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Biblio - Bibliographie IAL
Bibliographie IAL

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Recherche bibliographique scientifique

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Accueil > Références bibliographiques

biblio

2010



  • Greco, C, Bralet, M-P, Ailane, N, Dubart-Kupperschmitt, A, Rubinstein, E, Le Naour, F & Boucheix, C 2010, « E-cadherin/p120-catenin and tetraspanin Co-029 cooperate for cell motility control in human colon carcinoma », Cancer Res, vol. 70, no. 19, p. 7674-83, viewed sans date, .
    Résumé : Tumor invasion and metastasis are major obstacles to clinical treatment that rely on cell migration. Here, we elucidate a mechanism of colon carcinoma cell migration that is supported by the cell surface tetraspanin Co-029 (tspan8), which is known to favor tumor progression and metastasis. This mechanism is unmasked by silencing of E-cadherin or its associated adapter molecule p120-catenin (p120ctn), and it involves a switch in signaling between the collagen-binding integrins α(1)β(1) and α(2)β(1). Direct interaction between E-cadherin and Co-029 was documented by chemical cross-linking and immunohistologic analysis of colon carcinomas. High expression of Co-029 and cytoplasmic delocalization of p120ctn were each associated with poor prognosis. Cell motility was reduced severely by antibody-mediated disruption of Co-029 only when p120ctn was silenced, suggesting that tumor progression may be hindered by Co-029 targeting. Our findings define a function for tetraspanin Co-029 as a modifier of cancer cell motility and reveal an adhesion signaling network implicated in progression and metastasis.
    Mots-clés : Animals Antibodies, Genetic, Inbred BALB C Signal Transduction Tetraspanins Transduction, Monoclonal/immunology/pharmacology Antigens, Neoplasm/biosynthesis/genetics/immunology/ metabolism Cadherins/ metabolism Catenins/ metabolism Cell Line, Tumor Cell Movement/ physiology Colonic Neoplasms/genetics/ metabolism/pathology GTP Phosphohydrolases/metabolism Humans Immunohistochemistry Integrin alpha2beta1/metabolism Membrane Glycoproteins/biosynthesis/genetics/immunology/ metabolism Mice Mice.
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  • Gregoire, E, Hoti, E, Gorden, DL, de la Serna, S, Pascal, G & Azoulay, D 2010, « Utility or futility of prognostic scoring systems for colorectal liver metastases in an era of advanced multimodal therapy », Eur J Surg Oncol, vol. 36, no. 6, p. 568-74, viewed sans date, .
    Résumé : OBJECTIVES: To assess the general applicability of prognostic scores for colorectal liver metastases (CRLM). METHODS: Review of English language studies from 1980 to 2008 (Medline and Embase). Search keywords included "Colorectal neoplasms", "liver metastases", "liver resection", "prognostic scoring system". RESULTS: Six scoring systems and fourteen prognostic factors within these studies were identified. No prognostic factor was common in all scoring methods. Five scores retained the number of metastases as a prognostic factor. Size of metastases and time between the onset of the primary tumor and the discovery of metastases were present in four scores. Three scores predicted 5-year survival using carcinoembryonic antigen (CEA) and R1 resection. Only two scores were assessed preoperatively. Successive scoring methods had improved predictive accuracy compared to earlier systems. However, their applicability in general populations remains debatable. An evaluation of the scores applicability to different patient populations demonstrated that the models were minimally effective in predicting disease-specific survival and recurrence, suggesting that stratification of patients by clinical and pathologic factors alone, may be clinically unreliable and not applicable for selection of patients for surgery. CONCLUSION: The utility of prognostic models on general populations is inconsistent. Current clinicopathologic factors may be inadequate to determine disease prognosis in CRLM. Future attempts to develop prognostic scores should include additional biologic and clinical variables, and be validated in larger populations.
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  • Groheux, D, Giacchetti, S, Rubello, D, Al-Nahhas, A, Moretti, J-L, Espié, M & Hindié, E 2010, « The evolving role of PET/CT in breast cancer », Nucl Med Commun, vol. 31, no. 4, p. 271-3, viewed sans date, .
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  • Guediche, N, Brisset, S, Benichou, J-J, Guérin, N, Mabboux, P, Maurin, M-L, Bas, C, Laroudie, M, Picone, O, Goldszmidt, D, Prévot, S, Labrune, P & Tachdjian, G 2010, « Chromosomal breakpoints characterization of two supernumerary ring chromosomes 20 », Am J Med Genet A, vol. 152A, no. 2, p. 464-71, viewed sans date, .
    Résumé : The occurrence of an additional ring chromosome 20 is a rare chromosome abnormality, and no common phenotype has been yet described. We report on two new patients presenting with a supernumerary ring chromosome 20 both prenatally diagnosed. The first presented with intrauterine growth retardation and some craniofacial dysmorphism, and the second case had a normal phenotype except for obesity. Conventional cytogenetic studies showed for each patient a small supernumerary marker chromosome (SMC). Using fluorescence in situ hybridization, these SMCs corresponded to ring chromosomes 20 including a part of short and long arms of chromosome 20. Detailed molecular cytogenetic characterization showed different breakpoints (20p11.23 and 20q11.23 for Patient 1 and 20p11.21 and 20q11.21 for Patient 2) and sizes of the two ring chromosomes 20 (13.6 Mb for case 1 and 4.8 Mb for case 2). Review of the 13 case reports of an extra r(20) ascertained postnatally (8 cases) and prenatally (5 cases) showed varying degrees of phenotypic abnormalities. We document a detailed molecular cytogenetic chromosomal breakpoints characterization of two cases of supernumerary ring chromosomes 20. These results emphasize the need to characterize precisely chromosomal breakpoints of supernumerary ring chromosomes 20 in order to establish genotype-phenotype correlation. This report may be helpful for prediction of natural history and outcome, particularly in prenatal diagnosis.
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  • Guettier, C 2010, « [Intrahepatic biliary cystic lesions] », Ann Pathol, vol. 30, no. 6, p. 448-54.
    Résumé : Intrahepatic biliary cysts encompass a large lesional spectrum including hereditary diseases as polycystic liver disease or Caroli's syndrome, malformative lesions as non hereditary Caroli's disease or simple biliary cyst and true neoplastic lesions as cystadenoma or cystadenocarcinoma. The diagnostic approach of these lesions relies firstly on imaging. Nevertheless, the pathologist not exceptionally receives surgical specimens from cystic fenestration or liver specimen resection with one or several cystic lesions. The clues for pathological diagnosis of these lesions have to be known by pathologists. As regards neoplastic cystic lesions, true non-communicating cystic tumors and cystic variants of intraductal biliary tumors have to be distinguished; in both cases, the classification is now identical to the one of pancreatic cystic tumors.
    Mots-clés : Autosomal Recessive/diagnosis/pathology, Bile Duct Neoplasms/diagnosis/pathology Bile Ducts, Differential Humans Liver Diseases/classification/ diagnosis/pathology Liver Neoplasms/diagnosis/pathology Polycystic Kidney Diseases/complications Polycystic Kidney, Intrahepatic/ pathology Caroli Disease/diagnosis/pathology Cystadenocarcinoma/diagnosis/pathology Cystadenoma/diagnosis/pathology Cysts/classification/ diagnosis/pathology Diagnosis.
  • Guettier, C & Scoazec, JY 2010, « [What's new in hepatobiliary pathology?] », Ann Pathol, vol. 30, no. 6, p. 411-2.
    Résumé : Guettier, Catherine; Scoazec, Jean-Yves; Editorial; Introductory; France; Ann Pathol. 2010 Dec;30(6):411-2. doi: 10.1016/j.annpat.2010.09.005. Epub 2010 Nov 9.
    Mots-clés : Adult Biliary Tract Diseases Child Fatty Liver Hepatitis, Human Humans Infant, Neonatal Liver Diseases, Newborn Jaundice, Viral.

  • Guihard, S, Clay, D, Cocault, L, Saulnier, N, Opolon, P, Souyri, M, Pagès, G, Pouysségur, J, Porteu, F & Gaudry, M 2010, « The MAPK ERK1 is a negative regulator of the adult steady-state splenic erythropoiesis », Blood, vol. 115, no. 18, p. 3686-3694.
    Résumé : The mitogen-activated protein kinases (MAPKs) extracellular signal-regulated kinase 1 (ERK1) and ERK2 are among the main signal transduction molecules, but little is known about their isoform-specific functions in vivo. We have examined the role of ERK1 in adult hematopoiesis with ERK1(-/-) mice. Loss of ERK1 resulted in an enhanced splenic erythropoiesis, characterized by an accumulation of erythroid progenitors in the spleen, without any effect on the other lineages or on bone marrow erythropoiesis. This result suggests that the ablation of ERK1 induces a splenic stress erythropoiesis phenotype. However, the mice display no anemia. Deletion of ERK1 did not affect erythropoietin (EPO) serum levels or EPO/EPO receptor signaling and was not compensated by ERK2. Splenic stress erythropoiesis response has been shown to require bone morphogenetic protein 4 (BMP4)-dependent signaling in vivo and to rely on the expansion of a resident specialized population of erythroid progenitors, termed stress erythroid burst-forming units (BFU-Es). A great expansion of stress BFU-Es and increased levels of BMP4 mRNA were found in ERK1(-/-) spleens. The ERK1(-/-) phenotype can be transferred by bone marrow cells. These findings show that ERK1 controls a BMP4-dependent step, regulating the steady state of splenic erythropoiesis.
    Mots-clés : Anemia, Animals, Apoptosis, Blotting, Western, Bone Marrow Transplantation, Bone Morphogenetic Protein 4, Colony-Forming Units Assay, Erythroid Precursor Cells, Erythropoiesis, Erythropoietin, Flow Cytometry, Mice, Mice, Inbred C57BL, Mitogen-Activated Protein Kinase 3, Oxidants, Phenylhydrazines, Receptors, Erythropoietin, Reverse Transcriptase Polymerase Chain Reaction, RNA, Messenger, Signal Transduction, Spleen.
  • Hantz, S, Garnier-Geoffroy, F, Mazeron, MC, Garrigue, I, Merville, P, Mengelle, C, Rostaing, L, Saint Marcoux, F, Essig, M, Rerolle, JP, Cotin, S, Germi, R, Pillet, S, Lebranchu, Y, Turlure, P & Alain, S 2010, « Drug-resistant cytomegalovirus in transplant recipients: a French cohort study », J Antimicrob Chemother, vol. 65, no. 12, p. 2628-40.
    Résumé : OBJECTIVES: Cytomegalovirus (CMV) drug resistance is a therapeutic challenge in the transplant setting. No longitudinal cohort studies of CMV resistance in a real-life setting have been published in the valganciclovir era. We report findings for a French multicentre prospective cohort of 346 patients enrolled at initial diagnosis of CMV infection (clinical trial registered at clinicaltrials.gov: NCT01008540). PATIENTS AND METHODS: Patients were monitored for detection of CMV infection for >/=2 years. Real-time detection of resistance by UL97 and UL54 gene sequencing and antiviral phenotyping was performed if viral replication persisted for >21 days of appropriate antiviral treatment. Plasma ganciclovir assays were performed when resistance was suspected. RESULTS: Resistance was suspected in 37 (10.7%) patients; 18/37 (5.2% of the cohort) had virological resistance, associated with poorer outcome. Most cases involved single UL97 mutations, but four cases of multidrug resistance were due to UL54 mutations. In solid organ transplant recipients, resistance occurred mainly during primary CMV infection (odds ratio 8.78), but also in two CMV-seropositive kidney recipients. Neither CMV prophylaxis nor antilymphocyte antibody administration was associated with virological resistance. CONCLUSIONS: These data show the feasibility of surveying resistance. Virological resistance was frequent in patients failing antiviral therapy. More than 1/5 resistant isolates harboured UL54 mutations alone or combined with UL97 mutations, which conferred a high level of resistance and sometimes were responsible for cross-resistance, leading to therapeutic failure.
    Mots-clés : Adult Antiviral Agents/ pharmacology/therapeutic use Chemoprevention Child Child, Preschool Cohort Studies Cytomegalovirus/ drug effects/genetics Cytomegalovirus Infections/prevention & control/ virology DNA-Directed DNA Polymerase/genetics Drug Resistance.

