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Article ; Online: The Recurrent Liver MAN2A1-FER Oncoprotein Lacks Kinase Activity: Implications for the Use of Tyrosine Kinase Inhibitors.

Desaunay, Mathieu / Voisset, Edwige / Letard, Sebastien / Roche, Philippe / De Sepulveda, Paulo

Cellular and molecular gastroenterology and hepatology

2023 Volume 17, Issue 4, Page(s) 667–669

MeSH term(s)	Tyrosine Kinase Inhibitors ; Phosphorylation ; Signal Transduction ; Oncogene Proteins ; Liver
Chemical Substances	Tyrosine Kinase Inhibitors ; Oncogene Proteins
Language	English
Publishing date	2023-12-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2023.12.007
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Article ; Online: TET2 regulates immune tolerance in chronically activated mast cells.

Rigo, Riccardo / Chelbi, Rabie / Agopian, Julie / Letard, Sebastien / Griffon, Aurélien / Ghamlouch, Hussein / Vernerey, Julien / Ladopoulos, Vasileios / Voisset, Edwige / De Sepulveda, Paulo / Guittard, Geoffrey / Nunès, Jacques A / Bidaut, Ghislain / Göttgens, Berthold / Weber, Michael / Bernard, Olivier A / Dubreuil, Patrice / Soucie, Erinn

JCI insight

2022 Volume 7, Issue 7

Abstract: Mutation of the TET2 DNA-hydroxymethylase has been associated with a number of immune pathologies. The disparity in phenotype and clinical presentation among these pathologies leads to questions regarding the role of TET2 mutation in promoting disease ... ...

Abstract	Mutation of the TET2 DNA-hydroxymethylase has been associated with a number of immune pathologies. The disparity in phenotype and clinical presentation among these pathologies leads to questions regarding the role of TET2 mutation in promoting disease evolution in different immune cell types. Here we show that, in primary mast cells, Tet2 expression is induced in response to chronic and acute activation signals. In TET2-deficient mast cells, chronic activation via the oncogenic KITD816V allele associated with mastocytosis, selects for a specific epigenetic signature characterized by hypermethylated DNA regions (HMR) at immune response genes. H3K27ac and transcription factor binding is consistent with priming or more open chromatin at both HMR and non-HMR in proximity to immune genes in these cells, and this signature coincides with increased pathological inflammation signals. HMR are also associated with a subset of immune genes that are direct targets of TET2 and repressed in TET2-deficient cells. Repression of these genes results in immune tolerance to acute stimulation that can be rescued with vitamin C treatment or reiterated with a Tet inhibitor. Overall, our data support a model where TET2 plays a direct role in preventing immune tolerance in chronically activated mast cells, supporting TET2 as a viable target to reprogram the innate immune response for innovative therapies.
MeSH term(s)	DNA-Binding Proteins/metabolism ; Dioxygenases/metabolism ; Immune Tolerance ; Mast Cells/immunology ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; Proto-Oncogene Proteins ; Dioxygenases (EC 1.13.11.-)
Language	English
Publishing date	2022-04-08
Publishing country	United States
Document type	Journal Article
ISSN	2379-3708
ISSN (online)	2379-3708
DOI	10.1172/jci.insight.154191
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Article ; Online: Comparison of effects of midostaurin, crenolanib, quizartinib, gilteritinib, sorafenib and BLU-285 on oncogenic mutants of KIT, CBL and FLT3 in haematological malignancies.

Weisberg, Ellen / Meng, Chengcheng / Case, Abigail E / Sattler, Martin / Tiv, Hong L / Gokhale, Prafulla C / Buhrlage, Sara J / Liu, Xiaoxi / Yang, Jing / Wang, Jinhua / Gray, Nathanael / Stone, Richard M / Adamia, Sophia / Dubreuil, Patrice / Letard, Sebastien / Griffin, James D

British journal of haematology

2019 Volume 187, Issue 4, Page(s) 488–501

Abstract: Mutations in two type-3 receptor tyrosine kinases (RTKs), KIT and FLT3, are common in both acute myeloid leukaemia (AML) and systemic mastocytosis (SM) and lead to hyperactivation of key signalling pathways. A large number of tyrosine kinase inhibitors ( ... ...

