Publications (37)208.75 Total impact
-
Article: Microbial dysbiosis and colon carcinogenesis: could colon cancer be considered a bacteria-related disease?
[show abstract] [hide abstract]
ABSTRACT: Colorectal cancer (CRC) is posing an increasingly important burden on the health care system, with western countries seeing a growing incidence of the disease. Except for germline DNA mutations which have been attributed to less than 5% of patients, little is known about the main causes of CRC. However, environment factors such as food, lifestyle and medication are now suspected to have a major influence on inducing cancers. Today, exhaustive quantitative and qualitative evaluation of all environmental factors is not possible. Various environment-induced diseases have been characterized based on colon microflora, also called microbiota, analyses. Growing data have shown specific changes in microflora (i.e. dysbiosis) in the stools of patients with colon cancer or those adherent to the colonic mucosa. Thus, it appears that microbiota may be considered a platform offering host and environment interactions for studying CRCs. The hypothesis that colon cancer might be a bacteria-related disease is suggested and perspectives are discussed.Therapeutic Advances in Gastroenterology 05/2013; 6(3):215-29. -
Article: Non-invasive assessment of liver graft fibrosis by transient elastography after liver transplantation.
[show abstract] [hide abstract]
ABSTRACT: BACKGROUND: Liver stiffness measurement (LSM) by transient elastography (TE) (FibroScan(®)) is a validated method of quantifying liver fibrosis in non-transplanted patients with hepatitis C virus (HCV). It could be useful in follow-up after liver transplantation (LT). The aim of this study was to assess the diagnostic accuracy of LSM in evaluating liver fibrosis after LT in patients with and without recurrent HCV. PATIENTS AND METHODS: Forty-three patients (mean age 57.6±9.9 years), 28 (65.1%) HCV-positive patients and 15 (34.9%) HCV-negative patients underwent gold standard liver biopsy and TE 55.8±4.9 months after transplantation. Liver fibrosis was scored on biopsy specimens according to METAVIR (F0-F4). Accuracy of TE and optimal stiffness cut-off values for fibrosis staging were determined by a receiver-operating characteristics (ROC) curve analysis. RESULTS: Median stiffness values were significantly different for METAVIR score less than 2 (5.8kPa) vs. METAVIR score greater to equal to 2 (9.6kPa) (P<0.001). The area under the ROC curve was 0.83 for METAVIR score greater to equal to 2 (95%CI: 0.71-0.95). The optimal stiffness cut-off value was 7kPa for METAVIR scores greater to equal to 2. The results were similar whether the patients had recurrent HCV infection or not. CONCLUSIONS: These results indicate that transient elastography accurately identifies LT recipients with significant fibrosis, irrespective of HCV status. It is a promising non-invasive tool to assess graft fibrosis progression after LT in patients with HCV recurrence, as well as for screening of late graft fibrosis of other etiologies. Transient elastography could reduce the use of invasive protocol biopsies.Gastroentérologie Clinique et Biologique 01/2013; · 0.80 Impact Factor -
Article: Recurring multicystic inflammatory pseudotumor of the liver: A case report.
[show abstract] [hide abstract]
ABSTRACT: Inflammatory pseudotumor (IPT) of the liver is a rare benign lesion for which imaging diagnosis remains a challenge. We report the case of a 39-year-old Algerian woman, who presented epigastric pains combined with fever and jaundice. Ultrasound, CT scan and MRI showed the presence of a 10cm-long multi-septated cystic mass of the left lobe, with peripheral enhancement. A left-hepatectomy was performed and histopathology revealed an IPT of the liver. During the 4 following years, the patient had three other recurrences of liver IPT at various locations distinct from the original, revealed by the same clinical symptoms. During these relapses, the lesions did regress thanks to a medical treatment. This observation underlines the difficulty of the diagnosis and treatment of liver IPT.Gastroentérologie Clinique et Biologique 12/2012; · 0.80 Impact Factor -
Article: Immunohistochemical Markers on Needle Biopsies Are Helpful for the Diagnosis of Focal Nodular Hyperplasia and Hepatocellular Adenoma Subtypes.