  • Haouas, H, Haouas, S, Uzan, G & Hafsia, A 2010, « Identification of new markers discriminating between myeloid and lymphoid acute leukemia », Hematology, vol. 15, no. 4, p. 193-203, viewed sans date, .
    Résumé : BACKGROUND: The heterogeneity of acute myeloid leukemia (AML) with respect to biology and clinical course resides in the fact that patients belonging to the same group show marked differences in their response to chemotherapy, necessitating a refinement of AML classification. METHODS: In order to define molecular markers for AML, we performed microarray analysis on peripheral blood cells from two M5 AML patients, and selected four differentially expressed genes to validate their expression by real-time quantitative PCR (RT-PCR). RESULTS: We have shown that two downregulated genes in AML, those encoding guanine nucleotide-binding protein gamma11 (GNG11) and amphiregulin (AREG), are also downregulated in B-lineage acute lymphoblastic leukemia (B-ALL) and T-lineage acute lymphoblastic leukemia (T-ALL) patients. A second gene, that encoding ceruloplasmin (CP), is upregulated in AML but not in B-ALL and T-ALL. The level of expression of these genes varies from one patient to another. CONCLUSION: Since the number of patients studied is limited, further studies are needed with a larger series of patients to evaluate the potential utility of GNG11, AREG and CP as molecular markers for AML subtype classification. Our study is the first to analyze these genes in AML, B-ALL, T-ALL and chronic leukemia (myeloid and lymphoid) patients by RT-PCR. This rapid and sensitive method could be used to screen these genes in different types of leukemia.
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  • Harambat, J, Fargue, S, Acquaviva, C, Gagnadoux, MF, Janssen, F, Liutkus, A, Mourani, C, Macher, MA, Abramowicz, D, Legendre, C, Durrbach, A, Tsimaratos, M, Nivet, H, Girardin, E, Schott, AM, Rolland, MO & Cochat, P 2010, « Genotype-phenotype correlation in primary hyperoxaluria type 1: the p.Gly170Arg AGXT mutation is associated with a better outcome », Kidney Int, vol. 77, no. 5, p. 443-9, viewed sans date, .
    Résumé : We sought to ascertain the long-term outcome and genotype-phenotype correlations available for primary hyperoxaluria type 1 in a large retrospective cohort study. We examined the clinical history of 155 patients (129 families primarily from Western Europe, North Africa, or the Middle East) as well as the enzymatic or genetic diagnosis. The median age at first symptom was 4 years, and at diagnosis 7.7 years, at which time 43% had reached end-stage renal disease. Presentations included: (1) early nephrocalcinosis and infantile renal failure, (2) recurrent urolithiasis and progressive renal failure diagnosed during childhood, (3) late onset with occasional stone passage diagnosed in adulthood, (4) diagnosis occurring on post-transplantation recurrence, and (5) family screening. The cumulative patient survival was 95, 86, and 74% at ages 10, 30, and 50 years, respectively, with the cumulative renal survival of 81, 59, 41, and 10% at ages 10, 20, 30, and 50 years, respectively; 72 patients had undergone a total of 97 transplantations. Among the 136 patients with DNA analysis, the most common mutation was p.Gly170Arg (allelic frequency 21.5%), with a median age at end-stage renal disease of 47 years for homozygotes, 35 years for heterozygotes, and 21 years for other mutations. Our results underscore the severe prognosis of primary hyperoxaluria type 1 and the necessity for early diagnosis and treatment, as well as confirm a better prognosis of the p.Gly170Arg mutation.
    Mots-clés : Amino Acid Substitution Arginine/metabolism Child Child, Chronic/genetics Mutation Phenotype Prognosis Retrospective Studies Transaminases/*genetics, Preschool Cohort Studies Genotype Heterozygote Homozygote Humans Hyperoxaluria, Primary/diagnosis/*genetics Infant Kidney Failure.