Abstract	Mutations in two type-3 receptor tyrosine kinases (RTKs), KIT and FLT3, are common in both acute myeloid leukaemia (AML) and systemic mastocytosis (SM) and lead to hyperactivation of key signalling pathways. A large number of tyrosine kinase inhibitors (TKIs) have been developed that target either FLT3 or KIT and significant clinical benefit has been demonstrated in multiple clinical trials. Given the structural similarity of FLT3 and KIT, it is not surprising that some of these TKIs inhibit both of these receptors. This is typified by midostaurin, which has been approved by the US Food and Drug Administration for mutant FLT3-positive AML and for KIT D816V-positive SM. Here, we compare the in vitro activities of the clinically available FLT3 and KIT inhibitors with those of midostaurin against a panel of cells expressing a variety of oncogenic FLT3 or KIT receptors, including wild-type (wt) FLT3, FLT3-internal tandem duplication (ITD), FLT3 D835Y, the resistance mutant FLT3-ITD+ F691L, KIT D816V, and KIT N822K. We also examined the effects of these inhibitors in vitro and in vivo on cells expressing mutations in c-CBL found in AML that result in hypersensitization of RTKs, such as FLT3 and KIT. The results show a wide spectrum of activity of these various mutations to these clinically available TKIs.
MeSH term(s)	Aniline Compounds/pharmacology ; Aniline Compounds/therapeutic use ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Benzimidazoles/pharmacology ; Benzimidazoles/therapeutic use ; Benzothiazoles/pharmacology ; Benzothiazoles/therapeutic use ; Cell Line, Tumor ; Drug Screening Assays, Antitumor ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/genetics ; Humans ; Mutant Proteins/drug effects ; Phenylurea Compounds/pharmacology ; Phenylurea Compounds/therapeutic use ; Piperidines/pharmacology ; Piperidines/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins c-cbl/drug effects ; Proto-Oncogene Proteins c-cbl/genetics ; Proto-Oncogene Proteins c-kit/drug effects ; Proto-Oncogene Proteins c-kit/genetics ; Pyrazines/pharmacology ; Pyrazines/therapeutic use ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Pyrroles/pharmacology ; Pyrroles/therapeutic use ; Sorafenib/pharmacology ; Sorafenib/therapeutic use ; Staurosporine/analogs & derivatives ; Staurosporine/pharmacology ; Staurosporine/therapeutic use ; Triazines/pharmacology ; Triazines/therapeutic use ; fms-Like Tyrosine Kinase 3/drug effects ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	Aniline Compounds ; Antineoplastic Agents ; Benzimidazoles ; Benzothiazoles ; Mutant Proteins ; Phenylurea Compounds ; Piperidines ; Protein Kinase Inhibitors ; Pyrazines ; Pyrazoles ; Pyrroles ; Triazines ; gilteritinib ; avapritinib (513P80B4YJ) ; quizartinib (7LA4O6Q0D3) ; Sorafenib (9ZOQ3TZI87) ; Proto-Oncogene Proteins c-cbl (EC 2.3.2.27) ; FLT3 protein, human (EC 2.7.10.1) ; KIT protein, human (EC 2.7.10.1) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1) ; CBL protein, human (EC 6.3.2.-) ; Staurosporine (H88EPA0A3N) ; midostaurin (ID912S5VON) ; crenolanib (LQF7I567TQ)
Language	English
Publishing date	2019-07-15
Publishing country	England
Document type	Comparative Study ; Journal Article
ZDB-ID	80077-6
ISSN	1365-2141 ; 0007-1048
ISSN (online)	1365-2141
ISSN	0007-1048
DOI	10.1111/bjh.16092
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Article ; Online: Screening of candidate G-quadruplex ligands for the human c-KIT promotorial region and their effects in multiple in-vitro models.

Zorzan, Eleonora / Da Ros, Silvia / Musetti, Caterina / Shahidian, Lara Zorro / Coelho, Nuno Filipe Ramos / Bonsembiante, Federico / Létard, Sébastien / Gelain, Maria Elena / Palumbo, Manlio / Dubreuil, Patrice / Giantin, Mery / Sissi, Claudia / Dacasto, Mauro

Oncotarget

2016 Volume 7, Issue 16, Page(s) 21658–21675

Abstract: Stabilization of G-quadruplex (G4) structures in promoters is a novel promising strategy to regulate gene expression at transcriptional and translational levels. c-KIT proto-oncogene encodes for a tyrosine kinase receptor. It is involved in several ... ...