[show abstract] [hide abstract]
ABSTRACT: Phenotypic identification of focal nodular hyperplasia (FNH) and hepatocellular adenoma (HCA) subtypes using immunohistochemical markers has been developed from their molecular characteristics. Our objective was to evaluate the sensitivity of these markers in the definitive diagnosis of these lesions by core needle biopsies. A total of 239 needle biopsies paired with their surgical resection specimen (group A) or without an associated resection specimen (group B) were reviewed. Using a step-by-step algorithm after standard staining, appropriate immunostaining analyses were performed to determine the certainty of diagnosis of FNH, HNF1α-inactivated HCA, inflammatory HCA, β-catenin-activated HCA, or unclassified HCA. The diagnosis of FNH was certain or probable on routine stains in 53% of needle biopsies of group A, whereas after glutamine synthetase staining, the diagnosis was certain in 86.7% as compared with 100% on the corresponding surgical specimen (P=0.04). In needle biopsies of group A, the diagnosis of HCA was certain on routine stains in 58.6% as compared with 94.3% on surgical specimens. After specific immunostaining, diagnosis was established on biopsies with 74.3% certainty, including all HCA subtypes, with similar distribution in surgical specimens. For each "certain diagnosis" paired diagnostic test (biopsy and surgical specimen), a positive correlation was observed (P<0.001). No significant difference was observed between groups A and B for FNH (P=0.714) or for HCA subtypes (P=0.750). Compared with surgical specimens, immunohistochemical analysis performed on biopsies allowed the discrimination of FNH from HCA and the identification of HCA subtypes with good performance.The American journal of surgical pathology 10/2012; 36(11):1691-1699. · 4.06 Impact Factor -
Article: Automated liver volumetry in orthotopic liver transplantation using multiphase acquisitions on MDCT.
[show abstract] [hide abstract]
ABSTRACT: OBJECTIVE: The aim of this study was to test a new automated hepatic volumetry technique by comparing the accuracies and postprocessing times of manual and automated liver volume segmentation methods in a patient population undergoing orthotopic liver transplantation so that liver volume could be determined on pathology as the standard of reference. CONCLUSION: Both manual and automated multiphase MDCT-based volume measurements were strongly correlated to liver volume (Pearson correlation coefficient, r = 0.87 [p < 0.0001] and 0.90 [p < 0.0001], respectively). Automated multiphase segmentation was significantly more rapid than manual segmentation (mean time, 16 ± 5 [SD] and 86 ± 3 seconds, respectively; p = 0.01). Overall, automated liver volumetry based on multiphase CT acquisitions is feasible and more rapid than manual segmentation.American Journal of Roentgenology 06/2012; 198(6):W568-74. · 2.78 Impact Factor -
Article: Pulmonary cryptococcoma in a patient with Sézary syndrome treated with alemtuzumab.
European journal of dermatology: EJD 09/2011; 21(6):1018-20. · 2.53 Impact Factor -
Article: GNAS-activating mutations define a rare subgroup of inflammatory liver tumors characterized by STAT3 activation.
[show abstract] [hide abstract]
ABSTRACT: Mosaic G-protein alpha-subunit (GNAS)-activating mutations are responsible for the McCune-Albright (MCA) syndrome. This oncogene that activates the adenylate cyclase is also mutated in various tumor types leading to the accumulation of cyclic-AMP. Identification of a hepatocellular adenoma (HCA) in two MCA patients led us to search for GNAS activation in benign and malignant hepatocellular carcinogenesis. GNAS mutations were screened by sequencing 164 HCA, 245 hepatocellular carcinoma (HCC), and 17 fibrolamellar carcinomas. Tumors were characterized by quantitative RT-PCR, gene mutation screening and pathological reviewing. The consequences of wild type and mutant GNAS expression were analyzed in hepatocellular cell lines. A somatic GNAS-activating mutation was identified in 5 benign tumors and in 2 HCC. In benign tumors, GNAS mutations were exclusive from HNF1A, CTNNB1, and IL6ST mutations whereas one HCC demonstrated both CTNNB1 and GNAS mutations. Quantitative RT-PCR showed an activation of the IL-6 and interferon pathways in GNAS-mutated tumor tissues. Accordingly, pathological reviewing identified in GNAS-mutated tumors an inflammatory phenotype characterized by fibrosis and STAT3 activation. We further demonstrated in HCC cell lines that GNAS mutant expression induced inflammatory response and STAT3 activation. We identified for the first time the association between two rare diseases, MCA syndrome and HCA occurrence, but also that somatic GNAS-activating mutations in sporadic benign and malignant liver tumors are characterized by an inflammatory phenotype. These results showed a cross-talk between cyclic-AMP and JAK/STAT pathways in liver tumors and they reinforce the role of STAT3 activation in liver tumorigenesis.Journal of Hepatology 08/2011; 56(1):184-91. · 9.26 Impact Factor -
Article: Somatic mutations activating STAT3 in human inflammatory hepatocellular adenomas.