  • Hoogduijn, MJ, Popp, FC, Grohnert, A, Crop, MJ, van Rhijn, M, Rowshani, AT, Eggenhofer, E, Renner, P, Reinders, ME, Rabelink, TJ, van der Laan, LJ, Dor, FJ, Ijzermans, JN, Genever, PG, Lange, C, Durrbach, A, Houtgraaf, JH, Christ, B, Seifert, M, Shagidulin, M, Donckier, V, Deans, R, Ringden, O, Perico, N, Remuzzi, G, Bartholomew, A, Schlitt, HJ, Weimar, W, Baan, CC, Dahlke, MH & Group, MS 2010, « Advancement of mesenchymal stem cell therapy in solid organ transplantation (MISOT) », Transplantation, vol. 90, no. 2, p. 124-6, viewed sans date, .
    Résumé : There is evolving interest in the use of mesenchymal stem cells (MSC) in solid organ transplantation. Pre-clinical transplantation models show efficacy of MSC in prolonging graft survival and a number of clinical studies are planned or underway. At a recent meeting of the MISOT consortium (MSC In Solid Organ Transplantation) the advances of these studies were evaluated and mechanisms underlying the potential effects of MSC discussed. Continued discussion is required for definition of safety and eventually efficacy endpoints for MSC therapy in solid organ transplantation.
    Mots-clés : Cell, Cells/cytology/immunology/physiology, Culture, Graft, Humans, Immunophenotyping, Immunosuppression/methods, Kidney, Liver, Mesenchymal, Organ, Safety, Stem, Stromal, Survival/*physiology, T-Lymphocytes/immunology, Techniques, Therapy/methods, Tissue, Transplantation/*methods, Transplantation/*methods/physiology, Transplantation/immunology/physiology.
  • Hudson, TJ, Anderson, W, Artez, A, Barker, AD, Bell, C, Bernabe, RR, Bhan, MK, Calvo, F, Eerola, I, Gerhard, DS, Guttmacher, A, Guyer, M, Hemsley, FM, Jennings, JL, Kerr, D, Klatt, P, Kolar, P, Kusada, J, Lane, DP, Laplace, F, Youyong, L, Nettekoven, G, Ozenberger, B, Peterson, J, Rao, TS, Remacle, J, Schafer, AJ, Shibata, T, Stratton, MR, Vockley, JG, Watanabe, K, Yang, H, Yuen, MM, Knoppers, BM, Bobrow, M, Cambon-Thomsen, A, Dressler, LG, Dyke, SO, Joly, Y, Kato, K, Kennedy, KL, Nicolas, P, Parker, MJ, Rial-Sebbag, E, Romeo-Casabona, CM, Shaw, KM, Wallace, S, Wiesner, GL, Zeps, N, Lichter, P, Biankin, AV, Chabannon, C, Chin, L, Clement, B, de Alava, E, Degos, F, Ferguson, ML, Geary, P, Hayes, DN, Hudson, TJ, Johns, AL, Kasprzyk, A, Nakagawa, H, Penny, R, Piris, MA, Sarin, R, Scarpa, A, Shibata, T, van de Vijver, M, Futreal, PA, Aburatani, H, Bayes, M, Botwell, DD, Campbell, PJ, Estivill, X, Gerhard, DS, Grimmond, SM, Gut, I, Hirst, M, Lopez-Otin, C, Majumder, P, Marra, M, McPherson, JD, Nakagawa, H, Ning, Z, Puente, XS, Ruan, Y, Shibata, T, Stratton, MR, Stunnenberg, HG, Swerdlow, H, Velculescu, VE, Wilson, RK, Xue, HH, Yang, L, Spellman, PT, Bader, GD, Boutros, PC, Campbell, PJ, Flicek, P, Getz, G, Guigo, R, Guo, G, Haussler, D, Heath, S, Hubbard, TJ, Jiang, T, Jones, SM, Li, Q, Lopez-Bigas, N, Luo, R, Muthuswamy, L, Ouellette, BF, Pearson, JV, Puente, XS, Quesada, V, Raphael, BJ, Sander, C, Shibata, T, Speed, TP, Stein, LD, Stuart, JM, Teague, JW, Totoki, Y, Tsunoda, T, Valencia, A, Wheeler, DA, Wu, H, Zhao, S, Zhou, G, Stein, LD, Guigo, R, Hubbard, TJ, Joly, Y, Jones, SM, Kasprzyk, A, Lathrop, M, Lopez-Bigas, N, Ouellette, BF, Spellman, PT, Teague, JW, Thomas, G, Valencia, A, Yoshida, T, Kennedy, KL, Axton, M, Dyke, SO, Futreal, PA, Gerhard, DS, Gunter, C, Guyer, M, Hudson, TJ, McPherson, JD, Miller, LJ, Ozenberger, B, Shaw, KM, Kasprzyk, A, Stein, LD, Zhang, J, Haider, SA, Wang, J, Yung, CK, Cros, A, Liang, Y, Gnaneshan, S, Guberman, J, Hsu, J, Bobrow, M, Chalmers, DR, Hasel, KW, Joly, Y, Kaan, TS, Kennedy, KL, Knoppers, BM, Lowrance, WW, Masui, T, Nicolas, P, Rial-Sebbag, E, Rodriguez, LL, Vergely, C, Yoshida, T, Grimmond, SM, Biankin, AV, Bowtell, DD, Cloonan, N, deFazio, A, Eshleman, JR, Etemadmoghadam, D, Gardiner, BB, Kench, JG, Scarpa, A, Sutherland, RL, Tempero, MA, Waddell, NJ, Wilson, PJ, McPherson, JD, Gallinger, S, Tsao, MS, Shaw, PA, Petersen, GM, Mukhopadhyay, D, Chin, L, DePinho, RA, Thayer, S, Muthuswamy, L, Shazand, K, Beck, T, Sam, M, Timms, L, Ballin, V, Lu, Y, Ji, J, Zhang, X, Chen, F, Hu, X, Zhou, G, Yang, Q, Tian, G, Zhang, L, Xing, X, Li, X, Zhu, Z, Yu, Y, Yu, J, Yang, H, Lathrop, M, Tost, J, Brennan, P, Holcatova, I, Zaridze, D, Brazma, A, Egevard, L, Prokhortchouk, E, Banks, RE, Uhlen, M, Cambon-Thomsen, A, Viksna, J, Ponten, F, Skryabin, K, Stratton, MR, Futreal, PA, Birney, E, Borg, A, Borresen-Dale, AL, Caldas, C, Foekens, JA, Martin, S, Reis-Filho, JS, Richardson, AL, Sotiriou, C, Stunnenberg, HG, Thoms, G, van de Vijver, M, van't Veer, L, Calvo, F, Birnbaum, D, Blanche, H, Boucher, P, Boyault, S, Chabannon, C, Gut, I, Masson-Jacquemier, JD, Lathrop, M, Pauporte, I, Pivot, X, Vincent-Salomon, A, Tabone, E, Theillet, C, Thomas, G, Tost, J, Treilleux, I, Calvo, F, Bioulac-Sage, P, Clement, B, Decaens, T, Degos, F, Franco, D, Gut, I, Gut, M, Heath, S, Lathrop, M, Samuel, D, Thomas, G, Zucman-Rossi, J, Lichter, P, Eils, R, Brors, B, Korbel, JO, Korshunov, A, Landgraf, P, Lehrach, H, Pfister, S, Radlwimmer, B, Reifenberger, G, Taylor, MD, von Kalle, C, Majumder, PP, Sarin, R, Rao, TS, Bhan, MK, Scarpa, A, Pederzoli, P, Lawlor, RA, Delledonne, M, Bardelli, A, Biankin, AV, Grimmond, SM, Gress, T, Klimstra, D, Zamboni, G, Shibata, T, Nakamura, Y, Nakagawa, H, Kusada, J, Tsunoda, T, Miyano, S, Aburatani, H, Kato, K, Fujimoto, A, Yoshida, T, Campo, E, Lopez-Otin, C, Estivill, X, Guigo, R, de Sanjose, S, Piris, MA, Montserrat, E, Gonzalez-Diaz, M, Puente, XS, Jares, P, Valencia, A, Himmelbauer, H, Quesada, V, Bea, S, Stratton, MR, Futreal, PA, Campbell, PJ, Vincent-Salomon, A, Richardson, AL, Reis-Filho, JS, van de Vijver, M, Thomas, G, Masson-Jacquemier, JD, Aparicio, S, Borg, A, Borresen-Dale, AL, Caldas, C, Foekens, JA, Stunnenberg, HG, van't Veer, L, Easton, DF, Spellman, PT, Martin, S, Barker, AD, Chin, L, Collins, FS, Compton, CC, Ferguson, ML, Gerhard, DS, Getz, G, Gunter, C, Guttmacher, A, Guyer, M, Hayes, DN, Lander, ES, Ozenberger, B, Penny, R, Peterson, J, Sander, C, Shaw, KM, Speed, TP, Spellman, PT, Vockley, JG, Wheeler, DA, Wilson, RK, Hudson, TJ, Chin, L, Knoppers, BM, Lander, ES, Lichter, P, Stein, LD, Stratton, MR, Anderson, W, Barker, AD, Bell, C, Bobrow, M, Burke, W, Collins, FS, Compton, CC, DePinho, RA, Easton, DF, Futreal, PA, Gerhard, DS, Green, AR, Guyer, M, Hamilton, SR, Hubbard, TJ, Kallioniemi, OP, Kennedy, KL, Ley, TJ, Liu, ET, Lu, Y, Majumder, P, Marra, M, Ozenberger, B, Peterson, J, Schafer, AJ, Spellman, PT, Stunnenberg, HG, Wainwright, BJ, Wilson, RK & Yang, H 2010, « International network of cancer genome projects », Nature, vol. 464, no. 7291, p. 993-8.
    Résumé : The International Cancer Genome Consortium (ICGC) was launched to coordinate large-scale cancer genome studies in tumours from 50 different cancer types and/or subtypes that are of clinical and societal importance across the globe. Systematic studies of more than 25,000 cancer genomes at the genomic, epigenomic and transcriptomic levels will reveal the repertoire of oncogenic mutations, uncover traces of the mutagenic influences, define clinically relevant subtypes for prognosis and therapeutic management, and enable the development of new cancer therapies.
    Mots-clés : DNA Methylation DNA Mutational Analysis/trends Databases, Genetic Genes, Human/ genetics Genomics/ organization & administration/trends Humans Intellectual Property International Cooperation Mutation Neoplasms/classification/ genetics/pathology/therapy, Medical/ organization & administration/trends Genome, Neoplasm/genetics Genetics.
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  • Ichai, P, Saliba, F, Antoun, F, Azoulay, D, Sebagh, M, Antonini, TM, Escaut, L, Delvart, V, Castaing, D & Samuel, D 2010, « Acute liver failure due to antitubercular therapy: Strategy for antitubercular treatment before and after liver transplantation », Liver Transpl, vol. 16, no. 10, p. 1136-46, viewed sans date, .
    Résumé : The standard antitubercular treatment (ATT), which consists of isoniazid (INH), rifampicin (RIF), ethambutol, and pyrazinamide (PZA), is the best available treatment for tuberculosis (TB). However, the hepatotoxicity of INH and PZA can be severe, and even after drug withdrawal, patients may require liver transplantation (LT). In these cases, the strategy for the treatment of TB is poorly defined. Between 1986 and 2008, 14 patients presented at our department with severe hepatitis secondary to INH and PZA treatment. Four of these patients were immunosuppressed: 2 after renal transplantation and 2 because of human immunodeficiency virus infection. In seven of the 14 patients an alternative ATT was begun on admission, which was well tolerated. Hepatitis improved spontaneously in 5 patients, and alternative ATT was continued for 9.3 ± 4.2 months; 1 patient deteriorated and underwent LT, and 1 patient died. ATT was stopped definitively in 2 patients. Six patients required urgent LT, and alternative ATT was started after transplantation and was successful. Five patients receiving RIF had an episode of acute rejection. In conclusion, hepatitis secondary to ATT can be successfully treated with alternative anti-TB regimens. The use of RIF in LT patients may lead to acute rejection. RIF should therefore be avoided in these patients.
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  • Innominato, PF, Lévi, FA & Bjarnason, GA 2010, « Chronotherapy and the molecular clock: Clinical implications in oncology », Adv Drug Deliv Rev, vol. 62, no. 9-10, p. 979-1001, viewed sans date, .
    Résumé : The circadian timing system drives daily rhythmic changes in drug metabolism and controls rhythmic events in cell cycle, DNA repair, apoptosis, and angiogenesis in both normal tissue and cancer. Rodent and human studies have shown that the toxicity and anticancer activity of common cancer drugs can be significantly modified by the time of administration. Altered sleep/activity rhythms are common in cancer patients and can be disrupted even more when anticancer drugs are administered at their most toxic time. Disruption of the sleep/activity rhythm accelerates cancer growth. The complex circadian time-dependent connection between host, cancer and therapy is further impacted by other factors including gender, inter-individual differences and clock gene polymorphism and/or down regulation. It is important to take circadian timing into account at all stages of new drug development in an effort to optimize the therapeutic index for new cancer drugs. Better measures of the individual differences in circadian biology of host and cancer are required to further optimize the potential benefit of chronotherapy for each individual patient.
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  • Innominato, PF, Palesh, O, Dhabhar, FS, Lévi, F & Spiegel, D 2010, « Regulation of circadian rhythms and hypothalamic-pituitary-adrenal axis: an overlooked interaction in cancer », Lancet Oncol, vol. 11, no. 9, p. 816-7, viewed sans date, .
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  • Jiang, XY, Forrest, D, Nicolini, F, Turhan, A, Guilhot, J, Yip, C, Holyoake, T, Jorgensen, H, Lambie, K, Saw, KM, Pang, E, Vukovic, R, Lehn, P, Ringrose, A, Yu, MA, Brinkman, RR, Smith, C, Eaves, A & Eaves, C 2010, « Properties of CD34(+) CML stem/progenitor cells that correlate with different clinical responses to imatinib mesylate », Blood, vol. 116, no. 12, p. 2112-2121, viewed sans date, <<Go to ISI>://WOS:000282137300019>.
    Résumé : Imatinib mesylate (IM) induces clinical remissions in chronic-phase chronic myeloid leukemia (CML) patients but IM resistance remains a problem. We recently identified several features of CML CD34(+) stem/progenitor cells expected to confer resistance to BCR-ABL-targeted therapeutics. From a study of 25 initially chronic-phase patients, we now demonstrate that some, but not all, of these parameters correlate with subsequent clinical response to IM therapy. CD34(+) cells from the 14 IM nonresponders demonstrated greater resistance to IM than the 11 IM responders in colony-forming cell assays in vitro (P < .001) and direct sequencing of cloned transcripts from CD34(+) cells further revealed a higher incidence of BCR-ABL kinase domain mutations in the IM nonresponders (10%-40% vs 0%-20% in IM responders, P < .003). In contrast, CD34(+) cells from IM nonresponders and IM responders were not distinguished by differences in BCR-ABL or transporter gene expression. Interestingly, one BCR-ABL mutation (V304D), predicted to de-stabilize the interaction between p210(BCR-ABL) and IM, was detectable in 14 of 20 patients. T315I mutant CD34(+) cells found before IM treatment in 2 of 20 patients examined were preferentially amplified after IM treatment. Thus, 2 properties of pretreatment CML stem/progenitor cells correlate with subsequent response to IM therapy. Prospective assessment of these properties may allow improved patient management.(Blood. 2010;116(12):2112-2121)

