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Hôpital-Camfrout, France

Guinde J.,Service dOncologie Thoracique | Laroumagne S.,Service dOncologie Thoracique | Kaspi E.,Service de Biologie Cellulaire | Kaspi E.,Aix - Marseille University | And 5 more authors.
Revue des Maladies Respiratoires | Year: 2015

The diagnosis of malignant pleural mesothelioma relies mostly on the pathological examination of pleural samples, validated by a panel of experts and generally obtained during medical or surgical thoracoscopy performed for the management of an exudative pleural effusion. In the absence of pleural effusion (dry-type mesothelioma), the diagnostic approach depends on the features of the lesions (pleural thickness, nodules and/or masses) and their pleural location. Ultrasound and CT-guided needle aspiration represent recognized alternative diagnostic techniques in these situations. We present the case of a patient, presenting a dry-type mesothelioma, whose diagnosis was obtained by endobronchial ultrasound (EBUS)-guided needle aspiration of a pleural mediastinal mass and confirmed by a CT-guided needle aspiration of another pleural mass in close contact with the chest wall. The samples have been compared and show quantitative and qualitative similarities. EBUS represents a minimally invasive alternative diagnostic technique for dry-type mesothelioma, showing thickness of the mediastinal pleura in contact with a central airway or when thoracoscopy, which remains the "gold standard" diagnostic approach, is not feasible. © 2015 SPLF.

Ianotto J.-C.,Institute Of Cancero Hematologie | Boyer-Perrard F.,Angers University Hospital Center | Gyan E.,CNRS Genetics, Immunotherapy, Chemistry & Cancer Laboratory | Laribi K.,Service dhematologie | And 16 more authors.
British Journal of Haematology | Year: 2013

Myeloproliferative neoplasm-related myelofibrosis is associated with cytopenic or proliferative phases, splenomegaly and constitutional symptoms. Few effective treatments are available and small series suggested that interferon could be an option for myelofibrosis therapy. We performed a retrospective study of pegylated-interferon α-2a (Peg-IFNα-2a) therapy in myelofibrosis. Sixty-two patients treated with Peg-IFNα-2a at 17 French and Belgian centres were included. Responses were determined based on the criteria established by the International Working Group for Myelofibrosis Research and Treatment. Mean follow-up was 26 months. Sixteen of 25 anaemic patients (64%) (eight concomitantly receiving recombinant erythropoietin) achieved a complete response and transfusion-independence was obtained in 5/13 patients (38·5%). Constitutional symptoms resolved in 82% of patients. All five leucopenic patients normalized their leucocyte counts, whereas a normal platelet count was obtained in 5/8 thrombocytopenic patients. Splenomegaly was reduced in 46·5% of patients, and complete resolution of thrombocytosis and leucocytosis were observed in 82·8% and 68·8% of patients, respectively. Side effects (mostly haematological) were mainly of grade 1-2. The only factor independently associated with treatment failure was a spleen enlargement of more than 6 cm below the costal margin. In conclusion, Peg-IFNα-2a induced high response rates with acceptable toxicity in a large proportion of patients with primary and secondary myelofibrosis, especially in early phases. © 2013 John Wiley & Sons Ltd.

Hamy A.-S.,Center des Maladies du Sein | Porcher R.,Center dEpidemiologie Clinique | Porcher R.,Paris West University Nanterre La Defense | Cuvier C.,Center des Maladies du Sein | And 12 more authors.
Reproductive BioMedicine Online | Year: 2014

