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Biblio - Bibliographie IAL
Bibliographie IAL

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Recherche bibliographique scientifique

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Accueil > Références bibliographiques

biblio

2009

  • Roque-Afonso, AM 2009, « Hepatitis B virus cellular immunity after liver transplantation: a role in preventing hepatitis B virus recurrence? », Liver Transpl, vol. 15, no. 3, p. 269-72.
    Résumé : Roque-Afonso, Anne Marie; Comment; Editorial; United States; Liver Transpl. 2009 Mar;15(3):269-72. doi: 10.1002/lt.21729.
    Mots-clés : CD4-Positive T-Lymphocytes/ immunology Hepatitis B virus/ immunology/physiology Hepatitis B, Cellular Immunization, Chronic/ immunology Humans Immunity, Passive/ methods Immunoglobulins/ therapeutic use Liver Transplantation/ immunology Recurrence Virus Replication/immunology.
  • Samri, A, Roque-Afonso, AM, Beran, O, Tateo, M, Teicher, E, Feray, C, Sebagh, M, Guettier, C, Dussaix, E, Vittecoq, D, Samuel, D, Autran, B & Duclos-Vallee, JC 2009, « Preservation of immune function and anti-hepatitis C virus (HCV) immune responses after liver transplantation in HIV-HCV coinfected patients (ANRS-HC08 "THEVIC" trial) », J Hepatol, vol. 51, no. 6, p. 1000-9.
    Résumé : BACKGROUND/AIMS: Liver transplantation (LT) in immune-suppressed human immunodeficiency virus (HIV) and hepatitis C virus (HCV) coinfected patients is feasible but raises questions regarding the severity of HCV recurrence on the liver graft and preservation of immune function. We investigated whether LT is deleterious to the immune system. METHODS: Fourteen HIV-HCV coinfected patients (HIV viral load [VL] <50 copies/ml; median CD4 count of 276/mm(3) pretransplantation) were grafted for HCV-cirrhosis and followed over 2 years. Nine patients received anti-HCV therapy post-transplantation. HCV and HIV VLs and degree of acute and chronic hepatitis were monitored. Peripheral blood T-cell phenotypes and interferon-gamma (IFN-gamma) immune responses against opportunistic pathogens, HCV, and HIV-1 p24 were evaluated. RESULTS: Median HCV VLs, CD4 counts, T-cell subsets, and IFN-gamma-producing T-cell frequencies against opportunistic pathogens and HIV-1 p24 did not change over time. HCV-specific T cells were observed ex vivo in two patients pretransplantation and in two others post-transplantation. HCV-specific in vitro amplification enabled the detection of HCV-specific IFN-gamma-producing responses in three further patients post-transplantation. Anti-HCV responses were observed independently of anti-HCV therapy and were undetectable in patients with severe hepatitis or liver fibrosis. CONCLUSIONS: These results demonstrate that LT in HIV-HCV coinfected patients is not deleterious to the immune system and does not alter immune responses directed against HCV, HIV, or opportunistic pathogens.
    Mots-clés : AIDS-Related Opportunistic Infections/immunology Adult CD4 Lymphocyte Count Carcinoma.
  • Samuel, D 2009, « MELD-Na as a prognostic score for cirrhotic patients: Hyponatremia and ascites are back in the game », J Hepatol, vol. 50, no. 4, p. 836-8.
    Résumé : Samuel, Didier; Comment; England; J Hepatol. 2009 Apr;50(4):836-8. doi: 10.1016/j.jhep.2008.12.015. Epub 2009 Jan 9.
  • Samuel, D 2009, « [Hepatic transplantation] », Gastroenterol Clin Biol, vol. 33, no. 1 Pt 1, p. 42.
    Résumé : Samuel, D; Editorial; France; Gastroenterol Clin Biol. 2009 Jan;33(1 Pt 1):42. doi: 10.1016/j.gcb.2008.11.003. Epub 2008 Dec 23.
    Mots-clés : &, Care, Continuity, data, Diseases/, Distribution, Donors/supply, Humans, Immunosuppression, Liver, numerical, of, Patient, surgery, Team, Tissue, Transplantation, Transplantation/methods/statistics.
  • Samuel, D 2009, « The option of liver transplantation for hepatitis B: where are we? », Dig Liver Dis, vol. 41 Suppl 2, p. S185-9.
    Résumé : Combination therapy with hepatitis B immunoglobulin (HBIG) plus nucleos(t)ide analogue have reduced the rate of hepatitis B virus (HBV) recurrence post-transplantation to less than 10% at long-term. HBV recurrence diagnosed after 3 years post-transplantation is extremely rare. Considering the cost and the constraints of HBV prophylaxis it was suggested to decrease the amount of HBIG given and possibly to discontinue HBIG administration. The additional debate was on the need to maintain or not any HBV prophylaxis at long-term or to maintain monoprophylaxis with one or two nucleos(t)ide analogues or to administer HBV vaccine: The supporters of this strategy argued that HBV recurrence can be easily controlled by administration of nucleos(t)ide analogues. However, it was shown that 50-80% of patients maintain HBV DNA in the liver, serum or peripheral mononuclear blood cells long-term after transplantation. In patients receiving monoprophylaxis with nucleos(t)ide analogues the risk of HBV reinfection increases with time due to HBV mutant strains. Vaccine protocols used to replace HBIG prophylaxis gave disappointing results. Combination protocols using low-doses of intramuscular HBIG plus nucleos(t)ide analogues have been associated with a low rate of HBV reinfection. In conclusion, long-term prophylaxis should be maintained in most patients except those with anti-HBs seroconversion.
    Mots-clés : Adenine/analogs & derivatives/therapeutic use Antiviral Agents/therapeutic use Drug Therapy.
  • Sarin, SK, Kumar, A, Almeida, JA, Chawla, YK, Fan, ST, Garg, H, de Silva, HJ, Hamid, SS, Jalan, R, Komolmit, P, Lau, GK, Liu, Q, Madan, K, Mohamed, R, Ning, Q, Rahman, S, Rastogi, A, Riordan, SM, Sakhuja, P, Samuel, D, Shah, S, Sharma, BC, Sharma, P, Takikawa, Y, Thapa, BR, Wai, CT & Yuen, MF 2009, « Acute-on-chronic liver failure: consensus recommendations of the Asian Pacific Association for the study of the liver (APASL) », Hepatol Int, vol. 3, no. 1, p. 269-82.
    Résumé : The Asian Pacific Association for the Study of the Liver (APASL) set up a working party on acute-on-chronic liver failure (ACLF) in 2004, with a mandate to develop consensus guidelines on various aspects of ACLF relevant to disease patterns and clinical practice in the Asia-Pacific region. Experts predominantly from the Asia-Pacific region constituted this working party and were requested to identify different issues of ACLF and develop the consensus guidelines. A 2-day meeting of the working party was held on January 22-23, 2008, at New Delhi, India, to discuss and finalize the consensus statements. Only those statements that were unanimously approved by the experts were accepted. These statements were circulated to all the experts and subsequently presented at the Annual Conference of the APASL at Seoul, Korea, in March 2008. The consensus statements along with relevant background information are presented in this review.
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  • Scoazec, JY, Sabourin, JC, Adle-Biassette, H, Bralet, MP, Chenard-Neu, MP, Cochand-Priollet, B, Guettier, C, Molinie, V, Paraf, F, Patey, N & Vielh, P 2009, « [Leading article from the editorial board] », Ann Pathol, vol. 29, no. 1, p. 1-2.
    Résumé : Scoazec, Jean-Yves; Sabourin, Jean-Christophe; Adle-Biassette, Homa; Bralet, Marie-Pierre; Chenard-Neu, Marie-Pierre; Cochand-Priollet, Beatrix; Guettier, Catherine; Molinie, Vincent; Paraf, Francois; Patey, Nathalie; Vielh, Philippe; Editorial; France; Ann Pathol. 2009 Feb;29(1):1-2. doi: 10.1016/j.annpat.2008.12.001. Epub 2009 Jan 31.
    Mots-clés : as, France, Humans, pathology/, Periodicals, Publishing, Topic, trends.