[show abstract] [hide abstract]
ABSTRACT: Inflammatory hepatocellular adenomas (IHCAs) are benign liver tumors. 60% of these tumors have IL-6 signal transducer (IL6ST; gp130) mutations that activate interleukin 6 (IL-6) signaling. Here, we report that 12% of IHCA subsets lacking IL6ST mutations harbor somatic signal transducer and activator of transcription 3 (STAT3) mutations (6/49). Most of these mutations are amino acid substitutions in the SH2 domain that directs STAT3 dimerization. In contrast to wild-type STAT3, IHCA STAT3 mutants constitutively activated the IL-6 signaling pathway independent of ligand in hepatocellular cells. Indeed, the IHCA STAT3 Y640 mutant homodimerized independent of IL-6 and was hypersensitive to IL-6 stimulation. This was associated with phosphorylation of tyrosine 705, a residue required for IL-6-induced STAT3 activation. Silencing or inhibiting the tyrosine kinases JAK1 or Src, which phosphorylate STAT3, impaired constitutive activity of IHCA STAT3 mutants in hepatocellular cells. Thus, we identified for the first time somatic STAT3 mutations in human tumors, revealing a new mechanism of recurrent STAT3 activation and underscoring the role of the IL-6-STAT3 pathway in benign hepatocellular tumorigenesis.Journal of Experimental Medicine 06/2011; 208(7):1359-66. · 13.85 Impact Factor -
Article: Non-invasive diagnostic imaging of hepatocellular carcinoma: targeting cellular characterization?
Journal of Hepatology 02/2011; 55(1):224-6. · 9.26 Impact Factor -
Article: Microbial dysbiosis in colorectal cancer (CRC) patients.
[show abstract] [hide abstract]
ABSTRACT: The composition of the human intestinal microbiota is linked to health status. The aim was to analyze the microbiota of normal and colon cancer patients in order to establish cancer-related dysbiosis. Stool bacterial DNA was extracted prior to colonoscopy from 179 patients: 60 with colorectal cancer, and 119 with normal colonoscopy. Bacterial genes obtained by pyrosequencing of 12 stool samples (6 Normal and 6 Cancer) were subjected to a validated Principal Component Analysis (PCA) test. The dominant and subdominant bacterial population (C. leptum, C. coccoides, Bacteroides/Prevotella, Lactobacillus/Leuconostoc/Pediococcus groups, Bifidobacterium genus, and E. coli, and Faecalibacterium prausnitzii species) were quantified in all individuals using qPCR and specific IL17 producer cells in the intestinal mucosa were characterized using immunohistochemistry. Pyrosequencing (Minimal sequence 200 nucleotide reads) revealed 80% of all sequences could be assigned to a total of 819 taxa based on default parameter of Classifier software. The phylogenetic core in Cancer individuals was different from that in Normal individuals according to the PCA analysis, with trends towards differences in the dominant and subdominant families of bacteria. Consequently, All-bacteria [log(10) (bacteria/g of stool)] in Normal, and Cancer individuals were similar [11.88±0.35, and 11.80±0.56, respectively, (P = 0.16)], according to qPCR values whereas among all dominant and subdominant species only those of Bacteroides/Prevotella were higher (All bacteria-specific bacterium; P = 0.009) in Cancer (-1.04±0.55) than in Normal (-1.40±0.83) individuals. IL17 immunoreactive cells were significantly expressed more in the normal mucosa of cancer patients than in those with normal colonoscopy. This is the first large series to demonstrate a composition change in the microbiota of colon cancer patients with possible impact on mucosal immune response. These data open new filed for mass screening and pathophysiology investigations.PLoS ONE 01/2011; 6(1):e16393. · 4.09 Impact Factor -
Article: Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage.