  • Jodon de Villeroché, V, Avouac, J, Ponceau, A, Ruiz, B, Kahan, A, Boileau, C, Uzan, G & Allanore, Y 2010, « Enhanced late-outgrowth circulating endothelial progenitor cell levels in rheumatoid arthritis and correlation with disease activity », Arthritis Res Ther, vol. 12, no. 1, p. R27, viewed sans date, .
    Résumé : INTRODUCTION: Angiogenesis and vasculogenesis are critical in rheumatoid arthritis (RA) as they could be a key issue for chronic synovitis. Contradictory results have been published regarding circulating endothelial progenitor cells (EPCs) in RA. We herein investigated late outgrowth EPC sub-population using recent recommendations in patients with RA and healthy controls. METHODS: EPCs, defined as Lin-/7AAD-/CD34+/CD133+/VEGFR-2+ cells, were quantified by flow cytometry in peripheral blood mononuclear cells (PBMCs) from 59 RA patients (mean age: 54 +/- 15 years, disease duration: 16 +/- 11 years) and 36 controls (mean age: 53 +/- 19 years) free of cardiovascular events and of cardiovascular risk factors. Concomitantly, late outgrowth endothelial cell colonies derived from culture of PBMCs were analyzed by colony-forming units (CFUs). RESULTS: RA patients displayed higher circulating EPC counts than controls (median 112 [27 to 588] vs. 60 [5 to 275]) per million Lin- mononuclear cells; P = 0.0007). The number of circulating EPCs positively correlated with disease activity reflected by DAS-28 score (r = 0.43; P = 0.0028) and lower counts were found in RA patients fulfilling remission criteria (P = 0.0069). Furthermore, late outgrowth CFU number was increased in RA patients compared to controls. In RA, there was no association between the number of EPCs and serum markers of inflammation or endothelial injury or synovitis. CONCLUSIONS: Our data, based on a well characterized definition of late outgrowth EPCs, demonstrate enhanced levels in RA and relationship with disease activity. This supports the contribution of vasculogenesis in the inflammatory articular process that occurs in RA by mobilization of EPCs.
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  • Johanet, C, Ballot, E & Chazouilleres, O 2010, « Significance of antibodies to soluble liver antigen/liver pancreas: response to the German study », Liver Int, vol. 30, no. 1, p. 156-157.
  • Kassis-Chikhani, N, Decre, D, Ichai, P, Sengelin, C, Geneste, D, Mihaila, L, Dussaix, E & Arlet, G 2010, « Outbreak of Klebsiella pneumoniae producing KPC-2 and SHV-12 in a French hospital », J Antimicrob Chemother, vol. 65, no. 7, p. 1539-40.
    Résumé : Kassis-Chikhani, Najiby; Decre, Dominique; Ichai, Philippe; Sengelin, Christian; Geneste, Delphine; Mihaila, Liliana; Dussaix, Elisabeth; Arlet, Guillaume; Letter; Research Support, Non-U.S. Gov't; England; J Antimicrob Chemother. 2010 Jul;65(7):1539-40. doi: 10.1093/jac/dkq132. Epub 2010 May 11.
    Mots-clés : Bacterial Proteins/ biosynthesis Cross Infection/epidemiology/microbiology Disease Outbreaks France Gene Transfer, Horizontal Hospitals Humans Klebsiella Infections/ epidemiology/ microbiology Klebsiella pneumoniae/ enzymology/isolation & purification Plasmids/analysis beta-Lactamases/ biosynthesis.
  • Kassis-Chikhani, N, Saliba, F, Carbonne, A, Neuville, S, Decre, D, Sengelin, C, Guerin, C, Gastiaburu, N, Lavigne-Kriaa, A, Boutelier, C, Arlet, G, Samuel, D, Castaing, D, Dussaix, E & Jarlier, V 2010, « Extended measures for controlling an outbreak of VIM-1 producing imipenem-resistant Klebsiella pneumoniae in a liver transplant centre in France, 2003-2004 », Euro Surveill, vol. 15, no. 46.
    Résumé : We report the successful control of an outbreak caused by imipenem-resistant VIM-1-producing Klebsiella pneumoniae (IR-Kp) in France. This outbreak occurred in a care centre for abdominal surgery that includes a 15-bed liver intensive care unit and performs more than 130 liver transplantations per year. The index case was a patient with acute liver failure transferred from a hospital in Greece for urgent liver transplantation who was carrying IR-Kp at admission as revealed by routine culture of a rectal swab. Infection control measures were undertaken and included contact isolation and promotion of hand hygiene with alcohol-based hand rub solution. Nevertheless, secondary IR-Kp cases were identified during the six following months from 3 December 2003 to 2 June 2004. From 2 June to 21 October, extended infection control measures were set up, such as cohorting IR-Kp carriers, contact patients and new patients in distinct sections with dedicated staff, limiting ward admission, and strict control of patient transfer. They led to a rapid control of the outbreak. The global attack rate of the IR-Kp outbreak was 2.5%, 13% in liver transplant patients and 0.4% in the other patients in the care centre (p<0.005). Systematic screening for IR-Kp of all patients admitted to the care centre is still maintained to date and no secondary IR-Kp case has been detected since 2 June 2004.
    Mots-clés : Anti-Bacterial Agents/pharmacology/therapeutic use Cross Infection/epidemiology/microbiology/ prevention & control Disease Outbreaks/ prevention & control Drug Resistance, Bacterial Female France/epidemiology Hospital Bed Capacity.
  • Lalioti, V, Sandoval, I, Cassio, D & Duclos-Vallee, JC 2010, « Molecular pathology of Wilson's disease: a brief », J Hepatol, vol. 53, no. 6, p. 1151-3.
    Résumé : Lalioti, Vassiliki; Sandoval, Ignacio; Cassio, Doris; Duclos-Vallee, Jean-Charles; Review; England; J Hepatol. 2010 Dec;53(6):1151-3. doi: 10.1016/j.jhep.2010.07.008. Epub 2010 Aug 13.
    Mots-clés : Adenosine Triphosphatases/genetics/metabolism Cation Transport Proteins/genetics/metabolism Copper/metabolism Hepatolenticular Degeneration/ genetics/metabolism/ pathology Humans Ion Transport Models, Biological Mutation Phosphorylation.
  • Lammer, J, Malagari, K, Vogl, T, Pilleul, F, Denys, A, Watkinson, A, Pitton, M, Sergent, G, Pfammatter, T, Terraz, S, Benhamou, Y, Avajon, Y, Gruenberger, T, Pomoni, M, Langenberger, H, Schuchmann, M, Dumortier, J, Mueller, C, Chevallier, P & Lencioni, R 2010, « Prospective randomized study of doxorubicin-eluting-bead embolization in the treatment of hepatocellular carcinoma: results of the PRECISION V study », Cardiovasc Intervent Radiol, vol. 33, no. 1, p. 41-52.
    Résumé : Transcatheter arterial chemoembolization (TACE) offers a survival benefit to patients with intermediate hepatocellular carcinoma (HCC). A widely accepted TACE regimen includes administration of doxorubicin-oil emulsion followed by gelatine sponge-conventional TACE. Recently, a drug-eluting bead (DC Bead) has been developed to enhance tumor drug delivery and reduce systemic availability. This randomized trial compares conventional TACE (cTACE) with TACE with DC Bead for the treatment of cirrhotic patients with HCC. Two hundred twelve patients with Child-Pugh A/B cirrhosis and large and/or multinodular, unresectable, N0, M0 HCCs were randomized to receive TACE with DC Bead loaded with doxorubicin or cTACE with doxorubicin. Randomization was stratified according to Child-Pugh status (A/B), performance status (ECOG 0/1), bilobar disease (yes/no), and prior curative treatment (yes/no). The primary endpoint was tumor response (EASL) at 6 months following independent, blinded review of MRI studies. The drug-eluting bead group showed higher rates of complete response, objective response, and disease control compared with the cTACE group (27% vs. 22%, 52% vs. 44%, and 63% vs. 52%, respectively). The hypothesis of superiority was not met (one-sided P = 0.11). However, patients with Child-Pugh B, ECOG 1, bilobar disease, and recurrent disease showed a significant increase in objective response (P = 0.038) compared to cTACE. DC Bead was associated with improved tolerability, with a significant reduction in serious liver toxicity (P < 0.001) and a significantly lower rate of doxorubicin-related side effects (P = 0.0001). TACE with DC Bead and doxorubicin is safe and effective in the treatment of HCC and offers a benefit to patients with more advanced disease.
    Mots-clés : Aged Antibiotics, Antineoplastic/ administration & dosage Carcinoma, Hepatocellular/ therapy Chemoembolization, Therapeutic/ methods Doxorubicin/ administration & dosage Drug Carriers Drug Implants Female Humans Liver Neoplasms/ therapy Male Prospective Studies Single-Blind Method Treatment Outcome.
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  • Lataillade, J-J, Albanese, P & Uzan, G 2010, « [Implication of hyaluronic acid in normal and pathological angiogenesis. Application for cellular engineering] », Ann Dermatol Venereol, vol. 137 Suppl 1, p. S15-22, viewed sans date, .
    Résumé : Angiogenesis is a physiological process that allows the formation of new blood vessels, either from the local vascular structures, or from circulating endothelial progenitor cells, mobilized from the bone marrow, and attracted to the neovascularization site. This mechanism is controlled by pro-angiogenic molecules. It is crucial to supply oxygen and nutrients to tissues during growth, embryonic development or tissue regeneration in response to injuries. Thus, the dermis part of the skin is highly vascularized by a dense network of small and medium arteries and of capillaries and venules. In case of injury, rapid tissue repair is possible through this vascular network. However, once the vascularization is restored in tissue repair, the process of angiogenesis is negatively regulated by anti-angiogenic molecules. Controling the balance between pro-and anti-angiogenic agents is crucial and its deregulation leads to serious disease. The extracellular matrix plays an important role in controlling angiogenesis, allowing at least, the distribution of growth factors and the regulation of endothelial cell migration. Among these matrix components, hyaluronic acid plays a major role in the mechanical properties of connective tissues in ensuring their hydration. This glycosaminoglycan is a large size polymer, whose breakdown products strongly act on angiogenesis, especially in pathological situations (cancer, inflammation). Regarding its biological and mechanical properties, hyaluronic acid is used as matrix in tissue engineering, for improving the revascularization of tissues like skin.
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  • Lataillade, J-J, Bey, E, Thepenier, C, Prat, M, Leclerc, T & Bargues, L 2010, « [Skin engineering for burns treatment] », Bull Acad Natl Med, vol. 194, no. 7, p. 1339-51, viewed sans date, .
    Résumé : Severely burned patients need effective and permanent wound coverage. The outcome of massive burn injuries has improved with the use of cultured epithelial autografts (CEA), despite their fragility, frequent failure to take, high cost and long-term tendency to contract. Combining CEA with dermal substitutes provides earlier skin closure and satisfactory functional results. Another promising line of research is skin regeneration with epidermal stem cells, which have the capacity to differentiate into keratinocytes, to promote wound repair, and to regenerate skin appendages. Human mesenchymal stem cells have been evaluated in radiation-induced skin damage.
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  • Lataillade, J-J, Brunet de la Grange, P, Uzan, G & Le Bousse-Kerdilès, M-C 2010, « [Are stem cells as old as their niches? The quest for eternal life..] », Med Sci (Paris), vol. 26, no. 6-7, p. 582-5, viewed sans date, .
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  • Le Naour, F 2010, « [Imaging by infrared spectroscopy and multimodal approaches. Applications to liver diseases] », Ann Pathol, vol. 30, no. 5 Suppl 1, p. 58-9.
    Résumé : Le Naour, Francois; France; Ann Pathol. 2010 Nov;30(5 Suppl 1):58-9. doi: 10.1016/j.annpat.2010.08.007. Epub 2010 Sep 16.
    Mots-clés : Humans Liver Diseases/ pathology Spectrophotometry, Infrared.
  • Lebrec, D, Thabut, D, Oberti, F, Perarnau, JM, Condat, B, Barraud, H, Saliba, F, Carbonell, N, Renard, P, Ramond, MJ, Moreau, R & Poynard, T 2010, « Pentoxifylline does not decrease short-term mortality but does reduce complications in patients with advanced cirrhosis », Gastroenterology, vol. 138, no. 5, p. 1755-62.
    Résumé : BACKGROUND & AIMS: Pentoxifylline, an inhibitor of tumor necrosis factor-alpha, is given to patients with liver diseases, but its effects in patients with advanced cirrhosis are unknown. We performed a randomized, placebo-controlled, double-blind trial of its effects in patients with cirrhosis. METHODS: A total of 335 patients with cirrhosis (Child-Pugh class C) were assigned to groups given either pentoxifylline (400 mg, orally, 3 times daily; n = 164) or placebo (n = 171) for 6 months. The primary end point was mortality at 2 months. Secondary end points were mortality at 6 months and development of liver-related complications. RESULTS: By 2 months, 28 patients in the pentoxifylline group (16.5%) and 31 in the placebo group (18.2%) had died (P = .84). At 6 months, 50 patients in the pentoxifylline group (30.0%) and 54 in the placebo group (31.5%) had died (P = .75). The proportions of patients without complications (eg, bacterial infection, renal insufficiency, hepatic encephalopathy, or gastrointestinal hemorrhage) were higher in the pentoxifylline group than in the placebo group at 2 months (78.6% vs 63.4%; P = .006) and 6 months (66.8% vs 49.7%; P = .002). The probability of survival without complications was higher in the pentoxifylline group than in the placebo group at 2 and 6 months (P = .04). In multivariate analysis, the factors associated with death were age, the Model for End-Stage Liver Disease score, and presence of early-stage carcinoma. Treatment with pentoxifylline was the only factor associated with liver-related complications. CONCLUSIONS: Although pentoxifylline does not decrease short-term mortality in patients with advanced cirrhosis, it does reduce the risk of complications.
    Mots-clés : Administration.

