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University of Rennes 1, Etablissement Francais Du Sang and Rennes University Hospital Center | Date: 2014-02-07

The present invention relates to methods and kits for predicting the survival time of a patient suffering from a diffuse large B-cell lymphoma (DLBCL). In particular, the present invention relates to a method for predicting the survival time of a patient suffering from a diffuse large B-cell lymphoma (DLBCL) comprising the step of i) determining the level of sPD-L1 in a blood sample obtained from the patient ii) comparing the level determined at step i) with a predetermined reference value and iii) concluding that the patient has a poor prognosis when the level determined at step i) is higher than the predetermined reference value or concluding that the patient has a good prognosis when the level determined at step i) is lower than the predetermined reference value.

Verin M.,Rennes University Hospital Center
European Journal of Human Genetics | Year: 2016

Primary brain calcification (PBC) is a dominantly inherited calcifying disorder of the brain. SLC20A2 loss-of-function variants account for the majority of families. Only one genomic deletion encompassing SLC20A2 and six other genes has been reported. We performed whole-exome sequencing (WES) in 24 unrelated French patients with PBC, negatively screened for sequence variant in the known genes SLC20A2, PDGFB, PDGFRB and XPR1. We used the CANOES tool to detect copy number variations (CNVs). We detected two deletions of exon 2 of SLC20A2 in two unrelated patients, which segregated with PBC in one family. We then reanalyzed the same series using a QMPSF assay including one amplicon in each exon of SLC20A2 and detected two supplemental partial deletions in two patients: one deletion of exon 4 and one deletion of exons 4 and 5. These deletions were missed by the first screening step of CANOES but could finally be detected after readjustment of bioinformatic parameters and use of a genotyping step of CANOES. This study reports the first partial deletions of SLC20A2 and strengthens its position as the major PBC-causative gene. It is possible to detect short CNVs from WES data, although the sensitivity of such tools should be evaluated in comparison with other methods.European Journal of Human Genetics advance online publication, 1 June 2016; doi:10.1038/ejhg.2016.50. © 2016 Macmillan Publishers Limited

Chester C.,Stanford University | Marabelle A.,Institute Of Gustave Roussy Service | Houot R.,University of Rennes 1 | Houot R.,Rennes University Hospital Center | And 2 more authors.
Current Opinion in Immunology | Year: 2015

Cancer immunotherapy is a rapidly evolving field that offers a novel paradigm for cancer treatment: therapies focus on enhancing the immune system's innate and adaptive anti-tumor response. Early immunotherapeutics have achieved impressive clinical outcomes and monoclonal antibodies are now integral to therapeutic strategies in a variety of cancers. However, only recently have antibodies targeting innate immune cells entered clinical development. Innate immune effector cells play important roles in generating and maintaining antitumor immunity. Antibody-dependent cell-mediated cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) are important innate immune mechanisms for tumor eradication. These cytolytic processes are initiated by the detection of a tumor-targeting antibody and can be augmented by activating co-stimulatory pathways or blocking inhibitory signals on innate immune cells. The combination of FDA-approved monoclonal antibodies with innate effector-targeting antibodies has demonstrated potent preclinical therapeutic synergy and early-phase combinatorial clinical trials are ongoing. © 2015 Elsevier Ltd.

Holzmeister J.,University of Zurich | Leclercq C.,Rennes University Hospital Center
The Lancet | Year: 2011

Implantable cardioverter defibrillators and cardiac resynchronisation therapy (CRT) have become standard of care in modern treatment for heart failure. Results from trials have provided ample evidence that CRT, in addition to its proven benefits in patients with symptomatic heart failure (New York Heart Association [NYHA] class III), might also reduce morbidity and mortality in those with mildly symptomatic heart failure (NYHA class II). As a result, the 2010 European Society of Cardiology guidelines now recommend CRT for both patient populations. In this review we summarise and critically assess the landmark randomised clinical trials REVERSE, MADIT-CRT, and RAFT. Furthermore, we discuss the rationale and available evidence for other emerging indications of CRT, including its use in patients with a mildly reduced left ventricular ejection fraction (>35), in those with a narrow QRS complex (≤120 ms), and in those with concomitant bradyarrhythmic pacemaker indications. We also focus on patients who do not respond to CRT, and on CRT optimisation. © 2011 Elsevier Ltd.

Brissot P.,University of Rennes 1 | Bardou-Jacquet E.,University of Rennes 1 | Jouanolle A.-M.,Rennes University Hospital Center | Loreal O.,University of Rennes 1
Trends in Molecular Medicine | Year: 2011

Iron disorders of genetic origin are mainly composed of iron overload diseases, the most frequent being HFE-related hemochromatosis. Hepcidin deficiency underlies iron overload in HFE-hemochromatosis as well as in several other genetic iron excess disorders, such as hemojuvelin or hepcidin-related hemochromatosis and transferrin receptor 2-related hemochromatosis. Deficiency of ferroportin, the only known cellular protein iron exporter, produces iron overload in the typical form of ferroportin disease. By contrast, genetically enhanced hepcidin production, as observed in matriptase-2 deficiency, generates iron-refractory iron deficiency anemia. Diagnosis of these iron storage disorders is usually established noninvasively through combined biochemical, imaging and genetic approaches. Moreover, improved knowledge of the molecular mechanisms accounting for the variations of iron stores opens the way of novel therapeutic approaches aiming to restore normal iron homeostasis. In this review, we will summarize recent findings about these various genetic entities that have been identified owing to an exemplary interplay between clinicians and basic scientists. © 2011 Elsevier Ltd.

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