111, a new VEGF-A isoform induced by genotoxic agents; resistance to proteolytic
&lt;br/&gt;
&lt;br/&gt;Author, co-author: MINEUR, P.; Colige, Alain; DELGAUDINE, Marie; Deroanne, Christophe; KESTELOOT, F.; Dubail, Johanne; GOTHOT, André; LAPIERE, Ch.; NOEL, A.; VOO, S.; Waltenberger; Nusgens; Lambert, Charles</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/143440">
    <title>Expression of matrix metalloproteinase-2 and mutant p53 is increased in hydatidiform mole as compared with normal placenta</title>
    <link>http://hdl.handle.net/2268/143440</link>
    <description>Title: Expression of matrix metalloproteinase-2 and mutant p53 is increased in hydatidiform mole as compared with normal placenta
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Petignat, P.; Laurini, R.; Goffin, Frédéric; Bruchim, I.; Bischof, P.
&lt;br/&gt;
&lt;br/&gt;Abstract: Matrix metalloproteinases (MMPs) are group of enzymes thought to play an important role in trophoblastic and tumor invasion. The aim of our study was to investigate the trophoblastic expression of MMPs and p53 in normal trophoblast and hydatidiform moles (HM). Paraffin sections of 45 specimens, including 14 complete hydatidiform moles (CM), 15 partial hydatidiform moles (PM), 8 atypical partial hydatidiform moles (aPM), and 8 controls were selected. Classification of HM was established on histologic criteria and supported by the DNA ploidy results. Tissue sections from each case were immunostained with monoclonal antibodies, cytokeratin-7, MMP-2, MMP-9, tissue inhibitors of metalloproteinases (TIMP)-1, and p53 wild type (p53wt) and mutant types (mutp53). Staining for cytokeratin-7 revealed a positive reaction in 93% of the samples. MMP-2 was mainly expressed in the syncytiotrophoblast of HM and found in 62% of aPM, 60% PM, and 93% CM. The mutp53 was mainly and focally expressed in syncytiotrophoblastic cells and was found in 63% of aPM, 80% PM, and 93% CM. Expression of MMP-2 and mutp53 was both significantly greater in HM vs control group (P &lt; 0.05) and greater in CM vs PM and aPM (P &lt; 0.05). No significant difference was observed for cytokeratin-7, MMP-9, TIMP-1, and p53wt between the HM subgroups and between HM and control group. MMP-2 and mutp53 are overexpressed in HM as compared with normal trophoblast and might participate in the invasive behavior of the HM.</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/143375">
    <title>Carcinomatose péritonéale d'origine indéterminée</title>
    <link>http://hdl.handle.net/2268/143375</link>
    <description>Title: Carcinomatose péritonéale d'origine indéterminée
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Marchal, Nathalie; GENNIGENS, Christine; JERUSALEM, Guy
&lt;br/&gt;
&lt;br/&gt;Abstract: La carcinomatose péritonéale est définie comme l'envahissement néoplasique secondaire du péritoine. Cette entité peut amener de nombreuses difficultés, à la fois sur le plan de son diagnostic, de sa mise au point et de la recherche de son origine ainsi que pour son traitement. Le cas clinique que nous relatons illustre les difficultés pouvant être rencontrées par l'équipe soignante face à une carcinomatose péritonéale et décrit l'importance d'une approche multidisciplinaire pour sa prise en charge. Lorsque son origine n'est pas déterminée avant l'instauration du traitement, la carcinomatose péritonéale entre dans le cadre des carcinomes de primitif inconnu (CAPI). Chez une femme, une telle présentation de CAPI en fait une entité particulière, facteur de meilleur pronostic, pour laquelle un traitement plus spécifique doit être instauré en première intention.</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/143374">
    <title>Pazopanib (Votrient) dans le traitement du cancer du rein et des sarcomes des tissus mous.</title>
    <link>http://hdl.handle.net/2268/143374</link>
    <description>Title: Pazopanib (Votrient) dans le traitement du cancer du rein et des sarcomes des tissus mous.