  • Lehmann-Che, J, André, F, Desmedt, C, Mazouni, C, Giacchetti, S, Turpin, E, Espié, M, Plassa, L-F, Marty, M, Bertheau, P, Sotiriou, C, Piccart, M, Symmans, WF, Pusztai, L & de Thé, H 2010, « Cyclophosphamide dose intensification may circumvent anthracycline resistance of p53 mutant breast cancers », Oncologist, vol. 15, no. 3, p. 246-52, viewed sans date, .
    Résumé : The predictive value of p53 for the efficacy of front-line anthracycline-based chemotherapy regimens has been a matter of significant controversy. Anthracyclines are usually combined with widely different doses of alkylating agents, which may significantly modulate tumor response to these combinations. We analyzed three series of de novo stage II-III breast cancer patients treated front line with anthracycline-based regimens of various cyclophosphamide dose intensities: 65 patients with estrogen receptor (ER)(-) tumors treated with anthracyclines alone (Institut Jules Bordet, Brussels), 51 unselected breast cancer patients treated with intermediate doses of cyclophosphamide (MD Anderson Cancer Center, Houston, TX), and 128 others treated with a dose-dense anthracycline-cyclophosphamide combination (St. Louis, Paris). After chemotherapy and surgery, pathologic complete response (pCR) was evaluated. p53 status was determined by a yeast functional assay on the pretreatment tumor sample. In a multivariate analysis of the pooled results, a lack of ER expression and high-dose cyclophosphamide administration were associated with a higher likelihood of pCR. A sharp statistical interaction was detected between p53 status and cyclophosphamide dose intensity. Indeed, when restricting our analysis to patients with ER(-) tumors, we confirmed that a mutant p53 status was associated with anthracycline resistance, but found that p53 inactivation was required for response to the dose-intense alkylating regimen. The latter allowed very high levels of pCR in triple-negative tumors. Thus, our data strongly suggest that cyclophosphamide dose intensification in ER(-) p53-mutated breast cancer patients could significantly improve their response.
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  • Lévi, F, Okyar, A, Dulong, S, Innominato, PF & Clairambault, J 2010, « Circadian timing in cancer treatments », Annu Rev Pharmacol Toxicol, vol. 50, p. 377-421, viewed sans date, .
    Résumé : The circadian timing system is composed of molecular clocks, which drive 24-h changes in xenobiotic metabolism and detoxification, cell cycle events, DNA repair, apoptosis, and angiogenesis. The cellular circadian clocks are coordinated by endogenous physiological rhythms, so that they tick in synchrony in the host tissues that can be damaged by anticancer agents. As a result, circadian timing can modify 2- to 10-fold the tolerability of anticancer medications in experimental models and in cancer patients. Improved efficacy is also seen when drugs are given near their respective times of best tolerability, due to (a) inherently poor circadian entrainment of tumors and (b) persistent circadian entrainment of healthy tissues. Conversely, host clocks are disrupted whenever anticancer drugs are administered at their most toxic time. On the other hand, circadian disruption accelerates experimental and clinical cancer processes. Gender, circadian physiology, clock genes, and cell cycle critically affect outcome on cancer chronotherapeutics. Mathematical and systems biology approaches currently develop and integrate theoretical, experimental, and technological tools in order to further optimize and personalize the circadian administration of cancer treatments.
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  • Li, X-M, Delaunay, F, Dulong, S, Claustrat, B, Zampera, S, Fujii, Y, Teboul, M, Beau, J & Lévi, F 2010, « Cancer inhibition through circadian reprogramming of tumor transcriptome with meal timing », Cancer Res, vol. 70, no. 8, p. 3351-60, viewed sans date, .
    Résumé : Circadian disruption accelerates cancer progression, whereas circadian reinforcement could halt it. Mice with P03 pancreatic adenocarcinoma (n = 77) were synchronized and fed ad libitum (AL) or with meal timing (MT) from Zeitgeber time (ZT) 2 to ZT6 with normal or fat diet. Tumor gene expression profiling was determined with DNA microarrays at endogenous circadian time (CT) 4 and CT16. Circadian mRNA expression patterns were determined for clock genes Rev-erbalpha, Per2, and Bmal1, cellular stress genes Hspa8 and Cirbp, and cyclin A2 gene Ccna2 in liver and tumor. The 24-hour patterns in telemetered rest-activity and body temperature and plasma corticosterone and insulin-like growth factor-I (IGF-I) were assessed. We showed that MT inhibited cancer growth by approximately 40% as compared with AL (P = 0.011) irrespective of calorie intake. Clock gene transcription remained arrhythmic in tumors irrespective of feeding schedule or diet. Yet, MT upregulated or downregulated the expression of 423 tumor genes, according to CT. Moreover, 36 genes involved in cellular stress, cell cycle, and metabolism were upregulated at one CT and downregulated 12 h apart. MT induced >10-fold circadian expression of Hspa8, Cirbp, and Ccna2 in tumors. Corticosterone or IGF-I patterns played no role in tumor growth inhibition. In contrast, MT consistently doubled the circadian amplitude of body temperature. Peak and trough respectively corresponded to peak expressions of Hspa8 and Cirbp in tumors. The reinforcement of the host circadian timing system with MT induced 24-hour rhythmic expression of critical genes in clock-deficient tumors, which translated into cancer growth inhibition. Targeting circadian clocks represents a novel potential challenge for cancer therapeutics.
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  • Machover, D, Delmas-Marsalet, B, Misra, SC, Ulusakarya, A, Gumus, Y, Frénoy, N, Guettier, C, Saffroy, R, Innominato, P, Almohamad, W, Brahimi, N, Haydar, M & Goldschmidt, E 2010, « Treatment with rituximab, dexamethasone, high-dose cytarabine, and oxaliplatin (R-DHAOx) produces a strong long-term antitumor effect in previously treated patients with follicular non-Hodgkin's lymphoma », Biomed Pharmacother, vol. 64, no. 2, p. 83-7, viewed sans date, .
    Résumé : BACKGROUND: We explored the addition of rituximab to high-dose cytarabine (ara-C), oxaliplatin (L-OHP), and dexamethasone [R-DHAOx], in resistant and relapsed patients with CD20-positive follicular non-Hodgkin's lymphoma. METHODS: Twenty-two patients were included; they were treated previously with one to five chemotherapy regimens, including 13 patients who had also received rituximab. R-DHAOx consisted of rituximab, 375mg/m(2), day 1; dexamethasone, 40mg/d, days one to four; L-OHP, 130mg/m(2), day 1; and ara-C, 2000mg/m(2) every 12 h, day 2. Courses were repeated every 21 days for eight courses. RESULTS: Twenty-one patients (95%) achieved a complete response and one had a partial response. Responses were obtained in patients with and without resistance to prior treatment, either alone or combined with rituximab. The median follow-up time was 58.3 months (range, 8.7-92.6 months). Progression-free survival reached a plateau at 84% at 38.2 months. Only two of the 21 complete responders have relapsed. Tumor molecular markers disappeared in all 10 complete responders whose markers were found before treatment. Peripheral neuropathy related to the cumulative dose of L-OHP, and myelosuppression were the most prominent toxic effects. CONCLUSIONS: R-DHAOx is highly active for salvage treatment of patients with follicular non-Hodgkin's lymphoma, and it produces long-term antitumor efficacy.
    Mots-clés : Adult Aged Antibodies, Biological/metabolism, Follicular/ drug therapy Male Middle Aged Neoplasm Recurrence, Local/drug therapy Organoplatinum Compounds/administration & dosage Peripheral Nervous System Diseases/chemically induced Treatment Outcome Tumor Markers, Monoclonal, Monoclonal/ administration & dosage/adverse effects Antibodies, Murine-Derived Antineoplastic Combined Chemotherapy Protocols/ administration & dosage Cytarabine/administration & dosage Dexamethasone/administration & dosage Disease-Free Survival Drug Resistance, Neoplasm Female Humans Lymphoma.
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  • Mackiewicz, V, Cammas, A, Desbois, D, Marchadier, E, Pierredon, S, Beaulieux, F, Dussaix, E, Vagner, S & Roque-Afonso, AM 2010, « Nucleotide variability and translation efficiency of the 5' untranslated region of hepatitis A virus: update from clinical isolates associated with mild and severe hepatitis », J Virol, vol. 84, no. 19, p. 10139-47.
    Résumé : Mutations in the internal ribosome entry site (IRES) of hepatitis A virus (HAV) have been associated with enhanced in vitro replication and viral attenuation in animal models. To address the possible role of IRES variability in clinical presentation, IRES sequences were obtained from HAV isolates associated with benign (n = 8) or severe (n = 4) hepatitis. IRES activity was assessed using a bicistronic dual-luciferase expression system in adenocarcinoma (HeLa) and hepatoma (HuH7) cell lines. Activity was higher in HuH7 than in HeLa cells, except for an infrequently isolated genotype IIA strain. Though globally low, significant variation in IRES-dependent translation efficiency was observed between field isolates, reflecting the low but significant genetic variability of this region (94.2% +/- 0.5% nucleotide identity). No mutation was exclusive of benign or severe hepatitis, and variations in IRES activity were not associated with a clinical phenotype, indirectly supporting the preponderance of host factors in determining the clinical presentation.
    Mots-clés : 5' Untranslated Regions/ genetics Acute Disease Adolescent Adult Base Sequence Cell Line Child DNA Primers/genetics DNA, Site-Directed Mutation Nucleic Acid Conformation Phylogeny Protein Biosynthesis RNA, Viral/chemistry/ genetics Virulence/genetics Young Adult, Viral/genetics France Genetic Variation Genotype HeLa Cells Hepatitis A/ virology Hepatitis A virus/ genetics/isolation & purification/ pathogenicity/physiology Humans Middle Aged Molecular Sequence Data Mutagenesis.
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  • Maigne, G, Ferlicot, S, Galacteros, F, Belenfant, X, Ulinski, T, Niaudet, P, Ronco, P, Godeau, B, Durrbach, A, Sahali, S, Lang, P, Lambotte, O & Audard, V 2010, « Glomerular lesions in patients with sickle cell disease », Medicine (Baltimore), vol. 89, no. 1, p. 18-27, viewed sans date, .
    Résumé : Sickle cell disease (SCD) is an increasing cause of chronic kidney disease, but the spectrum of glomerular lesions and their underlying mechanisms remain poorly described. We reviewed 18 renal biopsies from patients with SCD and glomerular involvement and studied the expression of hypoxic markers in the biopsy specimens. Four histopathologic variants were distinguished: focal segmental glomerulosclerosis (FSGS) (39%), membranoproliferative glomerulonephritis (28%), thrombotic microangiopathy glomerulopathy (17%), and specific sickle cell disease glomerulopathy (17%). Chronic organ damage and history of acute chest syndrome were associated with the occurrence of SCD glomerulopathy. All patients exhibited macroalbuminuria but only 6 patients displayed impaired renal function. SCD was not associated with a specific FSGS histologic variant. Long-term follow-up analysis revealed that 50% of patients exhibited chronic kidney disease. Regardless of the histologic variants, immunohistochemistry did not reveal a specific induction of hypoxic markers (inducible nitric oxide synthase [iNOS], nitrotyrosine, hypoxia-inducible factor [HIF]-1 alpha) at the time of renal biopsy. This large study shows that a wide spectrum of glomerular lesions is associated with SCD. Whatever lesions are observed, the renal prognosis is poor, and early renoprotective treatment is necessary. Hypoxic state does not seem to play a key role in the progression of glomerular lesions, but its potential role at an early stage of glomerular injury requires further investigation.
    Mots-clés : Adolescent Adult Anemia, Focal Segmental/epidemiology/*etiology/pathology Humans Male Thrombotic Microangiopathies/epidemiology/*etiology/pathology, Membranoproliferative/epidemiology/*etiology/pathology Glomerulosclerosis, Sickle Cell/*complications Child Female Glomerulonephritis.