  • Surace, C, Arpicco, S, Dufaÿ-Wojcicki, A, Marsaud, V, Bouclier, C, Clay, D, Cattel, L, Renoir, J-M & Fattal, E 2009, « Lipoplexes targeting the CD44 hyaluronic acid receptor for efficient transfection of breast cancer cells », Molecular Pharmaceutics, vol. 6, no. 4, p. 1062-1073.
    Résumé : Lipoplexes containing a hyaluronic acid-dioleoylphosphatidylethanolamine (HA-DOPE) conjugate were designed to target the CD44 receptor on breast cancer cells. Cationic liposomes composed of a mixture of [2-(2,3-didodecyloxypropyl)hydroxyethyl]ammonium bromide (DE) and dioleoylphosphatidylethanolamine (DOPE) with or without HA-DOPE were prepared, characterized, and used to form a complex with plasmid DNA pCMV-luc. Lipoplexes displayed a negative zeta potential and a mean diameter between 250-300 nm. Cytotoxicity and transfection efficiency of the lipoplexes were determined on the MDA-MB-231and MCF-7 breast cancer cell lines. Cytotoxicity was not modified by the presence of HA-DOPE. However HA-DOPE increased the level of transfection on CD44-expressing MDA-MB-231 cells compared to the MCF-7 line, which expresses very low levels of CD44. The transfection on the MDA-MB-231 cells was highly inhibited by anti-CD44 Hermes-1 antibody but not by the nonspecific anti-ErbB2 antibody. In conclusion, cationic liposomes containing the HA-DOPE conjugate mediated good transfection on CD44 expressing cell lines in culture.
    Mots-clés : Antigens, CD44, Breast Neoplasms, Cell Survival, Drug Delivery Systems, Female, Gene Transfer Techniques, Humans, Hyaluronic Acid, Liposomes, Luciferases, Phosphatidylethanolamines, Reverse Transcriptase Polymerase Chain Reaction, RNA, Messenger, Transfection, Tumor Cells, Cultured.
  • Tateo, M, Roque-Afonso, AM, Antonini, TM, Medja, F, Lombes, A, Jardel, C, Teicher, E, Sebagh, M, Roche, B, Castaing, D, Samuel, D & Duclos-Vallee, JC 2009, « Long-term follow-up of liver transplanted HIV/hepatitis B virus coinfected patients: perfect control of hepatitis B virus replication and absence of mitochondrial toxicity », AIDS, vol. 23, no. 9, p. 1069-76.
    Résumé : BACKGROUND: In patients coinfected with hepatitis B virus (HBV) and human immunodeficiency virus (HIV), evolution toward cirrhosis and its complications is more rapid and severe than in patients infected with HBV alone. The outcome of liver transplantation in HBV-HIV-coinfected patients is poorly understood in terms of survival rate, HBV reactivation and mitochondrial toxicity on the liver graft. PATIENTS AND METHODS: Between November 2002 and June 2007, 13 HIV-positive patients underwent liver transplantation because of end-stage liver disease due to HBV with or without coinfection with hepatitis D or C virus. These patients were prospectively followed for an average of 32 +/- 5.2 months (range 10-63 months). RESULTS: All patients were alive at the end of the follow-up period and had normal liver function. Their HBV viral load was undetectable, no cccDNA was found in the liver graft and HIV infection was nonprogressive under antiretroviral therapy. Moreover, no mitochondrial toxicity was noted in the liver graft, as assessed by the spectrophotometric analysis of respiratory chain activities and by quantifying the mitochondrial DNA copy number. CONCLUSION: HBV-HIV-coinfected patients can successfully undergo liver transplantation with excellent results in terms of survival, control of HBV replication after transplantation and mitochondrial toxicity.
    Mots-clés : Adult Antiretroviral Therapy, Chronic/ complications/prevention & control Hepatitis C, Chronic/complications Hepatitis D, Highly Active/ adverse effects Female Follow-Up Studies Graft Survival HIV/physiology HIV Infections/ complications/mortality/virology Hepatitis B virus/physiology Hepatitis B.
  • Teicher, E, Abbara, C, Duclos-Vallee, JC, Antonini, T, Bonhomme-Faivre, L, Desbois, D, Samuel, D & Vittecoq, D 2009, « Enfuvirtide: a safe and effective antiretroviral agent for human immunodeficiency virus-infected patients shortly after liver transplantation », Liver Transpl, vol. 15, no. 10, p. 1336-42.
    Résumé : The aim of this study was to evaluate the impact of an enfuvirtide-based antiretroviral (ARV) regimen on the management of immunosuppression and follow-up in hepatitis C virus (HCV)/hepatitis B virus (HBV)/human immunodeficiency virus (HIV)-coinfected liver transplant patients in comparison with a lopinavir/ritonavir-based ARV regimen. Tacrolimus and cyclosporine trough concentrations were determined at a steady state during 3 periods: after liver transplantation without ARV treatment (period 1), at the time of ARV reintroduction (period 2), and 2 to 3 months after liver transplantation (period 3). The findings for 22 HIV-coinfected patients were compared (18 with HCV and 4 with HBV); 11 patients were treated with enfuvirtide and were matched with 11 lopinavir/ritonavir-exposed patients. During period 1, tacrolimus and cyclosporine A doses were 8 and 600 mg/day, respectively, and the trough concentrations were within the therapeutic range in both groups. In period 2, the addition of lopinavir/ritonavir to the immunosuppressant regimen enabled a reduction in the dose of immunosuppressants required to maintain trough concentrations within the therapeutic range (to 0.3 mg/day for tacrolimus and 75 mg/day for cyclosporine). Immunosuppressant doses were not modified by the reintroduction of enfuvirtide, there being no change in the mean trough concentrations over the 3 periods. CD4 cell counts remained at about 200 cells/mm3. The HIV RNA viral load remained undetectable. Both groups displayed signs of mild cytolysis and cholestasis due to the recurrence of HCV, whereas no renal insufficiency was observed. Enfuvirtide is an attractive alternative to standard ARV therapy, facilitating the management of drug-drug interactions shortly after liver transplantation. Moreover, the lack of liver toxicity renders this drug valuable in the event of a severe HCV recurrence.
    Mots-clés : Adult Anti-Retroviral Agents/ therapeutic use Cyclosporine/therapeutic use Dose-Response Relationship.
  • Thibault, V, Laperche, S, Akhavan, S, Servant-Delmas, A, Belkhiri, D & Roque-Afonso, AM 2009, « Impact of hepatitis B virus genotypes and surface antigen variants on the performance of HBV real time PCR quantification », J Virol Methods, vol. 159, no. 2, p. 265-70.
    Résumé : Quantitative PCR assays used to monitor hepatitis B virus (HBV) load differ in their ability to detect different HBV variants. This study evaluated the performance of the Abbott RT PCR assay for quantitating DNA from different HBV genotypes and from HBV variants bearing HBsAg gene mutations. The study was performed on a randomly-selected sample with a viral load >6logIU/mL for each genotype and on 25 HBsAg variants. Each sample was assayed using the Abbott RT assay and with the Roche Cobas AmpliPrep-Cobas TaqMan as a reference method. All HBV genotypes were detected with the Abbott RT assay with an equivalent dynamic range (1-8logIU/mL). For each genotype, the data suggest that the assay was linear over the entire dilution range (r(2): 0.985-0.995). For the 25 HBsAg variants, viral titres determined with the two assays correlated well (r(2): 0.929). The mean difference between the two methods was -0.295 (95% CI: -0.520 to -0.071). The difference was lower than 1log unit in all but two cases. In conclusion, the Abbott RT assay can detect and quantify DNA from different HBV variants with equivalent performance and is thus suitable for routine monitoring of patients with chronic HBV infections.
    Mots-clés : &, Antigens/genetics, B, Chain, Genotype, Hepatitis, Humans, isolation, Load/, methods, Mutation, Polymerase, purification, Reaction/, Surface, Viral, virus/.

  • Tran, TA, Fabre, M, Pariente, D, Craiu, I, Haroche, J, Charlotte, F, Eid, P, Durrbach, A, Taoufik, Y & Kone-Paut, I 2009, « Erdheim-Chester disease in childhood: a challenging diagnosis and treatment », J Pediatr Hematol Oncol, vol. 31, no. 10, p. 782-6, viewed sans date, .
    Résumé : Erdheim-Chester disease is a rare, non-Langerhans systemic histiocytosis characterized by bilateral sclerosis of the metaphyseal regions of the long bones and infiltration in other organs. The histopathologic hallmark is defined by a mononuclear infiltrate of foamy histiocytes and rare pathognomonic Touton giant cells with extensive fibrosis. This condition is exceptional in children. We report here a case of Erdheim-Chester disease in a 10-year-old girl with retroperitoneal infiltration and bone involvement, for whom the diagnosis was only established after a 3-year course with multiple biopsies. It is also the first pediatric case successfully treated with interferon-alpha suggesting that interferon-alpha can be a safe and efficient first-line therapy for this disease in children.
    Mots-clés : Bone, Cell, Child, Disease/*diagnosis/*drug, Diseases, Erdheim-Chester, Female, Humans, Induction, Interferon-alpha/therapeutic, Movement, Remission, Therapy, use.
  • Trocello, JM, Chappuis, P, Chaine, P, Remy, P, Debray, D, Duclos-Vallee, JC & Woimant, F 2009, « [Wilson disease] », Presse Med, vol. 38, no. 7-8, p. 1089-98.
    Résumé : Wilson Disease must be considered in very varied circumstances, including in patients older than 50 years. Its diagnosis is not based on a single test but on a group of findings. The copper levels may be difficult to interpret. Molecular biology can confirm the diagnosis in only 80% of cases. The advice of the reference center is necessary before beginning treatment: chelators or zinc salts. Lifetime treatment is required. Follow-up of these patients must be regular and multidisciplinary and should be conducted in association with the reference center. Inclusion in the national registry for Wilson Disease must be suggested to all patients. Contact: cmr.wilson@lrb.aphp.fr.
    Mots-clés : Messenger/genetics Registries Zinc/therapeutic use, Physiologic Patient Care Team Penicillamine/therapeutic use Phenotype RNA.