Abstract	Stabilization of G-quadruplex (G4) structures in promoters is a novel promising strategy to regulate gene expression at transcriptional and translational levels. c-KIT proto-oncogene encodes for a tyrosine kinase receptor. It is involved in several physiological processes, but it is also dysregulated in many diseases, including cancer. Two G-rich sequences able to fold into G4, have been identified in c-KIT proximal promoter, thus representing suitable targets for anticancer intervention. Herein, we screened an "in house" library of compounds for the recognition of these G4 elements and we identified three promising ligands. Their G4-binding properties were analyzed and related to their antiproliferative, transcriptional and post-transcriptional effects in MCF7 and HGC27 cell lines. Besides c-KIT, the transcriptional analysis covered a panel of oncogenes known to possess G4 in their promoters.From these studies, an anthraquinone derivative (AQ1) was found to efficiently downregulate c-KIT mRNA and protein in both cell lines. The targeted activity of AQ1 was confirmed using c-KIT-dependent cell lines that present either c-KIT mutations or promoter engineered (i.e., α155, HMC1.2 and ROSA cells).Present results indicate AQ1 as a promising compound for the target therapy of c-KIT-dependent tumors, worth of further and in depth molecular investigations.
Language	English
Publishing date	2016-04-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.7808
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Article ; Online: Dual protein kinase and nucleoside kinase modulators for rationally designed polypharmacology.

Hammam, Kahina / Saez-Ayala, Magali / Rebuffet, Etienne / Gros, Laurent / Lopez, Sophie / Hajem, Berengere / Humbert, Martine / Baudelet, Emilie / Audebert, Stephane / Betzi, Stephane / Lugari, Adrien / Combes, Sebastien / Letard, Sebastien / Casteran, Nathalie / Mansfield, Colin / Moussy, Alain / De Sepulveda, Paulo / Morelli, Xavier / Dubreuil, Patrice

Nature communications

2017 Volume 8, Issue 1, Page(s) 1420

Abstract: Masitinib, a highly selective protein kinase inhibitor, can sensitise gemcitabine-refractory cancer cell lines when used in combination with gemcitabine. Here we report a reverse proteomic approach that identifies the target responsible for this ... ...

Abstract	Masitinib, a highly selective protein kinase inhibitor, can sensitise gemcitabine-refractory cancer cell lines when used in combination with gemcitabine. Here we report a reverse proteomic approach that identifies the target responsible for this sensitisation: the deoxycytidine kinase (dCK). Masitinib, as well as other protein kinase inhibitors, such as imatinib, interact with dCK and provoke an unforeseen conformational-dependent activation of this nucleoside kinase, modulating phosphorylation of nucleoside analogue drugs. This phenomenon leads to an increase of prodrug phosphorylation of most of the chemotherapeutic drugs activated by this nucleoside kinase. The unforeseen dual activity of protein kinase inhibition/nucleoside kinase activation could be of great therapeutic benefit, through either reducing toxicity of therapeutic agents by maintaining effectiveness at lower doses or by counteracting drug resistance initiated via down modulation of dCK target.
MeSH term(s)	A549 Cells ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Crystallography, X-Ray ; Deoxycytidine/analogs & derivatives ; Deoxycytidine/pharmacology ; Deoxycytidine Kinase/chemistry ; Deoxycytidine Kinase/metabolism ; Drug Design ; Drug Resistance, Neoplasm ; Enzyme Activation/drug effects ; Humans ; Imatinib Mesylate/chemistry ; Imatinib Mesylate/pharmacology ; Models, Biological ; Models, Molecular ; Phosphorylation ; Polypharmacology ; Protein Kinase Inhibitors/chemistry ; Protein Kinase Inhibitors/pharmacology ; Proteomics ; Thiazoles/chemistry ; Thiazoles/pharmacology
Chemical Substances	Antineoplastic Agents ; Protein Kinase Inhibitors ; Thiazoles ; Deoxycytidine (0W860991D6) ; Imatinib Mesylate (8A1O1M485B) ; gemcitabine (B76N6SBZ8R) ; Deoxycytidine Kinase (EC 2.7.1.74) ; masitinib (M59NC4E26P)
Language	English
Publishing date	2017-11-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2041-1723
ISSN (online)	2041-1723
DOI	10.1038/s41467-017-01582-5
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Article ; Online: Dual Role of the Tyrosine Kinase Syk in Regulation of Toll-Like Receptor Signaling in Plasmacytoid Dendritic Cells.