&lt;br/&gt;
&lt;br/&gt;Author, co-author: GENNIGENS, Christine; JERUSALEM, Guy
&lt;br/&gt;
&lt;br/&gt;Abstract: Renal cell carcinoma accounts for 3% of all malignant tumors. Until a few years ago, immunotherapy (Interferon and/or Interleukin-2) was the only approved systemic treatment in the metastatic setting. Better knowledge of renal cell cancer biology drew attention on the fundamental role of angiogenesis. Several strategies targeting angiogenesis have been developed including VEGF and VEGFR inhibitors. They are now the standard treatment in first and second line. Pazopanib, a VEGFR tyrosine kinase inhibitor, is one of the treatment options recommended for patients with metastatic renal cell carcinoma, in first line and after cytokines failure. Since more recently, pazopanib is also approved in the treatment of metastatic soft tissue sarcoma, after failure of at least one line of chemoterapy. In this paper, we will review the mechanism of action and the clinical results of pazopanib in renal cell carcinoma and sarcoma.</description>
  </item>
  <item rdf:about="http://hdl.handle.net/2268/142799">
    <title>REGULATION DE L'EXPRESSION ET DE LA REPLICATION DU VIRUS T-LYMPHOTROPE HUMAIN DE TYPE I (HTLV-1) PAR LE COMPLEXE MINICHROMOSOME MAINTENANCE 2-7 (MCM2-7)</title>
    <link>http://hdl.handle.net/2268/142799</link>
    <description>Title: REGULATION DE L'EXPRESSION ET DE LA REPLICATION DU VIRUS T-LYMPHOTROPE HUMAIN DE TYPE I (HTLV-1) PAR LE COMPLEXE MINICHROMOSOME MAINTENANCE 2-7 (MCM2-7)
&lt;br/&gt;
&lt;br/&gt;Author, co-author: Barez, Pierre-Yves
&lt;br/&gt;
&lt;br/&gt;Abstract: Premier rétrovirus humain découvert, le virus HTLV-1 infecte environ 20 millions de personnes de part le monde. Il est l’agent causal de la leucémie à cellules T de l’adulte (ATL) et d’une maladie neurodégénérative chronique appelée HAM/TSP (HTLV-1 associated myelopathy/Tropical spastic paraparesis). Le complexe MCM2-7 semble jouer un rôle important dans la biologie des virus, notamment celles du virus EBV (Epstein-Barr virus), KSHV (Kaposi’s sarcoma associated virus) ou Influenza. C’est également le cas pour le virus HTLV-1 puisque nous avons observé le recrutement de ce complexe au niveau du promoteur viral. L’utilité de ce recrutement ne semble pas jouer dans la réplication du virus mais est plutôt d’ordre transcriptionnel. Ainsi, comme nous l’avons démontré, la surexpression de MCM3 favorise la transactivation du LTR par la protéine Tax. Cette propriété est dépendante de l’interaction existant entre Tax et cette sous-unité du complexe MCM2-7, ainsi que de son domaine carboxy-terminal. Enfin, nos observations indiquent aussi que MCM3 pourrait être nécessaire à la localisation nucléaire de Tax. Ce travail a donc permis d’identifier de nouveaux mécanismes par lesquels Tax assure la persistance virale et conduit au développement de maladies associées à HTLV-1.; First human retrovirus discovered, HTLV-1 infects approximately 20 million individuals worldwide. HTLV-1 is the etiological agent of adult T-cell leukemia and a neurodegenerative disorder called HAM/TSP (HTLV-1 associated myelopathy/Tropical spastic paraparesis). The MCM2-7 complex seems to play a key role in the biology of viruses, such as EBV (Epstein-Barr virus), KSHV (Kaposi’s sarcoma associated virus) or Influenza. This is also the case for HTLV-1 virus because we revealed the recruitment of MCM2-7 onto the viral promoter. The role of this interaction does not pertain to viral replication but is involved in transcriptional regulation. In fact, overexpression of MCM3 increases Tax transactivation activity dependently on Tax/MCM3 interaction and MCM3 carboxy-terminal domain. Finally, our observations indicate that MCM3 is likely required for Tax nuclear shuttling. This work thus gives insights into new mechanisms by which Tax ensures the viral persistence and leads to the development of HTLV-1 associated diseases.</description>
  </item>
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