[show abstract] [hide abstract]
ABSTRACT: Maturity onset diabetes of the young type 3 (MODY3) is a consequence of heterozygous germline mutation in HNF1A. A subtype of hepatocellular adenoma (HCA) is also caused by biallelic somatic HNF1A mutations (H-HCA), and rare HCA may be related to MODY3. To better understand a relationship between the development of MODY3 and HCA, we compared both germline and somatic spectra of HNF1A mutations. We compared 151 somatic HNF1A mutations in HCA with 364 germline mutations described in MODY3. We searched for genotoxic and oxidative stress features in HCA and surrounding liver tissue. A spectrum of HNF1A somatic mutations significantly differed from the germline changes in MODY3. In HCA, we identified a specific hot spot at codon 206, nonsense and frameshift mutations mainly in the NH(2)-terminal part, and almost all amino acid substitutions were restricted to the POU-H domain. The high frequency of G-to-T tranversions, predominantly found on the nontranscribed DNA strand, suggested a genotoxic mechanism. However, no features of oxidative stress were observed in the nontumor liver tissue. Finally, in a few MODY3 patients with HNF1A germline mutation leading to amino acid substitutions outside the POU-H domain, we identified a different subtype of HCA either with a gp130 and/or CTNNB1 activating mutation. Germline HNF1A mutations could be associated with different molecular subtypes of HCA. H-HCA showed mutations profoundly inactivating hepatocyte nuclear factor-1alpha function; they are associated with a genotoxic signature suggesting a specific toxicant exposure that could be associated with genetic predisposition.Diabetes 07/2010; 59(7):1836-44. · 8.29 Impact Factor -
Article: Self-expanding metallic stent for ischemic colonic obstruction.
The American Journal of Gastroenterology 10/2009; 104(9):2372-3. · 7.28 Impact Factor -
Article: Cannabinoid CB2 receptor potentiates obesity-associated inflammation, insulin resistance and hepatic steatosis.
[show abstract] [hide abstract]
ABSTRACT: Obesity-associated inflammation is of critical importance in the development of insulin resistance and non-alcoholic fatty liver disease. Since the cannabinoid receptor CB2 regulates innate immunity, the aim of the present study was to investigate its role in obesity-induced inflammation, insulin resistance and fatty liver. Murine obesity models included genetically leptin-deficient ob/ob mice and wild type (WT) mice fed a high fat diet (HFD), that were compared to their lean counterparts. Animals were treated with pharmacological modulators of CB2 receptors. Experiments were also performed in mice knock-out for CB2 receptors (Cnr2 -/-). In both HFD-fed WT mice and ob/ob mice, Cnr2 expression underwent a marked induction in the stromal vascular fraction of epididymal adipose tissue that correlated with increased fat inflammation. Treatment with the CB2 agonist JWH-133 potentiated adipose tissue inflammation in HFD-fed WT mice. Moreover, cultured fat pads isolated from ob/ob mice displayed increased Tnf and Ccl2 expression upon exposure to JWH-133. In keeping, genetic or pharmacological inactivation of CB2 receptors decreased adipose tissue macrophage infiltration associated with obesity, and reduced inductions of Tnf and Ccl2 expressions. In the liver of obese mice, Cnr2 mRNA was only weakly induced, and CB2 receptors moderately contributed to liver inflammation. HFD-induced insulin resistance increased in response to JWH-133 and reduced in Cnr2 -/- mice. Finally, HFD-induced hepatic steatosis was enhanced in WT mice treated with JWH-133 and blunted in Cnr2 -/- mice. These data unravel a previously unrecognized contribution of CB2 receptors to obesity-associated inflammation, insulin resistance and non-alcoholic fatty liver disease, and suggest that CB2 receptor antagonists may open a new therapeutic approach for the management of obesity-associated metabolic disorders.PLoS ONE 02/2009; 4(6):e5844. · 4.09 Impact Factor -
Article: Liver cirrhosis: intravoxel incoherent motion MR imaging--pilot study.
[show abstract] [hide abstract]
ABSTRACT: To retrospectively evaluate a respiratory-triggered diffusion-weighted (DW) magnetic resonance (MR) imaging sequence combined with parallel acquisition to allow the calculation of pure molecular-based (D) and perfusion-related (D*, f) diffusion parameters, on the basis of the intravoxel incoherent motion (IVIM) theory, to determine if these parameters differ between patients with cirrhosis and patients without liver fibrosis. The institutional review board approved this retrospective study; informed consent was waived. IVIM DW imaging was tested on three alkane phantoms, on which the signal-intensity decay curves according to b factors were logarithmically plotted. Ten b factors (0, 10, 20, 30, 50, 80, 100, 200, 400, 800 sec/mm(2)) were used in patients. Patients with documented liver cirrhosis (cirrhotic liver group, n = 12) and patients without chronic liver disease (healthy liver group, n = 25) were included. The mean liver D, D*, and f values were measured and compared with the apparent diffusion coefficient (ADC) computed by using four b values (0, 200, 400, 800 sec/mm(2)). Liver ADC and D, f, and D* parameters were compared between the cirrhotic liver group and healthy liver group. Means were compared by using the Student t test. Signal-intensity decay curves were monoexponential on phantoms and biexponential in patients. In vivo, mean ADC values were significantly higher than D in the healthy liver group (ADC = 1.39 x 10(-3) mm(2)/sec +/- 0.2 [standard deviation] vs D = 1.10 x 10(-3) mm(2)/sec +/- 0.7) and in the cirrhotic liver group (ADC = 1.23 x 10(-3) mm(2)/sec +/- 0.4 vs D = 1.19 x 10(-3) mm(2)/sec +/- 0.5) (P = .03). ADC and D* were significantly reduced in the cirrhotic liver group compared with those in the healthy liver group (respective P values of .03 and .008). Restricted diffusion observed in patients with cirrhosis may be related to D* variations, which reflect decreased perfusion, as well as alterations in pure molecular water diffusion in cirrhotic livers.Radiology 01/2009; 249(3):891-9. · 5.73 Impact Factor -
Article: Liver resection for hepatocellular carcinoma.
