Center Hospitalier Lyon Sud 165

Pierre-Bénite, France

Center Hospitalier Lyon Sud 165

Pierre-Bénite, France
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Pomier C.,University of Lyon | Rabaaoui S.,University of Lyon | Pouliquen J.-F.,Institute Pasteur Of La Guyane | Couppie P.,Center Hospitalier Of Cayenne | And 7 more authors.
Journal of General Virology | Year: 2013

Upon antiretroviral therapy (ART) human immunodeficiency virus (HIV)/human T-cell lymphotropic virus type 1 (HTLV-1) co-infected individuals frequently develop neurological disorders through hitherto unknown mechanisms. Here, we show that effective anti-HIV ART increases HTLV-1 proviral load through a polyclonal integration pattern of HTLV-1 in both CD4+ and CD8+ T-cell subsets that is reminiscent of that typically associated with HTLV-1-related inflammatory conditions. These data indicate that preventing ART-triggered clonal expansion of HTLV-1- infected cells in co-infected individuals deserves investigation. © 2013 SGM.


Karam M.,University of Lyon | Thenoz M.,University of Lyon | Capraro V.,University of Lyon | Capraro V.,University of Liège | And 13 more authors.
Neoplasia (United States) | Year: 2014

Although numerous factors have been found to modulate hTERT transcription, the mechanism of its repression in certain leukemias remains unknown. We show here that DEK represses hTERT transcription through its enrichment on the hTERT promoter in cells from chronic and acute myeloid leukemias, chronic lymphocytic leukemia, but not acute lymphocytic leukemias where hTERT is overexpressed. We isolated DEK from the hTERT promoter incubated with nuclear extracts derived from fresh acute myelogenous leukemia (AML) cells and from cells expressing Tax, an hTERT repressor encoded by the human T cell leukemia virus type 1. In addition to the recruitment of DEK, the displacement of two potent known hTERT transactivators from the hTERT promoter characterized both AML cells and Tax-expressing cells. Reporter and chromatin immunoprecipitation assays permitted to map the region that supports the repressive effect of DEK on hTERT transcription, which was proportionate to the level of DEK-promoter association but not with the level of DEK expression. Besides hTERT repression, this context of chromatin redistribution of DEK was found to govern about 40% of overall transcriptional modifications, including those of cancer-prone genes. In conclusion, DEK emerges as an hTERT repressor shared by various leukemia subtypes and seems involved in the deregulation of numerous genes associated with leukemogenesis. © 2014 Neoplasia Press, Inc. All rights reserved.


Kolopp-Sarda M.-N.,Center Hospitalier Lyon Sud 165 | Chapuis-Cellier C.,Center Hospitalier Lyon Sud 165 | Dimet I.,Center Hospitalier Lyon Sud 165 | Lombard C.,Center Hospitalier Lyon Sud 165
Revue Francophone des Laboratoires | Year: 2012

Cold is responsible for clinical symptoms in some subjects, caused by seric or plasmatic proteins precipitation in small or medium vessels, as cryoglobulins or cryofibrinogen. Cryoglobulins are constituted with monoclonal or polyclonal immunoglobulins, with sometimes rheumatoid factor activity. They are essential or secondary in immunoproliferative, autoimmune or infectious diseases. Cutaneous vasculitis (purpura, Raynaud phenomenon), arthralgies, peripheral neuropathies or renal failure are the main cryoglobulinemic symptoms. Cryofibrinogen, associated with fibronectin and others plasmatic proteins, is involved in cold triggered thrombotic events (purpura, livedo, ulceration, necrosis). Strict pre-analytic conditions are essential to evidence cryoproteins in serum or plasma: blood sample, transport and coagulation at 37 °C. Cryoprotein analysis must be initiated in evocating clinical context, because of difficulties in cryoglobulinemia or cryofibrinogenemia diagnosis: first, these cryoproteins could be present in asymptomatic subjects, second, cryoprotein concentration is not proportional to symptom severity. Nevertheless, biologic study is essential, even in low concentration, because of potential renal or neoplasic complications of these cryoproteins. © 2012 - Elsevier Masson SAS - Tous droits réservés.


PubMed | Center Hospitalier Lyon Sud 165 and University of Lyon
Type: Journal Article | Journal: Neoplasia (New York, N.Y.) | Year: 2014

Although numerous factors have been found to modulate hTERT transcription, the mechanism of its repression in certain leukemias remains unknown. We show here that DEK represses hTERT transcription through its enrichment on the hTERT promoter in cells from chronic and acute myeloid leukemias, chronic lymphocytic leukemia, but not acute lymphocytic leukemias where hTERT is overexpressed. We isolated DEK from the hTERT promoter incubated with nuclear extracts derived from fresh acute myelogenous leukemia (AML) cells and from cells expressing Tax, an hTERT repressor encoded by the human T cell leukemia virus type 1. In addition to the recruitment of DEK, the displacement of two potent known hTERT transactivators from the hTERT promoter characterized both AML cells and Tax-expressing cells. Reporter and chromatin immunoprecipitation assays permitted to map the region that supports the repressive effect of DEK on hTERT transcription, which was proportionate to the level of DEK-promoter association but not with the level of DEK expression. Besides hTERT repression, this context of chromatin redistribution of DEK was found to govern about 40% of overall transcriptional modifications, including those of cancer-prone genes. In conclusion, DEK emerges as an hTERT repressor shared by various leukemia subtypes and seems involved in the deregulation of numerous genes associated with leukemogenesis.

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