Anti-Müllerian hormone (AMH) levels fall during chemotherapy. Treatment-induced amenorrhoea is a reversible phenomenon, but few data are available on long-term AMH changes in breast cancer. The aim of the study was to describe serum AMH levels before, during and in the long term after chemotherapy, and to show a potential AMH recovery. Between May 2010 and June 2011, we selected 134 women aged 18-43 years at the time of breast cancer diagnosis who received chemotherapy between 2005 and 2011, and had not undergone an oophorectomy or had previous cytotoxic treatment. The AMH levels were assessed before, during and 4 months to 5.5 years after the end of chemotherapy. During chemotherapy, AMH was undetectable in 69% of women. After chemotherapy, a significant increase in AMH was found, with an average magnitude of +1.2% per month (95% credibility interval: 0.7 to 1.6). Older age and 12 months of amenorrhoea were found to be associated with a lower AMH recovery rate, whereas baseline AMH and number of chemotherapy cycles were not. The process of AMH changes during and after chemotherapy is dynamic, and shows recovery after ovarian injury. Caution should be exercised in interpreting individual AMH assessment in this context. © 2014 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.

Verger E.,Service de Biologie Cellulaire | Cassinat B.,Service de Biologie Cellulaire | Chauveau A.,Brest University Hospital Center | Chauveau A.,University of Western Brittany | And 14 more authors.
Blood | Year: 2015

Myeloproliferative neoplasmsare clonal disorders characterized by the presence of several gene mutations associated with particular hematologic parameters, clinical evolution, and prognosis.Few therapeutic options are available, among which interferon α (IFNα)presents interesting properties like the ability to induce hematologic responses (HRs) andmolecular responses (MRS) inpatients with JAK2 mutation.We reportonthe response to IFNatherapy in a cohort of 31 essential thrombocythemia (ET) patients with CALR mutations (mean follow-up of 11.8 years).HRwas achievedin all patients.MedianCALRmutant allelicburden (%CALR) significantly decreased from 41% at base line to 26%after treatment, and 2patients even achieved complete MR. In contrast, %CALR was not significantly modified in ET patients treated with hydroxyurea or aspirin only. Next-generation sequencing identified additional mutations in 6 patients (affecting TET2, ASXL1, IDH2, and TP53 genes). The presence of additional mutations was associated with poorer MR on CALR mutant clones, withonlyminorornoMRS in this subsetofpatients.Analysisof theevolutionof the different variant allele frequencies showed that the mutated clones had a differential sensitivity to IFNα in a given patient, but no new mutation emerged during treatment. In all, this study shows that IFNa induces high rates of HRs and MRS in CALR-mutated ET, and that the presence of additional nondriver mutations may influence the MR to therapy. © 2015 by The American Society of Hematology.

Zassadowski F.,Service de Biologie Cellulaire | Zassadowski F.,French Institute of Health and Medical Research | Pokorna K.,French Institute of Health and Medical Research | Ferre N.,French Institute of Health and Medical Research | And 14 more authors.
Leukemia | Year: 2015

We recently identified that the MEK/ERK1/2 pathway synergized with retinoic acid (RA) to restore both transcriptional activity and RA-induced differentiation in RA-resistant acute promyelocytic leukemia (APL) cells. To target the MEK/ERK pathway, we identified glycogen synthase kinase-3β (GSK-3β) inhibitors including lithium chloride (LiCl) as activators of this pathway in APL cells. Using NB4 (RA-sensitive) and UF-1 (RA-resistant) APL cell lines, we observed that LiCl as well as synthetic GSK-3β inhibitors decreased proliferation, induced apoptosis and restored, in RA-resistant cells, the expression of RA target genes and the RA-induced differentiation. Inhibition of the MEK/ERK1/2 pathway abolished these effects. These results were corroborated in primary APL patient cells and translated in vivo using an APL preclinical mouse model in which LiCl given alone was as efficient as RA in increasing survival of leukemic mice compared with untreated mice. When LiCl was combined with RA, we observed a significant survival advantage compared with mice treated by RA alone. In this work, we demonstrate that LiCl, a well-tolerated agent in humans, has antileukemic activity in APL and that it has the potential to restore RA-induced transcriptional activation and differentiation in RA-resistant APL cells in an MEK/ERK-dependent manner. © 2015 Macmillan Publishers Limited.

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