  • Marron, M, Boffetta, P, Zhang, Z-F, Zaridze, D, Wünsch-Filho, V, Winn, DM, Wei, Q, Talamini, R, Szeszenia-Dabrowska, N, Sturgis, EM, Smith, E, Schwartz, SM, Rudnai, P, Purdue, MP, Olshan, AF, Eluf-Neto, J, Muscat, J, Morgenstern, H, Menezes, A, McClean, M, Matos, E, Mates, IN, Lissowska, J, Levi, F, Lazarus, P, La Vecchia, C, Koifman, S, Kelsey, K, Herrero, R, Hayes, RB, Franceschi, S, Fernandez, L, Fabianova, E, Daudt, AW, Dal Maso, L, Curado, MP, Cadoni, G, Chen, C, Castellsague, X, Boccia, S, Benhamou, S, Ferro, G, Berthiller, J, Brennan, P, Møller, H & Hashibe, M 2010, « Cessation of alcohol drinking, tobacco smoking and the reversal of head and neck cancer risk », Int J Epidemiol, vol. 39, no. 1, p. 182-96, viewed sans date, .
    Résumé : BACKGROUND: Quitting tobacco or alcohol use has been reported to reduce the head and neck cancer risk in previous studies. However, it is unclear how many years must pass following cessation of these habits before the risk is reduced, and whether the risk ultimately declines to the level of never smokers or never drinkers. METHODS: We pooled individual-level data from case-control studies in the International Head and Neck Cancer Epidemiology Consortium. Data were available from 13 studies on drinking cessation (9167 cases and 12 593 controls), and from 17 studies on smoking cessation (12 040 cases and 16 884 controls). We estimated the effect of quitting smoking and drinking on the risk of head and neck cancer and its subsites, by calculating odds ratios (ORs) using logistic regression models. RESULTS: Quitting tobacco smoking for 1-4 years resulted in a head and neck cancer risk reduction [OR 0.70, confidence interval (CI) 0.61-0.81 compared with current smoking], with the risk reduction due to smoking cessation after > or =20 years (OR 0.23, CI 0.18-0.31), reaching the level of never smokers. For alcohol use, a beneficial effect on the risk of head and neck cancer was only observed after > or =20 years of quitting (OR 0.60, CI 0.40-0.89 compared with current drinking), reaching the level of never drinkers. CONCLUSIONS: Our results support that cessation of tobacco smoking and cessation of alcohol drinking protect against the development of head and neck cancer.
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  • Martinez, F, Kamar, N, Pallet, N, Lang, P, Durrbach, A, Lebranchu, Y, Adem, A, Barbier, S, Cassuto-Viguier, E, Glowaki, F, Le Meur, Y, Rostaing, L, Legendre, C, Hermine, O, Choukroun, G & Neo, PSI 2010, « High dose epoetin beta in the first weeks following renal transplantation and delayed graft function: Results of the Neo-PDGF Study », Am J Transplant, vol. 10, no. 7, p. 1695-700, viewed sans date, .
    Résumé : Erythropoietin promotes nephroprotection in animal models of ischemia-reperfusion injury. Neorecormon and Prevention of Delayed Graft Function (Neo-PDGF) is a French open-label multicenter randomized study to evaluate the effect of high doses of epoetin beta (EPO-beta) during the first 2 weeks of renal transplantation on renal function in patients at risk for delayed graft function (DGF). One hundred and four patients were included in the study. Patients randomized in treatment group (A) received four injections of EPO-beta (30.000 UI each), given before surgery and at 12 h, 7 days and 14 days posttransplantation. Patients randomized in control group (B) did not receive EPO-beta. Immunosuppression included induction with basiliximab and maintenance therapy with steroids, mycophenolate mofetil and tacrolimus. At 1 month posttransplant, the estimated glomerular filtration rate (MDRD formula) was 42.5 +/- 19.0 mL/min in the EPO-beta group and 44.0 +/- 16.3 mL/min in the control group (p = ns). The frequency of DGF was similar in both groups (32% vs. 38.8%; p = ns). No difference in the incidence of serious adverse events was observed. (ClinicalTrials.gov number, NCT00815867.).
    Mots-clés : Adrenal Cortex Hormones/therapeutic use Aged Antibodies.
  • Melin, P, Chousterman, M, Fontanges, T, Ouzan, D, Rotily, M, Lang, JP, Marcellin, P & Cacoub, P 2010, « Effectiveness of chronic hepatitis C treatment in drug users in routine clinical practice: results of a prospective cohort study », Eur J Gastroenterol Hepatol, vol. 22, no. 9, p. 1050-7.
    Résumé : OBJECTIVE: Injection drug users are often excluded from hepatitis C virus (HCV) treatment. This study compares sustained virological response, adherence, and quality of life in patients with or without a history of illicit drug use in routine clinical practice. METHODS: This is a post-hoc analysis of a prospective, observational study conducted in 1860 patients who received peginterferon alpha-2b/ribavirin combination therapy. Nondrug users (NDUs) were defined as patients without a history of drug addiction; former drug users (FDUs) as patients who had stopped using illicit drugs or opioid maintenance therapy and active drug users (ADUs) as patients using illicit drugs or on opioid maintenance therapy. Virological response, adherence, and the health-related quality of life were assessed by the measure of HCV RNA in the serum, self-report and 36-item short-form health survey Questionnaire, respectively. RESULTS: The analyzed population included 1038 (56%) NDUs, 578 (31%) FDUs, and 244 (13%) ADUs. About 85% of ADUs were on opioid maintenance therapy and 25% used illicit drugs. Although ADUs had a more chaotic lifestyle and more psychiatric disorders, sustained virological response of ADUs (58%) did not differ from that of NDUs (49%) and FDUs (51%) (P=0.133). Adherence rates were 39% in NDUs and FDUs, and 37% in ADUs (P=0.883). Health-related quality of life was improved in the three groups after the end of treatment. CONCLUSION: Our study suggests that HCV therapy in ADUs on opioid maintenance therapy is as effective as in other HCV patients. The effectiveness of HCV therapy in illicit drug users needs to be evaluated in further studies.
    Mots-clés : Analgesics, Combination Hepatitis C, Opioid/administration & dosage Antiviral Agents/ administration & dosage Cohort Studies Drug Therapy.

  • Michelon, H, Konig, J, Durrbach, A, Quteineh, L, Verstuyft, C, Furlan, V, Ferlicot, S, Letierce, A, Charpentier, B, Fromm, MF & Becquemont, L 2010, « SLCO1B1 genetic polymorphism influences mycophenolic acid tolerance in renal transplant recipients », Pharmacogenomics, vol. 11, no. 12, p. 1703-13, viewed sans date, .
    Résumé : AIMS: This study aimed to determine the influence of gene candidates on mycophenolic acid (MPA) response during the first year of renal transplantation. MATERIALS & METHODS: A total of 218 renal transplant recipients who received MPA from the first day of transplantation at a fixed dose of 2 g/day were genotyped for ABCB1, ABCC2, UGT2B7, UGT1A9, SLCO1B1, SLCO1B3 and IMPDH1 polymorphisms. Clinical end points were MPA-related adverse drug reactions (ADRs) and acute rejection episodes during the first year post-transplantation. RESULTS: After correction for multiple statistical testing, SLCO1B1 (encoding the hepatic uptake transporter OATP1B1) was the only gene associated with MPA-related ADRs, showing a 75% risk reduction in favor of a protective effect of the SLCO1B1*5 allele (p = 0.002). In vitro experiments showed that MPA metabolites MPA-phenyl-glucuronide and MPA-acyl-glucuronide are substrates of OATP1B1. Their transport was decreased in the presence of the variant transporter (OATP1B1*5). CONCLUSION: These results suggest for the first time that carriers of the SLCO1B1*5 allele seem to be protected from MPA-related ADRs.
    Mots-clés : Single Nucleotide Retrospective Studies Substrate Specificity Transfection.