  • Uzan, G, Vanneaux, V, Delmau, C, Ayoubi, F, Gluckman, E & Larghero, J 2009, « [Cord blood circulating endothelial progenitors: perspectives for clinical use in cardiovascular diseases] », Bull Acad Natl Med, vol. 193, no. 3, p. 537-43; discussion 543-4, viewed sans date, .
    Résumé : The discovery of circulating endothelial progenitor cells (EPCs) in adult peripheral blood has opened up many exciting possibilities in vascular biology. Several studies have confirmed the existence of EPCs, as well as their bone marrow origin and their ability to integrate into vascular structures at sites of neoangiogenesis. EPCs appear to be naturally involved in the prevention of ischemia by participating directly in the vascularization process. Given their tropism for sites of neoangiogenesis, EPCs have clear therapeutic potential for treating ischemic diseases. If associated with other cell therapy products, they could improve tissue regeneration by promoting graft vascularization. However, the use of EPCs as a cell therapy product is limited by their rarity in peripheral blood. Cord blood contains many more EPCs, which are functional and can be expanded in culture. Their clinical use will require expansion in strictly controlled conditions and rigorous validation in preclinical models. EPCs could also serve as a quality markerforfrozen cord blood, showing the presence of non hematopoietic stem cells.
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  • Villeneuve, J, Block, A, Le Bousse-Kerdilès, M-C, Lepreux, S, Nurden, P, Ripoche, J & Nurden, AT 2009, « Tissue inhibitors of matrix metalloproteinases in platelets and megakaryocytes: a novel organization for these secreted proteins », Exp Hematol, vol. 37, no. 7, p. 849-56, viewed sans date, .
    Résumé : OBJECTIVE: Expression of tissue inhibitors of matrix metalloproteinases (TIMPs) is one way that activated platelets intervene in tissue remodeling and angiogenesis. Our study was designed to investigate their synthesis in megakaryocytes (MKs) and their storage in platelets. MATERIALS AND METHODS: TIMP expression in MKs derived from blood CD34(+) progenitor cells of normal donors and a megakaryocytic cell line (CHRF-288-11) grown in serum-free conditions and platelets from normal donors or two patients with gray platelet syndrome was studied by immunofluorescence labeling, reverse transcription-polymerase chain reaction, and western blotting. RESULTS: Biosynthesis of TIMPs 1-4 in MKs was indicated by presence of their messenger RNAs as shown by polymerase chain reaction and of their proteins. Immunofluorescence labeling suggested a primarily granular localization of TIMPs in MKs and platelets. But when colocalization with von Willebrand factor, fibrinogen, P-selectin, and other alpha-granule proteins was assessed in platelets by confocal microscopy, TIMP-1, -2, and -4 were localized as distinct fluorescent patches apart from the established alpha-granule markers and largely independent of platelet metalloproteinases. TIMP-3 differed for it also had an alpha-granule location. Western blotting confirmed the presence of TIMPs 1-4 in platelets and thrombin activation resulted in their extensive release to the medium. Platelets from two patients with gray platelet syndrome, congenitally deficient in alpha-granules, showed sparse labeling of von Willebrand factor and fibrinogen confined to vestigial alpha-granules; however, localization of the TIMPs was unchanged. CONCLUSIONS: TIMPs are synthesized and organized in MKs and platelets independently of other secreted proteins present in alpha-granule pools.
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  • Wakabayashi, T, Craessaerts, K, Bammens, L, Bentahir, M, Borgions, F, Herdewijn, P, Staes, A, Timmerman, E, Vandekerckhove, J, Rubinstein, E, Boucheix, C, Gevaert, K & De Strooper, B 2009, « Analysis of the gamma-secretase interactome and validation of its association with tetraspanin-enriched microdomains », Nat Cell Biol, vol. 11, no. 11, p. 1340-6, viewed sans date, .
    Résumé : Gamma-secretase, an aspartyl protease that belongs to the iCLiPs (intramembrane cleaving proteases) family, is a multiprotein complex that consists of presenilin (PS), nicastrin (NCT), Aph-1 and Pen-2 (ref. 1). It is responsible for generation of the beta-amyloid peptide (Abeta), the primary component of senile plaques in the brains of patients with Alzheimer's disease. Although the four components are necessary and sufficient for gamma-secretase activity, additional proteins are possibly involved in its regulation. Consequently, we purified proteins associated with the active gamma-secretase complex from reconstituted PS-deficient fibroblasts, using tandem affinity purification (TAP) and identified a series of proteins that transiently interact with the gamma-secretase complex and are probably involved in complex maturation, membrane trafficking and, importantly, the tetraspanin web. Tetraspanins form detergent-resistant microdomains in the cell membrane and regulate cell adhesion, cell signalling and proteolysis. Association of the gamma-secretase complex with tetraspanin-enriched microdomains provides an explanation for the previously documented localization of gamma-secretase to raft-like domains. Thus, these studies suggest that maintenance of the integrity of tetraspanin microdomains contributes to the refinement of proteolytic activity of the gamma-secretase complex.
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  • Wasmuth, HE, Tag, CG, Van de Leur, E, Hellerbrand, C, Mueller, T, Berg, T, Puhl, G, Neuhaus, P, Samuel, D, Trautwein, C, Kanse, SM & Weiskirchen, R 2009, « The Marburg I variant (G534E) of the factor VII-activating protease determines liver fibrosis in hepatitis C infection by reduced proteolysis of platelet-derived growth factor BB », Hepatology, vol. 49, no. 3, p. 775-80.
    Résumé : Genetic risk factors play an important role for the progression of liver fibrosis in chronic hepatitis C virus (HCV) infection, but functional data on specific alleles and their related proteins are limited. Platelet-derived growth factor BB (PDGF-BB) is one of the strongest mitogens for hepatic stellate cells and is considered as a critical soluble mediator of liver fibrosis in vitro and in vivo. The biological activity of PDGF-BB is dependent on its degradation by the factor VII-activating protease (FSAP). Here, we demonstrate that a coding polymorphism (G534E) in the gene for FSAP is significantly associated with severe HCV-induced liver fibrosis (odds ratio, 2.59; P = 0.017), which is independent of age, gender, and presence of diabetes in multivariate analysis. These genetic findings were replicated in a cohort of patients with liver transplantation due to HCV-induced cirrhosis (OR, 2.56; P = 0.011). Functional dissection of the association demonstrates that the single amino acid change encoded by G534E in the FSAP protein does not influence PDGFbeta receptor or alpha-smooth muscle actin expression but completely abrogates FSAP-mediated inhibition of PDGF-BB-induced proliferation of primary stellate cells in vitro. Conclusion: The G534E variant of FSAP is a risk locus for HCV-induced liver fibrosis and cirrhosis by determining PDGF-BB-mediated hepatic stellate cell proliferation through a single amino acid substitution in FSAP. FSAP G534E might be useful for risk stratification in patients with HCV infection.
    Mots-clés : Adult Aged Alleles Case-Control Studies Cell Proliferation/drug effects Cells, Genetic/ genetics Proto-Oncogene Proteins c-sis Risk Factors Serine Endopeptidases/ genetics.

  • Weber, A, Groyer-Picard, M-T & Dagher, I 2009, « Hepatocyte transplantation techniques: large animal models », Methods Mol Biol, vol. 481, p. 83-96, viewed sans date, .
    Résumé : The poor hepatocyte engraftment efficiency and the low level of their expansion in the host liver are a major limitation to cell therapy for the treatment of life-threatening liver diseases. Many rodent models have shown that liver repopulation via transplanted hepatocytes occurs only when liver growth capacity is impaired for an extended period of time. However, these models are not transposable to the clinics and to date there is no safe method to achieve this result in a clinical setting.Therefore, it is necessary to define on large animal models strategies that provide to transplanted hepatocytes sufficient proliferation stimuli to induce their division and that could permit a direct extrapolation to humans. Such procedures should be transposable to patients. We have defined a protocol of liver partial portal branch embolisation and shown that it induces the proliferation of transplanted hepatocytes in non-human primates (Macaca mulatta). This animal model is also appropriate to evaluate the lentiviral-mediated ex vivo gene therapy approach, since simian hepatocytes are efficiently transduced by HIV-1-derived lentivirus vectors.
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  • Weber, A, Groyer-Picard, M-T, Franco, D & Dagher, I 2009, « Hepatocyte transplantation in animal models », Liver Transpl, vol. 15, no. 1, p. 7-14, viewed sans date, .
    Résumé : More than 30 years after the first hepatocyte transplant to treat the Gunn rat, the animal model for Crigler-Najjar syndrome, there are still a number of impediments to hepatocyte transplantation. Numerous animal models are still used in work aimed at improving hepatocyte engraftment and/or long-term function. Although other cell sources, particularly hepatic and extrahepatic stem cells, are being explored, adult hepatocytes remain the cells of choice for the treatment of liver diseases by cell therapy. In recent years, diverse approaches have been developed in various animal models to enhance hepatocyte transduction and amplification in vitro and cell engraftment and functionality in vivo. They have led to significant progress in hepatocyte transplantation for the treatment of patients with metabolic diseases and for bridging patients with acute injury until their own livers regenerate. This review presents and considers the results of this work with a special emphasis on procedures that might be clinically applicable.
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  • Weng, HL, Liu, Y, Chen, JL, Huang, T, Xu, LJ, Godoy, P, Hu, JH, Zhou, C, Stickel, F, Marx, A, Bohle, RM, Zimmer, V, Lammert, F, Mueller, S, Gigou, M, Samuel, D, Mertens, PR, Singer, MV, Seitz, HK & Dooley, S 2009, « The etiology of liver damage imparts cytokines transforming growth factor beta1 or interleukin-13 as driving forces in fibrogenesis », Hepatology, vol. 50, no. 1, p. 230-43.
    Résumé : It is unknown whether transforming growth factor beta1 (TGF-beta1) signaling uniformly participates in fibrogenic chronic liver diseases, irrespective of the underlying origin, or if other cytokines such as interleukin (IL)-13 share in fibrogenesis (e.g., due to regulatory effects on type I pro-collagen expression). TGF-beta1 signaling events were scored in 396 liver tissue samples from patients with diverse chronic liver diseases, including hepatitis B virus (HBV), hepatitis C virus (HCV), Schistosoma japonicum infection, and steatosis/steatohepatitis. Phospho-Smad2 staining correlated significantly with fibrotic stage in patients with HBV infection (n = 112, P < 0.001) and steatosis/steatohepatitis (n = 120, P < 0.01), but not in patients with HCV infection (n = 77, P > 0.05). In tissue with HBx protein expression, phospho-Smad2 was detectable, suggesting a functional link between viral protein expression and TGF-beta1 signaling. For IL-13, immunostaining correlated with fibrotic stage in patients with HCV infection and steatosis/steatohepatitis. IL-13 protein was more abundant in liver tissue lysates from three HCV patients compared with controls, as were IL-13 serum levels in 68 patients with chronic HCV infection compared with 20 healthy volunteers (72.87 +/- 26.38 versus 45.41 +/- 3.73, P < 0.001). Immunohistochemistry results suggest that IL-13-mediated liver fibrogenesis may take place in the absence of phospho-signal transducer and activator of transcription protein 6 signaling. In a subgroup of patients with advanced liver fibrosis (stage > or =3), neither TGF-beta nor IL-13 signaling was detectable. Conclusion: Depending on the cause of liver damage, a predominance of TGF-beta or IL-13 signaling is found. TGF-beta1 predominance is detected in HBV-related liver fibrogenesis and IL-13 predominance in chronic HCV infection. In some instances, the underlying fibrogenic mediator remains enigmatic.
    Mots-clés : beta1/, Cirrhosis/, Diseases/etiology, etiology, Factor, Growth, Humans, Interleukin-13/, Liver, physiology, Transforming.
  • Wyplosz, B, Van der Vliet, D, Consigny, PH, Calmus, Y, Mamzer-Bruneel, MF, Guillemain, R, Malvy, D, Samuel, D, Vittecoq, D & Launay, O 2009, « [Vaccinations for the traveling adult solid organ transplant recipient (excluding hematopoietic stem cell transplant recipients)] », Med Mal Infect, vol. 39, no. 4, p. 225-33.
    Résumé : Progress in transplantation technique has offered a growing number of solid organ transplant recipients the opportunity to travel to tropical and low-income countries. The issue of vaccine-preventable diseases is a challenging question in immunocompromised patients including those with solid organ transplant. Since the response to vaccines is weakened in case of chronic organ failure, candidates should be vaccinated early in the course of the disease. Clinicians should implement a vaccinal strategy until the patient is scheduled for transplantation and monitor its efficacy by serological assays. Live attenuated vaccines (such as yellow fever, measles-mumps-rubella, or chicken pox) are contra-indicated in solid organ transplant recipients and, when indicated, should be administered prior to transplantation, particularly in foreign-born patients highly likely to visit friends and relatives in endemic areas. Vaccinations for transplant recipients considering international travel should be realized according to the risk of acquiring vaccine-preventable diseases but also on both tolerance and immune response which are affected by degree and duration of immunosuppression, comorbidities, and type of organ transplanted. Routine and specific vaccinations for solid organ transplant recipients, as well as travel-related vaccination (such as hepatitis A, typhoid, meningococcal meningitis, rabies, tick-born encephalitis, Japanese encephalitis, and cholera) should be considered during a specific pretravel medical consultation. However, vaccination should be avoided in the 6 months following transplantation when patients are usually receiving the highest doses of immunosuppressive drugs. In this comprehensive review, we provide vaccination schedules based on published studies and guidelines for vaccination of solid organ transplant recipients.
    Mots-clés : Adult, Humans, Organ, Transplantation, Travel, Vaccines.