Aouar, Besma / Kovarova, Denisa / Letard, Sebastien / Font-Haro, Albert / Florentin, Jonathan / Weber, Jan / Durantel, David / Chaperot, Laurence / Plumas, Joel / Trejbalova, Katerina / Hejnar, Jiri / Nunès, Jacques A / Olive, Daniel / Dubreuil, Patrice / Hirsch, Ivan / Stranska, Ruzena

PloS one

2016 Volume 11, Issue 6, Page(s) e0156063

Abstract: Crosslinking of regulatory immunoreceptors (RR), such as BDCA-2 (CD303) or ILT7 (CD85g), of plasmacytoid dendritic cells (pDCs) efficiently suppresses production of type-I interferon (IFN)-α/β and other cytokines in response to Toll-like receptor (TLR) 7/ ...

Abstract	Crosslinking of regulatory immunoreceptors (RR), such as BDCA-2 (CD303) or ILT7 (CD85g), of plasmacytoid dendritic cells (pDCs) efficiently suppresses production of type-I interferon (IFN)-α/β and other cytokines in response to Toll-like receptor (TLR) 7/9 ligands. This cytokine-inhibitory pathway is mediated by spleen tyrosine kinase (Syk) associated with the ITAM-containing adapter of RR. Here we demonstrate by pharmacological targeting of Syk that in addition to the negative regulation of TLR7/9 signaling via RR, Syk also positively regulates the TLR7/9 pathway in human pDCs. Novel highly specific Syk inhibitor AB8779 suppressed IFN-α, TNF-α and IL-6 production induced by TLR7/9 agonists in primary pDCs and in the pDC cell line GEN2.2. Triggering of TLR9 or RR signaling induced a differential kinetics of phosphorylation at Y352 and Y525/526 of Syk and a differential sensitivity to AB8779. Consistent with the different roles of Syk in TLR7/9 and RR signaling, a concentration of AB8779 insufficient to block TLR7/9 signaling still released the block of IFN-α production triggered via the RR pathway, including that induced by hepatitis B and C viruses. Thus, pharmacological targeting of Syk partially restored the main pDC function-IFN-α production. Opposing roles of Syk in TLR7/9 and RR pathways may regulate the innate immune response to weaken inflammation reaction.
MeSH term(s)	Cytokines/metabolism ; Dendritic Cells/drug effects ; Dendritic Cells/metabolism ; Humans ; Immunity, Innate ; Phosphorylation/drug effects ; Protein Kinase Inhibitors/pharmacology ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Syk Kinase/antagonists & inhibitors ; Syk Kinase/metabolism ; Toll-Like Receptors/agonists ; Toll-Like Receptors/metabolism
Chemical Substances	Cytokines ; Protein Kinase Inhibitors ; Toll-Like Receptors ; Syk Kinase (EC 2.7.10.2)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0156063
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Article: Oncogenic tyrosine kinase of malignant hemopathy targets the centrosome.

Delaval, Bénédicte / Létard, Sébastien / Lelièvre, Hélène / Chevrier, Véronique / Daviet, Laurent / Dubreuil, Patrice / Birnbaum, Daniel

Cancer research

2005 Volume 65, Issue 16, Page(s) 7231–7240

Abstract: Myeloproliferative disorders (MPD) are malignant diseases of hematopoietic progenitor cells. Many MPDs result from a chromosomal translocation that creates a fusion gene encoding a chimeric kinase. The fibroblast growth factor receptor 1 (FGFR1)-MPD is ... ...