  • Mitjavila-Garcia, MT, Bonnet, ML, Yates, F, Haddad, R, Oudrhiri, N, Feraud, O, Magniez, A, Makhlouf, M, Vallot, C, Rougeulle, C, Bennaceur-Griscelli, A & Turhan, AG 2010, « Partial Reversal of the Methylation Pattern of the X-linked Gene HUMARA during Hematopoietic Differentiation of Human Embryonic Stem Cells », Journal of Molecular Cell Biology, vol. 2, no. 5, p. 291-298, viewed sans date, <<Go to ISI>://WOS:000286428800009>.
    Résumé : Human embryonic stem cells (hESCs) can be induced to differentiate towards hematopoiesis with high efficiency. In this work, we analyzed the methylation status of the X-linked HUMARA (human androgen receptor) gene in hematopoietic cells derived from hESC line H9 before and after induction of hematopoietic differentiation. All passages of H9 and H9-derived hematopoietic cells displayed homogenous methylation pattern with disappearance of the same allele upon HpaII digestion. This pattern persisted in the great majority of different hematopoietic progenitors derived from H9, except in 11 of 86 individually plucked colonies in which an equal digestion of the HUMARA alleles has been found, suggesting that a methylation change occurring at this locus during differentiation. Interestingly, quantification of X inactive-specific transcript (XIST) RNA in undifferentiated H9 cell line and day 14 embryoid bodies (EB) by RT-PCR did not show any evidence of XIST expression either before or after differentiation. Thus, during self-renewal conditions and after induction of commitment towards the formation of EB, the methylation pattern of the HUMARA locus appears locked with the same unmethylated allele. However, hematopoietic differentiation seems to be permissive to the reversal of methylation status of HUMARA in some terminally differentiated progenitors. These data suggest that monitoring methylation of HUMARA gene during induced differentiation could be of use for studying hESC-derived hematopoiesis.
  • Moniaux, N & Faivre, J 2010, « Will nano-fibers permit to turn liver cell transplantation into a curative tool against liver failure? », J Hepatol, vol. 52, no. 2, p. 150-2.
    Résumé : Moniaux, Nicolas; Faivre, Jamila; Comment; Editorial; Review; England; J Hepatol. 2010 Feb;52(2):150-2. doi: 10.1016/j.jhep.2009.10.027. Epub 2009 Nov 10.
    Mots-clés : Animals, Engineering, Failure/, Hepatocytes/, Humans, Liver, Mice, Nanofibers, Nanotechnology, Scaffolds, Therapy, Tissue, Transplantation.
  • Mostafa, A, Taylor, SM, el-Daly, M, el-Hoseiny, M, Bakr, I, Arafa, N, Thiers, V, Rimlinger, F, Abdel-Hamid, M, Fontanet, A & Mohamed, MK 2010, « Is the hepatitis C virus epidemic over in Egypt? Incidence and risk factors of new hepatitis C virus infections », Liver Int, vol. 30, no. 4, p. 560-6.
    Résumé : OBJECTIVES: To estimate hepatitis C virus (HCV) incidence rates and identify risk factors for current HCV transmission with emphasis on the role of living with infected household family members in rural Egypt. METHODS: A 4-year population-based, cohort study of seronegative villagers was conducted to identify incident HCV seroconversion cases. A risk factor questionnaire and blood samples for anti-HCV EIA-3 and HCV RNA polymerase chain reaction testing were collected at two rounds of follow-up. Incidence rates, relative risks and 95% confidence interval (CI) were calculated based on a Poisson distribution. A matched case-control analysis to explore specific behavioural predictors of infection was conducted and odds ratios were obtained by conditional logistic regression. RESULTS: Twenty-five participants (11 females) seroconverted in 10,578 person years of follow-up (PY), (incidence rate of 2.4/1000 PY; 95% CI: 1.6-3.5). The median age at seroconversion was 26 years [interquartile range (IQR) 19-35] among males and 20 years (IQR 13-24) among females. The only significant risk factor identified for these cases was receiving injections [adjusted odds ratio (OR(adj))=3.3; 95% CI: 1.1-9.8]. Two of the 17 viraemic seroconvertors were infected with the same strain as at least one of their family members. CONCLUSION: This study identified the important role of injections in spreading HCV infection in this rural community. National healthcare awareness and infection control programmes should be strengthened to prevent further transmission. Screening of families of infected HCV subjects should be an essential part of case management for early detection and management.
    Mots-clés : Chronic/diagnosis/epidemiology Humans Incidence Logistic Models Male Middle Aged Odds Ratio Predictive Value of Tests Prognosis Risk Assessment Serologic Tests/methods Sex Distribution Socioeconomic Factors Young Adult.

  • Najjar, I, Grimont, A, Martin, N, Martin-Lanneree, S, Bonnet, ML, Guilhot, F, Chomel, JC, Lauret, E, Turhan, AG & Dusanter-Fourt, I 2010, « Distinct Functions of Stat5A and Stat5B in Chronic Myeloid Leukemia (CML): Stat5B Is Implicated in Survival and Self-Renewal and Stat5A in Imatinib Resistance », Blood, vol. 116, no. 21, p. 520-520, viewed sans date, <<Go to ISI>://WOS:000289662201317>.
    Résumé : Najjar, Imen Grimont, Adrien Martin, Nicolas Martin-Lanneree, Severine Bonnet, Marie Laure Guilhot, Francois Chomel, Jean-Claude Lauret, Evelyne Turhan, Ali G. Dusanter-Fourt, Isabelle 52nd Annual Meeting of the American-Society-of-Hematology (ASH) Dec 04-07, 2010 Orlando, FL Amer Soc Hematol
  • Nalpas, B, Lavialle-Meziani, R, Plancoulaine, S, Jouanguy, E, Nalpas, A, Munteanu, M, Charlotte, F, Ranque, B, Patin, E, Heath, S, Fontaine, H, Vallet-Pichard, A, Pontoire, D, Bourliere, M, Casanova, JL, Lathrop, M, Brechot, C, Poynard, T, Matsuda, F, Pol, S & Abel, L 2010, « Interferon gamma receptor 2 gene variants are associated with liver fibrosis in patients with chronic hepatitis C infection », Gut, vol. 59, no. 8, p. 1120-6.
    Résumé : BACKGROUND: Only a minority of patients with chronic hepatitis C virus (HCV) infection develops severe liver fibrosis, a process that may be controlled by human genetic factors. OBJECTIVE: To investigate the role of 384 single nucleotide polymorphisms (SNPs) located in 36 candidate genes related to the fibrogenesis/fibrolysis process. METHODS: Patients with chronic HCV infection were gathered from two French cohorts (prospectively and retrospectively). The overall sample consisted of 393 HCV-infected subjects without known risk factors for fibrosis progression, including 134 patients with severe liver fibrosis and 259 without severe fibrosis. RESULTS: Only two SNPs in strong linkage disequilibrium (LD) in the interferon gamma receptor 2 gene (IFNGR2) were significantly associated with liver fibrosis in both the prospective and the retrospective samples. The strongest association (p=8x10(-5)) was observed with the G/A SNP rs9976971 with an OR of severe fibrosis for AA versus AG or GG subjects at 2.95 (95% CI 1.70 to 5.11). This effect was higher (p=9x10(-7)) when taking into account the time of follow-up, and the hazard ratio of progression towards severe fibrosis for AA patients was 2.62 (1.76 to 3.91). Refined sequencing and analysis of the IFNGR2 region identified two additional variants in strong LD with rs9976971. No haplotypes derived from this cluster of four variants provided stronger evidence for association than rs9976971 alone. CONCLUSIONS: This identification of a cluster of four IFNGR2 variants strongly associated with fibrosis progression in chronic HCV infection underlines the role of IFNgamma in the development of liver fibrosis that may pave the way for new treatments.
    Mots-clés : Adult Aged Disease Progression Epidemiologic Methods Female Genetic Predisposition to Disease Genotype Haplotypes Hepatitis C, Chronic/ complications Humans Linkage Disequilibrium Liver Cirrhosis/ genetics/ virology Male Middle Aged Polymorphism, Interferon/ genetics Young Adult, Single Nucleotide Receptors.

  • Nicolini, FE, Chomel, JC, Roy, L, Legros, L, Chabane, K, Ducastelle, S, Nicolas-Virelizier, E, Michallet, M, Tigaud, I, Magaud, JP, Turhan, A, Guilhot, F & Hayette, S 2010, « The Durable Clearance of the T315I BCR-ABL Mutated Clone in Chronic Phase Chronic Myelogenous Leukemia Patients on Omacetaxine Allows Tyrosine Kinase Inhibitor Rechallenge », Clinical Lymphoma Myeloma & Leukemia, vol. 10, no. 5, p. 394-399, viewed sans date, <<Go to ISI>://WOS:000283610300010>.
    Résumé : Purpose: The onset of a BCR-ABL(T315I) mutation during the course of chronic myelogenous leukemia (CML) on tyrosine kinase inhibitors (TKIs) usually results in poor survival, and therapeutic options remain few in the absence of any allogeneic donor. Patients and Methods: We have investigated the affect of subcutaneous omacetaxine (OMA, or homoharringtonine) cycles on unmutated and T315I-mutated BCR-ABL transcripts in a series of 8 TKI-resistant chronic-phase CML patients and we have addressed the question of whether the administration of OMA could resensitize patients to TKIs. Patients were regularly monitored for total disease burden and for BCR-ABL(T315I) transcripts using a new quantitative sensitive technique (sensitivity threshold, 0.05%), for up to 27 cycles of OMA. Results: Overall, patients demonstrated hematologic, cytogenetic, or molecular improvement. An initial rapid decline and a sustained disappearance of T315I-mutated transcripts were observed in 50% of patients, after a median of 10.5 cycles (range, 3-27 cycles) of OMA. As the unmutated leukemic burden reduction was modest, 2 patients were submitted to nilotinib after 9 months of sustained BCR-ABLT315I transcripts negativity on OMA and mutated transcripts remained undetectable after a median follow-up of 12 months on nilotinib challenge. Conclusion: We suggest that OMA (ie, a non-targeted therapy) might provide a better disease control allowing the disappearance of the mutated clone probably elicited by the clone deselection after TKI release, and/or a preferential activity of OMA on the T315I-mutated cells through unknown mechanisms. These observations suggest that OMA could allow a safe TKI rechallenge in patients with resistant chronic-phase CML.