2008



  • Adam, R, de Haas, RJ, Wicherts, DA, Aloia, TA, Delvart, V, Azoulay, D, Bismuth, H & Castaing, D 2008, « Is hepatic resection justified after chemotherapy in patients with colorectal liver metastases and lymph node involvement? », J Clin Oncol, vol. 26, no. 22, p. 3672-80, viewed sans date, .
    Résumé : PURPOSE: For patients with colorectal liver metastases (CLM), regional lymph node (RLN) involvement is one of the worst prognostic factors. The objective of this study was to evaluate the ability of a multidisciplinary approach, including preoperative chemotherapy and hepatectomy, to improve patient outcomes. PATIENTS AND METHODS: Outcomes for a consecutively treated group of patients with CLM and simultaneous RLN involvement were compared with a cohort of patients without RLN involvement. Univariate and multivariate analysis of clinical variables was used to identify prognostic factors in this high-risk group. Results Of the 763 patients who underwent resection at our institution for CLM between 1992 and 2006, 47 patients (6%) were treated with hepatectomy and simultaneous lymphadenectomy. All patients had received preoperative chemotherapy. Five-year overall survival (OS) for patients with and without RLN involvement were 18% and 53%, respectively (P < .001). Five-year disease-free survival rates were 11% and 23%, respectively (P = .004). When diagnosed preoperatively, RLN involvement had an increased 5-year OS compared with intraoperative detection, although the difference was not significant (35% v 10%; P = .18). Location of metastatic RLN strongly influenced survival, with observed 5-year OS of 25% for pedicular, 0% for celiac, and 0% for para-aortic RLN (P = .001). At multivariate analysis, celiac RLN involvement and age >or= 40 years were identified as independent poor prognostic factors. CONCLUSION: Combined liver resection and pedicular lymphadenectomy is justified when RLN metastases respond to or are stabilized by preoperative chemotherapy, particularly in young patients. In contrast, this approach does not benefit patients with celiac and/or para-aortic RLN involvement, even when patients' disease is responding to preoperative chemotherapy.
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  • Adam, R, Wicherts, DA, de Haas, RJ, Aloia, T, Lévi, F, Paule, B, Guettier, C, Kunstlinger, F, Delvart, V, Azoulay, D & Castaing, D 2008, « Complete pathologic response after preoperative chemotherapy for colorectal liver metastases: myth or reality? », J Clin Oncol, vol. 26, no. 10, p. 1635-41, viewed sans date, .
    Résumé : PURPOSE: Complete clinical response (CCR) of colorectal liver metastases (CLM) following chemotherapy is of limited predictive value for complete pathologic response (CPR) and cure of the disease. The objective of this study was to determine predictive factors of CPR as well as its impact on survival. PATIENTS AND METHODS: From January 1985 to July 2006, 767 consecutive patients with CLM underwent liver resection after systemic chemotherapy. Patients with CPR were compared with patients without CPR. RESULTS: Twenty-nine of 767 (4%) patients had CPR, and none of these 29 patients had CCR. Patients with CPR (mean age, 54 years) had a mean number of 3.3 metastases at diagnosis (mean size, 29.3 mm). Objective response and stable disease were observed in 79% and 21% of cases, respectively. Postoperative mortality rate was 0%. After a median follow-up of 52.2 months (range, 1.1 to 193.0 months), overall 5-year survival was 76% for patients with CPR compared with 45% for patients without CPR (P = .004). Independent predictive factors for CPR were: age <or= 60 years, size of metastases <or= 3 cm at diagnosis, carcinoembryonic antigen (CEA) level at diagnosis <or= 30 ng/mL, and objective response following chemotherapy. The probability of CPR ranged from 0.2% when all factors were absent to 30.9% when all were present. CONCLUSION: CPR was observed in 4% of patients with CLM treated with preoperative chemotherapy. However, CPR may occur in almost one-third of objective responders age <or= 60 years with metastases <or= 3 cm and low CEA values. CPR is associated with uncommon high survival rates.
    Mots-clés : Adenocarcinoma/ drug therapy/ secondary/surgery Adult Aged Aged.
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  • Antonini, TM & Samuel, D 2008, « Transplantation et cancers », Oncologie, vol. 10, no. 6, p. 406 - 407.
    Résumé : L’incidence des cancers chez les patients transplantés est en train d’augmenter et le traitement immunosuppresseur, qui doit être maintenu afin d’éviter le rejet, en est une des principales causes. Les cancers de la peau, du sang et du système gastro-intestinal sont les plus fréquents. L’évolution de ces cancers est souvent plus agressive que dans la population générale et donc le dépistage et la prise en charge (avec la diminution des traitements immunosuppresseurs) de ces patients doivent être les plus rapides possibles. The incidence of cancer is increased in transplant recipients; this increase is due to the immunosuppressive treatment but this treatment must be maintained to prevent rejection. Skin cancer, posttransplant lymphoproliferative disorders (PDLT) and gastroenteric tumours are the most frequently observed malignancies. In this population, these cancers have a more aggressive course than in the general population, making indispensable their early detection and management, including the reduction of immunosuppressive treatment.
    Mots-clés : Cancer, De, Immunosuppression, novo, Transplantation, tumors.