[show abstract] [hide abstract]
ABSTRACT: The indications and the results for liver resection for hepatocellular cancer (HCC) depend on the stage of the tumor at diagnosis, the functional reserve of the liver, and the use of suitably adapted surgical techniques. This article briefly discusses liver resection for HCC in patients who do not have chronic liver disease and then discusses liver resection for HCC in patients who have chronic liver disease.Surgical Oncology Clinics of North America 08/2008; 17(3):607-33, ix. · 1.12 Impact Factor -
Article: Stents for palliation of obstructive metastatic colon cancer: impact on management and chemotherapy administration.
[show abstract] [hide abstract]
ABSTRACT: The more rapid and less complicated recovery after palliative stent insertion compared with surgery may theoretically facilitate the early administration of chemotherapy. A retrospective study. University tertiary care referral center. From January 1, 1996, to September 15, 2005, 58 patients with obstructing colon cancer and nonresectable synchronous metastases were treated with self-expanding colonic metallic stent (SEMS) (n = 31) or surgery (n = 27). Comparison of the use of SEMS and emergency surgery as palliative measures to treat obstructing colon cancer with special reference to time to chemotherapy administration and survival. Mortality and morbidity were comparable between the 2 groups. Median hospital stay was shorter after SEMS insertion than after surgery (median, 8.0 vs 13.5 days, respectively; P < .01). Incidence of stoma creation was lower in patients treated with SEMS than in patients treated with surgery (6% vs 37%, respectively; P = .02). The median time to chemotherapy administration was shorter after SEMS insertion than after surgery (14.0 vs 28.5 days, respectively; P = .002). Three patients with SEMS and 0 patients in the surgical group underwent a curative colonic and hepatic resection after downstaging by chemotherapy (P = .27). Two patients (6%) with SEMS and undergoing chemotherapy had a tumor perforation requiring emergency surgery. There was no difference in survival between the 2 groups (median survival, 13.7 months for SEMS vs 11.4 months for surgery; P = .19). Insertion of SEMS should be the first step to treat obstructing colon cancer with nonresectable synchronous metastases because it allows chemotherapy to be administered earlier, may increase the resectability rate of metastases, and favorably impacts survival. The risk of tumor perforation while receiving chemotherapy requires attention.Archives of Surgery 08/2007; 142(7):619-23; discussion 623. · 4.24 Impact Factor -
Article: The sphingosine 1-phosphate receptor S1P2 triggers hepatic wound healing.
[show abstract] [hide abstract]
ABSTRACT: Sphingosine 1-phosphate (S1P) is a bioactive sphingolipid produced by sphingosine kinase (SphK1 and 2). We previously showed that S1P receptors (S1P1, S1P2, and S1P3) are expressed in hepatic myofibroblasts (hMF), a population of cells that triggers matrix remodeling during liver injury. Here we investigated the function of these receptors in the wound healing response to acute liver injury elicited by carbon tetrachloride, a process that associates hepatocyte proliferation and matrix remodeling. Acute liver injury was associated with the induction of S1P2, S1P3, SphK1, and SphK2 mRNAs and increased SphK activity, with no change in S1P1 expression. Necrosis, inflammation, and hepatocyte regeneration were similar in S1P2-/- and wild-type (WT) mice. However, compared with WT mice, S1P2-/- mice displayed reduced accumulation of hMF, as shown by lower induction of smooth muscle alpha-actin mRNA and lower induction of TIMP-1, TGF-beta1, and PDGF-BB mRNAs, overall reflecting reduced activation of remodeling in response to liver injury. The wound healing response was similar in S1P3-/- and WT mice. In vitro, S1P enhanced proliferation of cultured WT hMF, and PDGF-BB further enhanced the mitogenic effect of S1P. In keeping with these findings, PDGF-BB up-regulated S1P2 and SphK1 mRNAs, increased SphK activity, and S1P2 induced PDGF-BB mRNA. These effects were blunted in S1P2-/- cells, and S1P2-/- hMF exhibited reduced mitogenic and comitogenic responses to S1P. These results unravel a novel major role of S1P2 in the wound healing response to acute liver injury by a mechanism involving enhanced proliferation of hMF.The FASEB Journal 08/2007; 21(9):2005-13. · 5.71 Impact Factor -
Article: Association of CYP1B1 germ line mutations with hepatocyte nuclear factor 1alpha-mutated hepatocellular adenoma.