Abstract	Myeloproliferative disorders (MPD) are malignant diseases of hematopoietic progenitor cells. Many MPDs result from a chromosomal translocation that creates a fusion gene encoding a chimeric kinase. The fibroblast growth factor receptor 1 (FGFR1)-MPD is characterized by the fusion of the FGFR1 kinase with various partners, including FOP. We show here that both normal FOP and FOP-FGFR1 fusion kinase localize to the centrosome. The fusion kinase encounters substrates at the centrosome where it induces strong phosphorylation on tyrosine residues. Treatment with FGFR1 kinase inhibitor SU5402 abolishes FOP-FGFR1-induced centrosomal phosphorylation and suppresses the proliferative and survival potentials of FOP-FGFR1 Ba/F3 cells. We further show that FOP-FGFR1 allows cells to overcome G1 arrest. Therefore, the FOP-FGFR1 fusion kinase targets the centrosome, activates signaling pathways at this organelle, and sustains continuous entry in the cell cycle. This could represent a potential new mechanism of oncogenic transformation occurring specifically at the centrosome.
MeSH term(s)	Animals ; Cell Cycle/physiology ; Cell Growth Processes/physiology ; Centrosome/enzymology ; Centrosome/metabolism ; G1 Phase/physiology ; Hematopoietic Stem Cells/enzymology ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Mice ; Myeloproliferative Disorders/enzymology ; Myeloproliferative Disorders/metabolism ; Myeloproliferative Disorders/pathology ; Oncogene Proteins, Fusion/metabolism ; Oncogene Proteins, Fusion/physiology ; Phosphorylation ; Pyrroles/pharmacology ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors ; Receptor, Fibroblast Growth Factor, Type 1 ; Receptors, Fibroblast Growth Factor/antagonists & inhibitors ; Receptors, Fibroblast Growth Factor/metabolism ; Receptors, Fibroblast Growth Factor/physiology ; S Phase/physiology
Chemical Substances	FOP-FGFR1 fusion protein, human ; Oncogene Proteins, Fusion ; Pyrroles ; Receptors, Fibroblast Growth Factor ; SU 5402 ; Fgfr1 protein, mouse (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, Fibroblast Growth Factor, Type 1 (EC 2.7.10.1)
Language	English
Publishing date	2005-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-04-4167
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Article: Suppressor of cytokine signaling 6 associates with KIT and regulates KIT receptor signaling.

Bayle, Julie / Letard, Sébastien / Frank, Ronald / Dubreuil, Patrice / De Sepulveda, Paulo

The Journal of biological chemistry

2004 Volume 279, Issue 13, Page(s) 12249–12259

Abstract: Suppressor of cytokine signaling (SOCS) proteins are a family of Src homology 2-containing adaptor proteins. Cytokine-inducible Src homology domain 2-containing protein, SOCS1, SOCS2, and SOCS3 have been implicated in the down-regulation of cytokine ... ...

Abstract	Suppressor of cytokine signaling (SOCS) proteins are a family of Src homology 2-containing adaptor proteins. Cytokine-inducible Src homology domain 2-containing protein, SOCS1, SOCS2, and SOCS3 have been implicated in the down-regulation of cytokine signaling. The function of SOCS4, 5, 6, and 7 are not known. KIT receptor signaling is regulated by protein tyrosine phosphatases and adaptor proteins. We previously reported that SOCS1 inhibited cell proliferation in response to stem cell factor (SCF). By screening the other members of SOCS family, we identified SOCS6 as a KIT-binding protein. Using KIT mutants and peptides, we demonstrated that SOCS6 bound directly to KIT tyrosine 567 in the juxtamembrane domain. To investigate the function of this interaction, we constitutively expressed SOCS6 in cell lines. Ectopic expression of SOCS6 in Ba/F3-KIT cell line decreased cell proliferation in response to SCF but not SCF-induced chemotaxis. SOCS6 reduced SCF-induced activation of ERK1/2 and p38 but not activation of AKT or STATs in Ba/F3, murine embryonic fibroblast (MEF), or COS-7 cells. SOCS6 did not impair ERK and p38 activation by other stimuli. These results indicate that SOCS6 binds to KIT juxtamembrane region, which affects upstream signaling components leading to MAPK activation. Our results indicate that KIT signaling is regulated by several SOCS proteins and suggest a putative function for SOCS6 as a negative regulator of receptor tyrosine kinases.
MeSH term(s)	Amino Acid Sequence ; Animals ; Anisomycin/pharmacology ; COS Cells ; Cell Division ; Cell Line ; Cell Movement ; Chemotaxis ; Down-Regulation ; Enzyme Activation ; Glutathione Transferase/metabolism ; Mice ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases/metabolism ; Molecular Sequence Data ; Mutation ; Peptides/chemistry ; Phosphorylation ; Protein Binding ; Protein Structure, Tertiary ; Proteins/metabolism ; Proto-Oncogene Proteins c-kit/metabolism ; Recombinant Fusion Proteins/metabolism ; Retroviridae/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Signal Transduction ; Stem Cell Factor/metabolism ; Suppressor of Cytokine Signaling Proteins ; Time Factors ; Two-Hybrid System Techniques ; Tyrosine/chemistry ; p38 Mitogen-Activated Protein Kinases ; src Homology Domains
Chemical Substances	Peptides ; Proteins ; Recombinant Fusion Proteins ; SOCS6 protein, human ; Stem Cell Factor ; Suppressor of Cytokine Signaling Proteins ; Tyrosine (42HK56048U) ; Anisomycin (6C74YM2NGI) ; Glutathione Transferase (EC 2.5.1.18) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2004-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M313381200
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Article ; Online: In aggressive forms of mastocytosis, TET2 loss cooperates with c-KITD816V to transform mast cells.