  • Arduise, C, Abache, T, Li, L, Billard, M, Chabanon, A, Ludwig, A, Mauduit, P, Boucheix, C, Rubinstein, E & Le Naour, F 2008, « Tetraspanins regulate ADAM10-mediated cleavage of TNF-alpha and epidermal growth factor », J Immunol, vol. 181, no. 10, p. 7002-13, viewed sans date, .
    Résumé : Several cytokines and growth factors are released by proteolytic cleavage of a membrane-anchored precursor, through the action of ADAM (a disintegrin and metalloprotease) metalloproteases. The activity of these proteases is regulated through largely unknown mechanisms. In this study we show that Ab engagement of several tetraspanins (CD9, CD81, CD82) increases epidermal growth factor and/or TNF-alpha secretion through a mechanism dependent on ADAM10. The effect of anti-tetraspanin mAb on TNF-alpha release is rapid, not relayed by intercellular signaling, and depends on an intact MEK/Erk1/2 pathway. It is also associated with a concentration of ADAM10 in tetraspanin-containing patches. We also show that a large fraction of ADAM10 associates with several tetraspanins, indicating that ADAM10 is a component of the "tetraspanin web." These data show that tetraspanins regulate the activity of ADAM10 toward several substrates, and illustrate how membrane compartmentalization by tetraspanins can control the function of cell surface proteins such as ectoproteases.
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  • Arnoult, D 2008, « Apoptosis-associated mitochondrial outer membrane permeabilization assays », Methods, vol. 44, no. 3, p. 229-34, viewed sans date, .
    Résumé : Following most cell death signals, pro-apoptotic Bcl-2 members as Bax and Bak are activated and oligomerize into the mitochondria outer membrane, triggering its permeabilization and release into the cytosol of soluble apoptogenic factors such as cytochrome c involved in caspase activation. Thus, in many studies focused on apoptosis, cytochrome c release within cells is frequently examined to assess Bax/Bak activation and mitochondrial outer membrane permeabilization. In addition, cytochrome c release can also be investigated in vitro in functional mitochondria that have been isolated from cultured cells, offering a number of advantages. Here, protocols for measuring cytochrome c release from intact cells as well as from isolated mitochondria is detailed. Finally, assays to investigate Bax/Bak activation and olimerization are also presented.
    Mots-clés : *Apoptosis, *Cell, Animals, Antagonist-Killer, bcl-2, bcl-2-Associated, c/*secretion, Cytochromes, Homologous, Humans, Membrane, Membranes/*metabolism, Mitochondrial, Permeability, Protein/chemistry/metabolism, X.

  • Arnoult, D, Skaletskaya, A, Estaquier, J, Dufour, C & Goldmacher, VS 2008, « The murine cytomegalovirus cell death suppressor m38.5 binds Bax and blocks Bax-mediated mitochondrial outer membrane permeabilization », Apoptosis, vol. 13, no. 9, p. 1100-10, viewed sans date, .
    Résumé : Apoptosis is increasingly implicated as an early line of defense against viral infections. Viruses have devised numerous strategies to delay apoptosis of infected cells. Many viruses encode cell death suppressors that target mitochondrial apoptotic signaling pathway, indicating the importance of this pathway in the anti-viral response. Human and primate cytomegaloviruses encode the viral mitochondria-localized inhibitor of apoptosis vMIA, but no overt homologue of vMIA was identified in any non-primate cytomegalovirus. Here we report that m38.5 protein encoded by murine cytomegalovirus, which is unrelated to vMIA in its amino acid sequence, delays death receptor ligation-induced cell death, and that m38.5 associates with Bax, recruits it to mitochondria, and blocks Bax-mediated but not Bak-mediated mitochondrial outer membrane permeabilization. Thus, primate and murine cytomegaloviruses have evolved non-homologous but functionally similar cell death suppressors selectively targeting the Bax-mediated branch of the mitochondrial apoptotic signaling pathway, indicating the importance of this branch in the response of diverse host organisms against cytomegalovirus infections.
    Mots-clés : Animals Antigens, CD95/metabolism Cell Death HCT116 Cells HeLa Cells Humans Mice Mitochondrial Membranes/*metabolism Muromegalovirus/*metabolism Permeability Protein Binding Protein Conformation Protein Transport RNA, Death Domain/metabolism Viral Proteins/*metabolism bcl-2-Associated X Protein/chemistry/*metabolism, Small Interfering/metabolism Receptors.
  • Arrais, TC, Van Dooren, S, Vandamme, AM, Brechot, C, Rimlinger, F, Silva, AE, Perez, RM, Ferraz, ML & Thiers, V 2008, « Change in hepatitis C virus genotype in hemodialysis patients after end-of-treatment response to interferon monotherapy–relapse or re-infection? », J Med Virol, vol. 80, no. 1, p. 80-6.
    Résumé : Hepatitis C virus (HCV) infection remains common among hemodialysis patients and its occurrence is related mainly to nosocomial spread. Although dialysis patients with HCV infection respond well to interferon-based therapy, relapse is frequent. This study aimed at a selected group of hemodialysis patients infected with HCV infection undergoing interferon therapy who achieved end-of-treatment virological response but became HCV-RNA positive again 6 months after end-of-treatment. It was evaluated whether de novo HCV-RNA positivity in these non-sustained responders occurred due to lack of clearance of HCV after the initial response to interferon-alpha (relapse) or due to re-infection with a new strain (re-infection). Genotyping by Inno-LiPA and by phylogenetic tree analysis using partial HCV-NS5B sequences at two evaluation points: pre-treatment (T0) and 6 months after end-of-treatment (T18). Non-sustained responders (n = 15) carried subtypes 1a (8 patients), 1b (4 patients), 3a (2 patients), and 4a (1 patient) before treatment. Identical subtypes were detected in 10 patients at T18. Five patients changed genotypes at T18, suggesting nosocomial re-infection. This study emphasizes the importance of epidemiologic measures to control the re-exposure of hemodialysis patients treated previously for HCV infection.
    Mots-clés : Genotype Hepacivirus/genetics Hepatitis C/ drug therapy/epidemiology/therapy/ virology Humans Interferons/ therapeutic use Phylogeny RNA, Viral/analysis Recurrence Renal Dialysis Retrospective Studies Viral Nonstructural Proteins/ genetics.