[show abstract] [hide abstract]
ABSTRACT: Biallelic somatic mutations of TCF1 coding for hepatocyte nuclear factor 1alpha (HNF1alpha) are found in 50% of the hepatocellular adenoma (HCA) cases usually associated with oral contraception. In rare cases, HNF1alpha germ line mutations could also predispose to familial adenomatosis. In order to identify new genetic factors predisposing to HNF1alpha-mutated HCA, we searched for mutations in genes involved in the metabolism of estrogen. For 10 genes (CYP1A1, CYP1A2, CYP3A4, CYP3A5, COMT, UGT2B7, NQO1, GSTM1, GSTP1, and GSTT1), we did not find mutations nor differences in the allele distribution among 32 women presenting HNF1alpha-mutated adenomas compared with 58 controls. In contrast, we identified a CYP1B1 germ line heterozygous mutation in 4 of 32 women presenting HNF1alpha-mutated adenomas compared with none in 58 controls. We confirmed these results with the identification of four additional CYP1B1 mutations in a second series of 26 cases. No mutations were found in the control group, which was extended to 98 individuals, and only a known rare genetic variant was observed in two controls (P = 0.0003). We did an ethoxyresorufin O-deethylase assay to evaluate the functional consequence of the CYP1B1 mutations. We found reduced enzymatic activity in each CYP1B1 variant. In addition, an E229K CYP1B1 mutation was found in a woman with a germ line HNF1alpha mutation in a familial adenomatosis context. In this large family, all three patients with adenomatosis bore both HNF1 and CYP1B1 germ line mutations. In conclusion, our data suggested that CYP1B1 germ line-inactivating mutations might increase the incidence of HCA in women with HNF1alpha mutations.Cancer Research 04/2007; 67(6):2611-6. · 7.86 Impact Factor -
Article: [Endocannabinoids: therapeutic perspectives in chronic liver diseases].
Gastroentérologie Clinique et Biologique 03/2007; 31(3):255-8. · 0.80 Impact Factor -
Article: Successful reuse of liver graft 13 years after initial transplantation.
[show abstract] [hide abstract]
ABSTRACT: The shortage of organ donors and the increased demand for liver transplantation has led to new strategies to increase the availability of liver grafts for transplantation. Occasionally, previous liver transplant recipients may experience brain death and become organ donors. Although this is a very rare situation, we and others have showed that reuse of liver grafts could be performed successfully within one week after transplantation. Late reuse has, however, not been reported to date. We report the first case in which a liver graft was successfully reused 13 years after the first transplantation.Transplantation 01/2007; 82(11):1547-8. · 4.00 Impact Factor
Top co-authors
Top Journals
- Hepatology (3)
- Gastroentérologie Clinique et Biologique (3)
- Gastroenterology (2)
- Journal of Hepatology (2)
- PLoS ONE (2)
Institutions
-
2007–2012
-
Hôpital Henri Mondor – Hôpitaux Universitaires Henri Mondor
Créteil, Ile-de-France, France -
Institut de Recherche Biomédicale des Armées (IRBA)
Marseille, Provence-Alpes-Cote d'Azur, France
-
-
2010–2011
-
Institut national de la santé et de la recherche médicale
- Unité de Génomique Fonctionnelle des Tumeurs Solides U674
Paris, Ile-de-France, France
-
-
2009–2011
-
Assistance Publique – Hôpitaux de Paris
Paris, Ile-de-France, France -
Université Paris-Est
Descartes, Centre, France
-
-
2005–2009
-
INSERM, GIP CYCERON
Caen, Basse-Normandie, France
-