  • Oberlin, E, Fleury, M, Clay, D, Petit-Cocault, L, Candelier, JJ, Mennesson, B, Jaffredo, T & Souyri, M 2010, « VE-cadherin expression allows identification of a new class of hematopoietic stem cells within human embryonic liver », Blood, vol. 116, no. 22, p. 4444-4455, viewed sans date, <<Go to ISI>://WOS:000284599900017>.
    Résumé : Edification of the human hematopoietic system during development is characterized by the production of waves of hematopoietic cells separated in time, formed in distinct embryonic sites (ie, yolk sac, truncal arteries including the aorta, and placenta). The embryonic liver is a major hematopoietic organ wherein hematopoietic stem cells (HSCs) expand, and the future, adult-type, hematopoietic cell hierarchy becomes established. We report herein the identification of a new, transient, and rare cell population in the human embryonic liver, which coexpresses VE-cadherin, an endothelial marker, CD45, a pan-hematopoietic marker, and CD34, a common endothelial and hematopoietic marker. This population displays an outstanding self-renewal, proliferation, and differentiation potential, as detected by in vitro and in vivo hematopoietic assays compared with its VE-cadherin negative counterpart. Based on VE-cadherin expression, our data demonstrate the existence of 2 phenotypically and functionally separable populations of multipotent HSCs in the human embryo, the VE-cadherin(+) one being more primitive than the VE-cadherin(-) one, and shed a new light on the hierarchical organization of the embryonic liver HSC compartment. (Blood. 2010;116(22):4444-4455)

  • Ousset, M, Bouquet, F, Fallone, F, Biard, D, Dray, C, Valet, P, Salles, B & Muller, C 2010, « Loss of ATM positively regulates the expression of hypoxia inducible factor 1 (HIF-1) through oxidative stress », Cell Cycle, vol. 9, no. 14, p. 2814-2822, viewed sans date, <<Go to ISI>://WOS:000281205500030>.
    Résumé : Ataxia Telangiectasia (AT) is an autosomal recessive disorder characterized by a wide variety of progressive clinical symptoms. This includes neuronal degeneration, oculocutaneous telangiectasias, diabetes mellitus, immunodeficiency, increased risk of cancer and sensitivity to ionizing radiation. The gene mutated in this disease, ATM (Ataxia Telangiectasia Mutated), encodes a protein kinase involved in DNA double strand breaks signalling and repair. ATM deficient cells also display an increase in oxidative stress, by poorly characterized mechanism(s), which clearly contributes to the neurodegenerative aspect of the disease. Despite these advances, the occurrence of the vascular abnormalities, glucose intolerance and insulin resistance remains poorly understood. In different cellular models where ATM expression was disrupted, we demonstrated that the absence of ATM leads to an increased expression of both subunits of the transcription factor Hypoxia Inducible Factor 1 (HIF-1). We also observed enhanced trans-activating functions of HIF-1. HIF-1 is the central regulator of responses to hypoxia which induces the transcription of genes involved in angiogenesis (e. g., VEGF-Vascular Endothelial Growth Factor) and cellular metabolism (e. g., GLUT-1). Interestingly, we demonstrated that ATM disruption positively regulates both expression and function of the basal glucose transporter GLUT-1 as well as the proangiogenic factor, VEGF. In addition, our results suggest that the absence of ATM increases HIF-1 proteins biosynthesis, and this effect is dependant on the oxidative stress existing in ATM deficient cells. Our compelling results highlight a new link between ATM deficiency and the clinical features of the disease and provide a molecular link between ATM downregulation and the increase in tumor angiogenesis observed in human breast cancers.
  • Paez Jimenez, A, Sharaf Eldin, N, Rimlinger, F, El-Daly, M, El-Hariri, H, El-Hoseiny, M, Mohsen, A, Mostafa, A, Delarocque-Astagneau, E, Abdel-Hamid, M, Fontanet, A, Mohamed, MK & Thiers, V 2010, « HCV iatrogenic and intrafamilial transmission in Greater Cairo, Egypt », Gut, vol. 59, no. 11, p. 1554-60.
    Résumé : OBJECTIVES: To document hepatitis C virus (HCV) intrafamilial transmission and assess its relative importance in comparison to other current modes of transmission in the country with the largest HCV epidemic in the world. HCV intrafamilial transmission was defined as HCV transmission among relatives living in the same household. DESIGN: Case-control study. Cases were adult patients with acute hepatitis C diagnosed in two 'fever hospitals' of Cairo. Controls were adult patients with acute hepatitis A diagnosed in the same two hospitals, and family members of cases. All consenting household members of cases provided blood for HCV serological and RNA testing. Homology of viral sequences (NS5b region) within households was used to ascertain HCV intrafamilial transmission. Exposures at risk for HCV during the 1-6 months previous to onset of symptoms were assessed in all cases and controls. RESULTS: From April 2002 to June 2007, 100 cases with acute hepatitis C, and 678 controls (416 household members and 262 patients with acute hepatitis A) were recruited in the study. Factors independently associated with HCV infection and their attributable fractions (AFs) were the following: having had a catheter (OR=5.0, 95% CI=1.4 to 17.8; AF=6.7%), an intravenous perfusion (OR=5.8, 95% CI=2.5 to 13.3; AF=20.1%), stitches (OR=2.0, 95% CI=1.3 to 6.6; AF=10.7%), gum treatment (OR=3.7, 95% CI=1.1 to 11.9; AF=3.8%) and being illiterate (OR=2.4, 95% CI=1.4 to 4.4). Of the 100 cases, 18 had viraemic HCV-infected household members. Three long-married (>15&emsp14;years) couples were infected with virtually identical sequences and none of the three index patients reported any exposure at risk, suggesting HCV intra-familial transmission. CONCLUSION: While three new HCV infections out of 100 could be linked to intra-familial transmission, parenteral iatrogenic transmission (dental care included) was accountable for 34.6% of these new infections. Thus, the relative contribution of intrafamilial transmission to HCV spread seems to be limited.
    Mots-clés : &, Acute, Adolescent, Adult, Aged, C/epidemiology/, Case-Control, Cross, disease, Egypt/epidemiology, Factors, Family, Female, Health, Hepacivirus/classification/isolation, Hepatitis, Humans, Infection/epidemiology/, Male, Middle, Phylogeny, purification, Risk, Studies, transmission, transmission/virology, Young.


  • Paule, B, Castagne, V, Picard, V, Saffroy, R, Adam, R, Guettier, C, Farinotti, R & Bonhomme-Faivre, L 2010, « MDR1 polymorphism role in patients treated with cetuximab and irinotecan in irinotecan refractory colorectal cancer », Med Oncol, vol. 27, no. 4, p. 1066-72, viewed sans date, .
    Résumé : The aim of the study was to evaluate the influence of the MDR1 C3435T polymorphism on the therapeutic response in 23 patients treated with cetuximab plus irinotecan for irinotecan refractory liver metastatic colorectal cancer considering their KRAS status. Indeed, irinotecan and its active metabolite (SN-38) are both substrates of P-glycoprotein (P-gp) encoded by MDR1. Patients received cetuximab and irinotecan up to progression. The overall survival was 55% at 10 months. Overall, four patients had an undetermined KRAS status and two patients with mutated KRAS were in progression disease. The response to treatment was observed after 3 months among the 17 wild-type KRAS patients. Two patients presented a progressive disease (1 TT and 1 CT), eight patients had a stable disease (5 CC and 3CT) and five patients had a partial response (3 CC and 2 CT). Importantly, 2 patients (2 TT) were in complete response and still alive 5 years after starting the treatment, which suggests that the combination of wild-type KRAS and MDR1 3435 TT may be a factor of good prognosis. These results suggest that EGFR inhibition by cetuximab may overcome this irinotecan resistance by abrogating drug efflux depending on MDR1 3435 polymorphism. Among patients resistant to irinotecan, it is still possible to use the association of cetuximab plus irinotecan to obtain a complete resection of hepatic metastases that is necessary to improve their survival.
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  • Peng, B, Xu, L, Cao, F, Wei, T, Yang, C, Uzan, G & Zhang, D 2010, « HSP90 inhibitor, celastrol, arrests human monocytic leukemia cell U937 at G0/G1 in thiol-containing agents reversible way », Mol Cancer, vol. 9, p. 79, viewed sans date, .
    Résumé : BACKGROUND: Because some of heat shock protein 90's (HSP90) clients are key cell cycle regulators, HSP90 inhibition can affect the cell cycle. Recently, celastrol is identified both as a novel inhibitor of HSP90 and as a potential anti-tumor agent. However, this agent's effects on the cell cycle are rarely investigated. In this study, we observed the effects of celastrol on the human monocytic leukemia cell line U937 cell cycle. RESULTS: Celastrol affected the proliferation of U937 in a dose-dependent way, arresting the cell cycle at G0/G1 with 400 nM doses and triggering cell death with doses above 1000 nM. Cell cycle arrest was accompanied by inhibition of HSP90 ATPase activity and elevation in HSP70 levels (a biochemical hallmark of HSP90 inhibition), a reduction in Cyclin D1, Cdk4 and Cdk6 levels, and a disruption of the HSP90/Cdc37/Cdk4 complex. The observed effects of celastrol on the U937 cell cycle were thiol-related, firstly because the effects could be countered by pre-loading thiol-containing agents and secondly because celastrol and thiol-containing agents could react with each other to form new compounds. CONCLUSIONS: Our results disclose a novel action of celastrol– causing cell cycle arrest at G0/G1 phase based upon thiol-related HSP90 inhibition. Our work suggests celastrol's potential in tumor and monocyte-related disease management.
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  • Pennarun, G, Hoffschir, F, Revaud, D, Granotier, C, Gauthier, LR, Mailliet, P, Biard, DS & Boussin, FD 2010, « ATR contributes to telomere maintenance in human cells », Nucleic Acids Research, vol. 38, no. 9, p. 2955-2963, viewed sans date, <<Go to ISI>://WOS:000277994600024>.
    Résumé : Telomere maintenance is essential to preserve genomic stability and involves several telomere-specific proteins as well as DNA replication and repair proteins. The kinase ATR, which has a crucial function in maintaining genome integrity from yeast to human, has been shown to be involved in telomere maintenance in several eukaryotic organisms, including yeast, Arabidopsis and Drosophila. However, its role in telomere maintenance in mammals remains poorly explored. Here, we report by using telomere-fluorescence in situ hybridization (Telo-FISH) on metaphase chromosomes that ATR deficiency causes telomere instability both in primary human fibroblasts from Seckel syndrome patients and in HeLa cells. The telomere aberrations resulting from ATR deficiency (i.e. sister telomere fusions and chromatid-type telomere aberrations) are mainly generated during and/or after telomere replication, and involve both leading and lagging strand telomeres as shown by chromosome orientation-FISH (CO-FISH). Moreover, we show that ATR deficiency strongly sensitizes cells to the G-quadruplex ligand 360A, enhancing sister telomere fusions and chromatid-type telomere aberrations involving specifically the lagging strand telomeres. Altogether, these data reveal that ATR plays a critical role in telomere maintenance during and/or after telomere replication in human cells.


  • Petillon, S, Vibert, E, Gorden, D-L, de la Serna, S, Salloum, C & Azoulay, D 2010, « Hepatectomy and intrahepatic biliary enteric anastomosis: a rescue surgery for obstructed metallic biliary stents in chronic pancreatitis », Gastroenterol Clin Biol, vol. 34, no. 4-5, p. 310-3, viewed sans date, .
    Mots-clés : Anastomosis, Chronic/complications Stents/ adverse effects, Obstructive/etiology/ surgery Male Middle Aged Pancreatitis, Roux-en-Y Biliary Fistula/etiology/ surgery Drainage Hepatectomy Humans Jaundice.
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