  • Avouac, J, Juin, F, Wipff, J, Couraud, PO, Chiocchia, G, Kahan, A, Boileau, C, Uzan, G & Allanore, Y 2008, « Circulating endothelial progenitor cells in systemic sclerosis: association with disease severity », Ann Rheum Dis, vol. 67, no. 10, p. 1455-60, viewed sans date, .
    Résumé : BACKGROUND: Heterogeneous data have been reported regarding the detection and number of circulating endothelial progenitor cells (EPCs) in systemic sclerosis (SSc). OBJECTIVE: We investigated the number of circulating EPCs using recent recommendations and we quantified their late outgrowth in patients with SSc and healthy controls. PATIENTS AND METHODS: EPCs, defined as Lin-/7AAD-/CD34+/CD133+/VEGFR-2+ cells, were quantified in 50 patients with SSc (mean age: 55 (16) years, disease duration: 9 (9) years) and 26 controls (mean age: 53 (19) years) by cell sorting/flow cytometry and by counting late outgrowth colony-forming units (CFU). RESULTS: Patients with SSc displayed higher circulating EPC counts than controls (median 86 (5-282) vs 49 (5-275)) EPCs for 1 million Lin- mononuclear cells; p = 0.01). Lower EPC counts were associated with the higher Medsger's severity score (p = 0.01) and with the presence of past and/or current digital ulcers (p = 0.026). There was no difference for the number of late outgrowth EPC-CFUs between patients with SSc and controls in cell culture evaluation. The formation of colonies was associated with higher levels of circulating EPCs (p = 0.02) and the number of colonies correlated with levels of EPCs (R = 0.73, p = 0.0004), validating our combination of fluorescence-activated cell sorter surface markers. CONCLUSIONS: We quantified circulating EPCs with an accurate combination of markers herein validated. Our data demonstrate increased circulating EPC levels in SSc, supporting their mobilisation from bone marrow. Furthermore, the subset of patients with digital vascular lesions and high severity score displayed low EPC counts, suggesting increased homing at this stage. The predictive value of this biomarker now warrants further evaluation.
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  • Avouac, J, Wipff, J, Goldman, O, Ruiz, B, Couraud, PO, Chiocchia, G, Kahan, A, Boileau, C, Uzan, G & Allanore, Y 2008, « Angiogenesis in systemic sclerosis: impaired expression of vascular endothelial growth factor receptor 1 in endothelial progenitor-derived cells under hypoxic conditions », Arthritis Rheum, vol. 58, no. 11, p. 3550-61, viewed sans date, .
    Résumé : OBJECTIVE: To assess angiogenesis and explore the expression and regulation of vascular endothelial growth factor (VEGF), VEGF receptor 1 (VEGFR-1), and VEGFR-2, the leading mediators of angiogenesis, in SSc patients and controls. METHODS: Late-outgrowth endothelial progenitor cells (EPCs), isolated from the peripheral blood of systemic sclerosis (SSc) patients and controls, and human umbilical vein endothelial cells (HUVECs) were assessed under normal and hypoxic conditions. Genomic background was evaluated in a large case-control study (including 659 patients with SSc and 511 controls) using tag single-nucleotide polymorphisms on VEGFR1 and VEGFR2 genes. RESULTS: EPCs from SSc patients had the phenotype of genuine endothelial cells and displayed in vitro angiogenic properties similar to those of HUVECs and control EPCs under basal conditions, as determined by flow cytometry, tube formation, and migration assay. However, after 6 hours of hypoxic exposure, EPCs from SSc patients exhibited lower induced expression of VEGFR-1 at the messenger RNA and protein levels, but similar VEGF and VEGFR-2 expression, compared with HUVECs or EPCs from healthy controls. There was no evidence of defective expression of hypoxia-inducible factor 1alpha. These results were supported by the lower serum levels of soluble VEGFR-1 found in SSc patients (n = 187) compared with healthy controls (n = 48) (mean +/- SD 163.7 +/- 98.5 versus 210.4 +/- 109.5 pg/ml; P = 0.0042). These abnormalities did not seem to be related to genomic background. CONCLUSION: Our findings shed new light on the possible role of VEGFR-1 in the main vascular disturbances that occur in SSc and lead to more severe disease.
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  • Avouac, J, Uzan, G, Kahan, A, Boileau, C & Allanore, Y 2008, « Endothelial progenitor cells and rheumatic disorders », Joint Bone Spine, vol. 75, no. 2, p. 131-7, viewed sans date, .
    Résumé : In human adults, new blood vessels may form via endothelial sprouting from pre-existing endothelial cells/angioblasts (angiogenesis) or via the recruitment of circulating endothelial progenitor cells (EPCs) (vasculogenesis). EPCs are a population of bone marrow-derived cells able to differentiate into mature endothelial cells and participating in the formation of new blood vessels. The molecular phenotype of EPCs and processes leading to their mobilization from bone marrow and homing to neovascularization sites remain unclear. There is still debate regarding methods for their quantification and isolation. In the field of rheumatology, EPCs have been studied in multiple myeloma and inflammatory rheumatic disorders. In myeloma, data suggest that EPCs could be reliable biomarkers of tumor angiogenesis, growth and antiangiogenic therapy efficacy. Recent studies suggest that EPCs are involved in synovial vascularization, and may contribute to the increased cardiovascular morbidity and mortality in rheumatoid arthritis, known features of this disease. In systemic lupus erythematosus, preliminary data suggest that EPCs are decreased. Results available in systemic sclerosis are consistent with the hypothesis that EPCs are recruited during active disease; however, their levels may be depleted as the disease progresses and under chronic ischemic conditions. EPCs are important in vasculogenesis, and may be involved in other systemic features of inflammatory rheumatic disorders.
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  • Bafna, S, Singh, AP, Moniaux, N, Eudy, JD, Meza, JL & Batra, SK 2008, « MUC4, a multifunctional transmembrane glycoprotein, induces oncogenic transformation of NIH3T3 mouse fibroblast cells », Cancer Res, vol. 68, no. 22, p. 9231-8.
    Résumé : Numerous studies have established the association of MUC4 with the progression of cancer and metastasis. An aberrant expression of MUC4 is reported in precancerous lesions, indicating its early involvement in the disease process; however, its precise role in cellular transformation has not been explored. MUC4 contains many unique domains and is proposed to affect cell signaling pathways and behavior of the tumor cells. In the present study, to decipher the oncogenic potential of MUC4, we stably expressed the MUC4 mucin in NIH3T3 mouse fibroblast cells. Stable ectopic expression of MUC4 resulted in increased growth, colony formation, and motility of NIH3T3 cells in vitro and tumor formation in nude mice when cells were injected s.c. Microarray analysis showed increased expression of several growth-associated and mitochondrial energy production-associated genes in MUC4-expressing NIH3T3 cells. In addition, expression of MUC4 in NIH3T3 cells resulted in enhanced levels of oncoprotein ErbB2 and its phosphorylated form (pY(1248)-ErbB2). In conclusion, our studies provide the first evidence that MUC4 alone induces cellular transformation and indicates a novel role of MUC4 in cancer biology.
    Mots-clés : Animals Cell Movement Cell Proliferation Cell Transformation, erbB-2/genetics Transfection, Neoplastic Gene Expression Profiling Mice Mucin-4/ physiology NIH 3T3 Cells Receptor.
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  • Ballot, E, Le Naour, F, Huguet, S, Tahiri, F, Samuel, D, Johanet, C & Duclos-Vallee, JC 2008, « Protéomique et hépatites auto-immunes : techniques et résultats », Immuno-analyse et biologie spécialisée, vol. 23, no. 5, p. 289-310.
    Résumé : Identifier la cible antigénique des autoanticorps est fondamentale, tant dans un cadre physiopathologique qu’analytique avec l’émergence dans le champ de la sérologie auto-immune de méthodes à « haut débit » à travers la technologie Luminex® ou les biopuces à antigènes. Un procédé récent d’identification de ces autoantigènes découle de l’analyse protéomique et permet d’appréhender les protéines telles qu’elles se présentent dans la cellule avec les modifications post-traductionnelles qui peuvent entrer dans la constitution des sites épitopiques. Cet article rapporte les différents moyens susceptibles d’être mis en oeuvre pour identifier un autoantigène. Une importance particulière sera apportée à l’analyse sérologique du protéome, combinaison de l’électrophorèse bidimensionnelle, de l’immunoblot, d’une analyse d’image et enfin, d’une identification des antigènes cibles des autoanticorps par spectrométrie de masse. Ces différents procédés seront ensuite illustrés à travers l’identification des principaux autoantigènes rencontrés dans les hépatites auto-immunes. Identification of autoantibodies targets is of importance for both physiopathology discussion and analytical research with the recent development of multiplexing system like Luminex® technology, built on flow cytometry or antigen biochip immunoassay. A new technique for antigen identification uses the proteomic analysis, which focuses on genes products, with their posttranslational modifications. Indeed, protein maturation can play an important role in epitopes generation. The purpose of this study is to review the main techniques for autoantigens identification, with a special development for the serological proteome analysis, combination of two-dimensional electrophoresis, immunoblotting assay, image analysis and mass spectrometry identification of interest immunoreactive spots. These techniques will be illustrated through identifications of the main autoantigens found in autoimmune hepatitis.
    Mots-clés : auto-antigènes, Autoantigen, Autoimmune, des, disease, Hepatitis, Identification, Mass, Proteome/*analysis, spectrometry.

  • Bekkal Brikci, F, Clairambault, J, Ribba, B & Perthame, B 2008, « An age-and-cyclin-structured cell population model for healthy and tumoral tissues », J Math Biol, vol. 57, no. 1, p. 91-110, viewed sans date, .
    Résumé : We present a nonlinear model of the dynamics of a cell population divided into proliferative and quiescent compartments. The proliferative phase represents the complete cell cycle (G (1)-S-G (2)-M) of a population committed to divide at its end. The model is structured by the time spent by a cell in the proliferative phase, and by the amount of Cyclin D/(CDK4 or 6) complexes. Cells can transit from one compartment to the other, following transition rules which differ according to the tissue state: healthy or tumoral. The asymptotic behaviour of solutions of the nonlinear model is analysed in two cases, exhibiting tissue homeostasis or tumour exponential growth. The model is simulated and its analytic predictions are confirmed numerically.
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  • Berlioz-Arthaud, A, Barny, S, Yvon, JF, Roque-Afonso, AM & Dussaix, E 2008, « [Laboratory based hepatitis A surveillance in New Caledonia: from an endemic to an epidemic pattern (1986-2007)] », Bull Soc Pathol Exot, vol. 101, no. 4, p. 336-42.
    Résumé : This study aimed at describing the evolution of the epidemiological pattern of hepatitis A in New Caledonia since 1986 and the recent epidemic which occurred in 2005-2006, regarding particularly its demographic and virological aspects and the public health response implemented. The annual or monthly activity records for Hepatitis A sero-diagnostic performed at the Pasteur Institute of New Caledonia were processed in a retrospective analysis (9723 samples tested for the detection of IgM to hepatitis A). Over the 2004-2006 period, a phylogenetic study of representative strains from New Caledonia and other Pacific islands was carried out by the French National Reference Laboratory for hepatitis A (Paul-Brousse hospital, Villejuif, France). RESULTS: The continuous improvement of hygiene that occurred in New Caledonia during the last two decades led to a dramatic drop in the frequency of hepatitis A among patients tested, ranging from an average value of 79 cases (14%) for the 1986-1999 period to 0 case from 2002. However, in 2005, a strong increasing number of confirmed cases was notified, mainly among young people (78% were under the age of 20). In 2006, this epidemic reached the island of Futuna where it involved more than 1% of the total population (56 cases). The phylogenetic study has confirmed the clonality of the virus circulating during this epidemic, not related to other regional strains (Fiji, Vanuatu, New Zealand) nor with a New Caledonian strain from the previous endemic period. This transition situation, with persistence of a high epidemic risk, should encourage the health authorities to implement adapted response strategies, based in particular on systematic case declaration and targeted immunisation programmes.
    Mots-clés : &, A, A/, Base, Caledonia/epidemiology, Chain, data, disease, Diseases/, Endemic, epidemiology, Hepatitis, Humans, Melanesia/epidemiology, New, numerical, Outbreaks/, Phylogeny, Polymerase, purification, Reaction, Reverse, Sequence, statistics, Transcriptase, virus/classification/genetics/isolation.

  • Bertho, JM, Roy, L, Souidi, M, Benderitter, M, Gueguen, Y, Lataillade, JJ, Prat, M, Fagot, T, De Revel, T & Gourmelon, P 2008, « New biological indicators to evaluate and monitor radiation-induced damage: an accident case report », Radiat Res, vol. 169, no. 5, p. 543-50, viewed sans date, .
    Résumé : The aim of this work was to use several new biological indicators to evaluate damage to the main physiological systems in a victim exposed accidentally to ionizing radiation. Blood samples were used for biological dosimetry and for measurement of the plasma concentrations of several molecules: Flt3 ligand to assess the hematopoietic system, citrulline as an indicator of the digestive tract, and several oxysterols as lipid metabolism and vascular markers. The cytogenetic evaluation estimated the dose to the victim to be between 4.2 and 4.8 Gy, depending on the methodology used. Monitoring the Flt3 ligand demonstrated the severity of bone marrow aplasia. In contrast, the citrulline concentration showed the absence of gastrointestinal damage. Variations in oxysterol concentrations suggested radiation-induced damage to the liver and the cardiovascular system. These results were correlated with those from classic biochemical markers, which demonstrated severe damage to the hematopoietic system and suggested the appearance of subclinical damage to the liver and cardiovascular system. These results demonstrate for the first time the importance of a multiparameter biological approach in the evaluation of radiation damage after accidental irradiation.
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  • Bogani, C, Ponziani, V, Guglielmelli, P, Desterke, C, Rosti, V, Bosi, A, Le Bousse-Kerdilès, M-C, Barosi, G, Vannucchi, AM & Consortium, MDR 2008, « Hypermethylation of CXCR4 promoter in CD34+ cells from patients with primary myelofibrosis », Stem Cells, vol. 26, no. 8, p. 1920-30, viewed sans date, .
    Résumé : Constitutive mobilization of CD34(+) cells in patients with primary myelofibrosis (PMF) has been attributed to proteolytic disruption of the CXCR4/SDF-1 axis and reduced CXCR4 expression. We document here that the number of circulating CD34(+)/CXCR4(+) cells in PMF patients, as well as the cellular CXCR4 expression, was directly related to CXCR4 mRNA level and that reduced CXCR4 mRNA level was not due to SDF-1-induced downregulation. To address whether epigenetic regulation contributes to defective CXCR4 expression, we studied the methylation status of the CXCR4 promoter using methylation-specific polymerase chain reaction and methylation-specific sequencing in the JAK2V617F-positive HEL cell line and in CD34(+) cells. We found that CD34(+) cells from PMF patients, unlike those from normal subjects, presented hypermethylation of CXCR4 promoter CpG island 1. Following incubation with the demethylating agent 5-Aza-2'-deoxycytidine (5-AzaD), the percentage of PMF CD34(+) cells expressing CXCR4 increased 3-10 times, whereas CXCR4 mRNA level increased approximately 4 times. 5-AzaD-treated PMF CD34(+) cells displayed almost complete reversal of CpG1 island 1 hypermethylation and showed enhanced migration in vitro in response to SDF-1. These data point to abnormal methylation of the CXCR4 promoter as a mechanism contributing to constitutive migration of CD34(+) cells in PMF. Disclosure of potential conflicts of interest is found at the end of this article.
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  • Botterel, F, Farrugia, C, Ichai, P, Costa, JM, Saliba, F & Bretagne, S 2008, « Real-time PCR on the first galactomannan-positive serum sample for diagnosing invasive aspergillosis in liver transplant recipients », Transpl Infect Dis, vol. 10, no. 5, p. 333-8.
    Résumé : Invasive aspergillosis (IA) is a life-threatening complication of liver transplantation. Detection of circulating galactomannan (GM) in serum samples is a method to improve the microbiological diagnosis in patients at risk for IA. However, the assay is hampered by false-positive results. The search for circulating Aspergillus DNA in the first GM-positive sample could improve the specificity of the test. Among 484 liver transplant recipients followed in a single center over 4 years, 25 patients had at least 1 GM-positive serum sample. The threshold of GM positivity was a ratio >or=1. These 25 patients were classified by the clinicians as probable IA (n=11), possible IA (n=2), and no IA (n=12) using the EORTC/MSG criteria with blinding to the polymerase chain reaction (PCR) results. After 1 mL aliquots of the first GM-positive serum sample were thawed, 2 independent DNA extractions were performed using the MagNA Pure Compact apparatus. Real-time amplification targeted at Aspergillus fumigatus mitochondrial DNA was performed on 10 microL of the final eluate in duplicate in the 2 independent DNA extractions using a LightCycler instrument. A sample was considered positive when the crossing point was <or=43 cycles in at least 2 out of the 4 replicates. Among the 13 probable or possible IA, 8 patients were PCR positive. The other 12 patients who had no IA were all PCR negative. Our data suggest that a concomitant real-time PCR performed on the first GM-positive sample improves the specificity of the first GM-positive assay result.
    Mots-clés : Adolescent Adult Aged Aspergillosis/blood/ diagnosis/etiology Aspergillus/genetics/ isolation & purification DNA Primers DNA, Fungal/ blood Female Humans Liver Transplantation/ adverse effects Male Mannans/ blood Middle Aged Opportunistic Infections/blood/ diagnosis/etiology Polymerase Chain Reaction Retrospective Studies Sensitivity and Specificity Young Adult.

  • Bouchahda, M, Macarulla, T, Spano, JP, Bachet, JB, Lledo, G, Andre, T, Landi, B, Tabernero, J, Karaboué, A, Domont, J, Levi, F & Rougier, P 2008, « Cetuximab efficacy and safety in a retrospective cohort of elderly patients with heavily pretreated metastatic colorectal cancer », Crit Rev Oncol Hematol, vol. 67, no. 3, p. 255-62, viewed sans date, .
    Résumé : BACKGROUND: Few data are available from clinical trials for elderly patients receiving cetuximab. PATIENTS AND METHODS: The clinical data of consecutive patients aged > or =70 years given cetuximab for metastatic CRC were retrospectively captured from hospital pharmacy registries in seven centers. RESULTS: Fifty-six patients received cetuximab+/-with irinotecan. Median age was 76 years (70-84), 86% of patients were pretreated with fluoropyrimidines, irinotecan and oxaliplatin and 69.6% had documented resistance to irinotecan. Objective response rate was 21% (95% CI: 11-32%). The median progression-free survival was 4.4 months (95% CI: 3.0-5.7 months) and the median overall survival was 16.0 months (95% CI: 13.5-18.5 months). Skin rash occurred in 75% of the patients (11% grade 3) and diarrhea in 80% (20% grades 3-4). CONCLUSION: Tolerability of cetuximab was acceptable in elderly patients with pretreated metastatic CRC. Efficacy appeared similar to that observed in younger patients.
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  • Camparo, P, Vasiliu, V, Molinie, V, Couturier, J, Dykema, KJ, Petillo, D, Furge, KA, Comperat, EM, Lae, M, Bouvier, R, Boccon-Gibod, L, Denoux, Y, Ferlicot, S, Forest, E, Fromont, G, Hintzy, MC, Laghouati, M, Sibony, M, Tucker, ML, Weber, N, Teh, BT & Vieillefond, A 2008, « Renal translocation carcinomas: clinicopathologic, immunohistochemical, and gene expression profiling analysis of 31 cases with a review of the literature », Am J Surg Pathol, vol. 32, no. 5, p. 656-70, viewed sans date, .
    Résumé : We report clinicopathologic features of a large series of renal translocation carcinomas from a multicentric study. Diagnosis was performed by cytogenetic examination of fresh material and/or by immunochemistry with antibodies directed against the C-terminal part of transcription factor E3 (TFE3) and native transcription factor EB (TFEB) proteins. Clinical data, follow-up, and histologic features were assessed. Antibodies against CK7, CD10, vimentin, epithelial membrane antigen, AE1-AE3, E-cadherin, alpha-methylacyl-coenzyme A racemase, melan A, and HMB45 were tested on tissue microarrays. Whole-genome microarray expression profiling was performed on 4 tumors. Twenty-nine cases were diagnosed as TFE3 and 2 as TFEB renal translocation carcinomas, including 13 males and 18 females, mean age 24.6 years. Two patients had a previous history of chemotherapy and 1 had a history of renal failure. Mean size of the tumor was 6.9 cm. Thirteen cases were > or = pT3 stage. Twelve cases were N+ or M+. Mean follow-up was 29.5 months. Three patients presented metastases and 5 have died. Mixed papillary and nested patterns with clear and/or eosinophilic cells represented the most consistent histologic appearance, with common foci of calcifications regardless of the type of translocation. Using a 30 mn incubation at room temperature, TFE3 immunostainings were positive in only 82% of our TFE3 translocation carcinomas. Both TFE3 and TFEB renal translocation carcinomas expressed CD10 and alpha-methylacyl-coenzyme A racemase in all cases. An expression of E-cadherin was observed in two-third of cases. Cytokeratins were expressed in less than one-third of cases. Melanocytic markers were expressed at least weakly in all cases except two. Unsupervised clustering on the basis of the gene expression profiling indicated a distinct subgroup of tumors. TRIM 63 glutathione S-transferase A1 and alanyl aminopeptidase are the main differentially expressed genes for this group of tumors. Our results suggest that these differentially expressed genes may serve as novel diagnostic or prognostic markers.
    Mots-clés : Adolescent Adult Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/analysis Carcinoma, Biological/analysis, Genetic Tumor Markers, Neoplastic Genome Humans Infant Kidney Neoplasms/chemistry/*genetics/*pathology Male Neoplasm Proteins/analysis Nephrectomy Tissue Array Analysis *Translocation, Renal Cell/chemistry/*genetics/*pathology Child Cytogenetic Analysis Female *Gene Expression Profiling Gene Expression Regulation.

  • Cantarovich, M, Durrbach, A, Hiesse, C, Ladouceur, M, Benoit, G & Charpentier, B 2008, « 20-year follow-up results of a randomized controlled trial comparing antilymphocyte globulin induction to no induction in renal transplant patients », Transplantation, vol. 86, no. 12, p. 1732-7, viewed sans date, .
    Résumé : BACKGROUND: The purpose of this study was to determine the impact of antilymphocyte globulin (ALG)-induction on long-term outcomes of postrenal transplantation. METHODS: Between January 1985 and January 1986, 123 consecutive renal transplants from deceased donors were performed at a single institution. Patients were randomized into two groups: group 1 (n=63, 40+/-10 year) received cyclosporine (CsA), prednisone, and azathioprine; and group 2 (n=60, 36+/-9 year) received ALG-induction, CsA, and prednisone and delayed initiation (45-90 days posttransplantation) of azathioprine if the CsA dose was less than 4 mg/kg per day. Target CsA trough levels were 150 to 250 ng/mL. Cytomegalovirus prophylaxis was not used. Human leukocyte antigen matching (2.4+/-1.1 vs. 2.6+/-1.2) and cold ischemia time (38+/-8 hr vs. 39+/-9 hr) did not differ. RESULTS: The incidence of acute rejection was lower in group 2 (28% vs. 75%, P<0.0001). The incidence of cytomegalovirus infection was 10% in group 1 and 18% in group 2 (P=0.41). The incidence of cancer was 22.2% in group 1 and 11.7% in group 2 (P=0.53) and the incidence of lymphoma did not differ (3% vs. 5%, P=0.77). Patient and graft survival in groups 1 and 2 at 1, 10, and 20 years were 100%/79% vs. 100%/93%, 83%/56% vs. 88%/51%, and 64%/43% vs. 54%/47%, respectively (log-rank test, P=0.18 and P=0.078). CONCLUSION: The use of ALG-induction resulted in a lower incidence of acute rejection and improved graft survival during the first year postrenal transplantation. Patient and graft survival at 20-year follow-up was not affected by ALG-induction.
    Mots-clés : Agents/*therapeutic, Analysis, Antilymphocyte, Azathioprine/therapeutic, Combined, Complications/epidemiology/*immunology/virology, Cyclosporine/therapeutic, Cytomegalovirus, effects/*physiology, Factors, Factors/*therapeutic, Follow-Up, Graft, Humans, Immunologic, Immunosuppressive, Infections/epidemiology, Kidney, Modality, Neoplasms/epidemiology, Postoperative, Prednisone/therapeutic, Rejection/*epidemiology, Serum/*therapeutic, Studies, Survival, Survival/drug, Therapy, Time, Transplantation/*immunology, use.
  • Castaing, D 2008, « Surgical anatomy of the biliary tract », HPB (Oxford), vol. 10, no. 2, p. 72-6.
    Résumé : An intimate knowledge of the morphological, functional, and real anatomy is a prerequisite for obtaining optimal results in the complex surgery of extra and intrahepatic cholangiocarcinoma. A complete presentation of the surgical anatomy of the bile ducts includes study of the liver, hepatic surface, margins, and scissures. The frequent variations from the normal anatomy are described and an overview of the blood supply and lymphatics of the biliary tract is presented.
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  • Chabanon, A, Desterke, C, Rodenburger, E, Clay, D, Guerton, B, Boutin, L, Bennaceur-Griscelli, A, Pierre-Louis, O, Uzan, G, Abecassis, L, Bourgeade, M-F, Lataillade, J-J & Le Bousse-Kerdilès, M-C 2008, « A cross-talk between stromal cell-derived factor-1 and transforming growth factor-beta controls the quiescence/cycling switch of CD34(+) progenitors through FoxO3 and mammalian target of rapamycin », Stem Cells, vol. 26, no. 12, p. 3150-61, viewed sans date, .
    Résumé : Cell cycle regulation plays a fundamental role in stem cell biology. A balance between quiescence and proliferation of hematopoietic stem cells in interaction with the microenvironment is critical for sustaining long-term hematopoiesis and for protection against stress. We analyzed the molecular mechanisms by which stromal cell-derived factor-1 (SDF-1) exhibited a cell cycle-promoting effect and interacted with transforming growth factor-beta (TGF-beta), which has negative effects on cell cycle orchestration of human hematopoietic CD34(+) progenitor cells. We demonstrated that a low concentration of SDF-1 modulated the expression of key cell cycle regulators such as cyclins, cyclin-dependent kinase inhibitors, and TGF-beta target genes, confirming its cell cycle-promoting effect. We showed that a cross-talk between SDF-1- and TGF-beta-related signaling pathways involving phosphatidylinositol 3-kinase (PI3K)/Akt phosphorylation participated in the control of CD34(+) cell cycling. We demonstrated a pivotal role of two downstream effectors of the PI3K/Akt pathway, FoxO3a and mammalian target of rapamycin, as connectors in the SDF-1-/TGF-beta-induced control of the cycling/quiescence switch and proposed a model integrating a dialogue between the two molecules in cell cycle progression. Our data shed new light on the signaling pathways involved in SDF-1 cell cycle-promoting activity and suggest that the balance between SDF-1- and TGF-beta-activated pathways is critical for the regulation of hematopoietic progenitor cell cycle status.
    Mots-clés : Antigens, CD34/biosynthesis Cell Cycle Chemokine CXCL12/ metabolism Forkhead Transcription Factors/ metabolism Hematopoiesis Hematopoietic Stem Cells/cytology Humans Models.
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  • Chakvetadze, C, Bani-Sadr, F, Slama, L, Pialoux, G, Roque-Afonso, AM & Dussaix, E 2008, « Sustained alanine aminotransferase increase during hepatitis A due to concomitant lymphogranuloma venereum infection in an HIV-1 positive patient », Gastroenterol Clin Biol, vol. 32, no. 6-7, p. 657-9.
    Résumé : Chakvetadze, C; Bani-Sadr, F; Slama, L; Pialoux, G; Roque-Afonso, A-M; Dussaix, E; Case Reports; Letter; France; Gastroenterol Clin Biol. 2008 Jun-Jul;32(6-7):657-9. doi: 10.1016/j.gcb.2008.04.026. Epub 2008 Jun 12.
    Mots-clés : A/, Adult, Alanine, Blood, blood/, complications, Hepatitis, HIV, Hiv-1, Humans, Infections/, Lymphogranuloma, Male, Transaminase/, Venereum/.

  • Chaligné, R, Tonetti, C, Besancenot, R, Roy, L, Marty, C, Mossuz, P, Kiladjian, J-J, Socié, G, Bordessoule, D, Le Bousse-Kerdilès, M-C, Vainchenker, W & Giraudier, S 2008, « New mutations of MPL in primitive myelofibrosis: only the MPL W515 mutations promote a G1/S-phase transition », Leukemia, vol. 22, no. 8, p. 1557-66, viewed sans date, .
    Résumé : MPL (or thrombopoietin receptor, TPO-R) 515 mutations have recently been described in 5-10% of primitive myelofibrosis (PMF) cases as decisive oncogenic events capable of triggering the disease. Here we report additional mutations located in exon 10 of MPL in PMF patients. We investigated whether these new mutations also lead to cell transformation. MPL exon 10 was systematically sequenced in 100 PMF patients. Seven different mutations were found in eight patients. We introduced each MPL mutant in Ba/F3 cells to determine whether they correspond to gain-of-function mutations. Only MPL W515 mutations induced (1) Ba/F3 proliferation independently of growth factors, (2) tumorigenesis in nude mice, (3) spontaneous activation of JAK/STAT, RAS/MAPK and PI3K transduction pathways and (4) increased S phase of cell cycle. Similar to all other myeloproliferative disorder oncogenic events identified to date, these results demonstrate that only the detected MPL W515 mutations trigger spontaneous MPL activation leading to a G(1)/S transition activation. The other mutations are devoid of significant transforming activity but may synergize with JAK2 V617F or other not yet characterized molecular events.
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  • Chevaliez, S, Balanant, J, Maillard, P, Lone, YC, Lemonnier, FA & Delpeyroux, F 2008, « Role of class I human leukocyte antigen molecules in early steps of echovirus infection of rhabdomyosarcoma cells », Virology, vol. 381, no. 2, p. 203-14, viewed sans date, .
    Résumé : Several echoviruses use decay accelerating factor (DAF) as a cell surface receptor. However, most of them require additional cell surface coreceptors. We investigated the respective roles of DAF and class I human leukocyte antigen (HLA) molecules in the early steps of the echovirus 11 (EV11) lifecycle in rhabdomyosarcoma (RD) cells. EV11 infection was inhibited at an early stage by anti-beta2-microglobulin (beta2m) and anti-HLA monoclonal antibodies and by a soluble monochain HLA class I molecule. Expression of class I HLA molecules restored the early steps of the EV11 lifecycle, but its expression was not sufficient for EV11 replication and particle production. Expression of HLA class I molecules was associated with leukocyte cell line permissiveness to EV11 infection. In conclusion, HLA class I molecules are involved in the early steps of EV11 infection of RD cells and appear to participate in a complex interplay of surface molecules acting as coreceptors, including DAF.
    Mots-clés : Animals Antibodies, CD55/metabolism CHO Cells Cell Line, Monoclonal/pharmacology Antigens, Tumor Cricetinae Cricetulus Echovirus Infections/*metabolism Enterovirus B.

  • Chiche, L & Adam, R 2008, « [Role and technical aspects of surgery for liver metastases from urological malignancies] », Prog Urol, vol. 18 Suppl 7, p. S256-60, viewed sans date, .
    Résumé : The liver is the third localisation of metastatic urological tumours after the bone and the lungs. Most frequently, it occurs as a multimetastatic disease for which surgery is not feasible. Nevertheless, when the metastasis is unique and when resection can be complete, it can be proposed if the localisation and the global prognosis permit. Recent therapeutic progress, including new improved drugs, progress in surgical procedures and the multisciplinary approach, lead to propose tumorectomy or hepatectomy for a few selected patients with hepatic metastasis from urological tumours.
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  • Chomel, J-C, Villalva, C, Sorel, N, Chazelas, F, Guilhot, F & Turhan, AG 2008, « Evaluation of beta-catenin activating mutations in chronic myeloid leukemia », Leuk Res, vol. 32, no. 5, p. 838-9, viewed sans date, .
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  • Clairambault, J 2008, « A step toward optimization of cancer therapeutics. Physiologically based modeling of circadian control on cell proliferation », IEEE Eng Med Biol Mag, vol. 27, no. 1, p. 20-4, viewed sans date, .
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  • Clairambault, J & Hoyer, D 2008, « Rhythms from seconds to days: part 2. Cell proliferation », IEEE Eng Med Biol Mag, vol. 27, no. 1, p. 16, viewed sans date, .
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