Soucie, Erinn / Hanssens, Katia / Mercher, Thomas / Georgin-Lavialle, Sophie / Damaj, Gandhi / Livideanu, Cristina / Chandesris, Maria Olivia / Acin, Yolène / Létard, Sebastien / de Sepulveda, Paulo / Hermine, Olivier / Bernard, Olivier A / Dubreuil, Patrice

Blood

2012 Volume 120, Issue 24, Page(s) 4846–4849

Abstract: Although a role for oncogenic KIT in driving mast cell disease is clear, the mechanisms driving the multiple phenotypic and clinical manifestations of this disorder are not well elucidated. We now show, using a large cohort of mastocytosis patients, ... ...

Abstract	Although a role for oncogenic KIT in driving mast cell disease is clear, the mechanisms driving the multiple phenotypic and clinical manifestations of this disorder are not well elucidated. We now show, using a large cohort of mastocytosis patients, including an almost equal number of aggressive and nonaggressive cases of systemic mastocytosis, that in contrast to the oncogenic KITD816V, TET2 mutation statistically associates with aggressive forms of the disease. By infecting primary murine bone marrow-derived mast cells with KITD816V, we also observe a significant and competitive growth advantage for KITD816V in Tet2-nullizygous compared with wild-type cells. TET2-deficient cells display increased proliferation and can survive in the absence of cytokines. Taken together, these data demonstrate a oncogenic cooperation in mast cells and reveal TET2 mutation as a potential marker to diagnose and predict severe forms of mastocytosis.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Amino Acid Substitution ; Animals ; Bone Marrow Cells/metabolism ; Cell Survival/genetics ; Cell Transformation, Neoplastic/genetics ; Cells, Cultured ; Cohort Studies ; DNA-Binding Proteins/genetics ; Female ; Humans ; Male ; Mast Cells/metabolism ; Mast Cells/pathology ; Mastocytosis/genetics ; Mastocytosis/pathology ; Mice ; Mice, Knockout ; Middle Aged ; Mutation ; Proto-Oncogene Proteins/genetics ; Proto-Oncogene Proteins c-kit/genetics ; Time Factors ; Transfection
Chemical Substances	DNA-Binding Proteins ; Proto-Oncogene Proteins ; TET2 protein, human (EC 1.13.11.-) ; Tet2 protein, mouse (EC 1.13.11.-) ; Proto-Oncogene Proteins c-kit (EC 2.7.10.1)
Language	English
Publishing date	2012-10-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2011-12-397588
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Article ; Online: Familial hematological malignancies: new IDH2 mutation.

Hamadou, Walid-Sabri / Bourdon, Violaine / Létard, Sébastien / Brenet, Fabienne / Laarif, Sofien / Besbes, Sawsen / Paci, Angelo / David, Muriel / Penard-Lacronique, Virginie / Youssef, Yosra Ben / Laatiri, Mohamed-Adnène / Eisinger, François / Mari, Véronique / Gesta, Paul / Dreyfus, Hélène / Bonadona, Valérie / Dugast, Catherine / Zattara, Hélène / Faivre, Laurence /

Noguchi, Testsuro / Khélif, Abderrahim / Salem, Chaker Ben / Dubreuil, Patrice / Sobol, Hagay / Soua, Zohra

Annals of hematology

2016 Volume 95, Issue 12, Page(s) 1943–1947

Abstract: Isocitrate dehydrogenase IDH 1 and IDH 2 mutations were reported in several cancer forms, especially in hematological malignancies, but were never been investigated in familial aggregation. The aim of this study is to determine whether germline ... ...

Abstract	Isocitrate dehydrogenase IDH 1 and IDH 2 mutations were reported in several cancer forms, especially in hematological malignancies, but were never been investigated in familial aggregation. The aim of this study is to determine whether germline isocitrate dehydrogenase genes mutations are involved.We targeted IDH1 and IDH2 genes in 104 familial cases belonging to Tunisian and French populations, including several forms of hematological malignancies and cosegregated solid tumors.We report one IDH1 variant: c.315 G>T, p.Gly105Gly in 15 % of cases, which was assigned to the worst outcome in several studies. Three IDH2 variants were found, among them, one intronic substitution c.543+45 G>A (rs142033117) and two new variants not previously described: c.389 A>T, p.Lys130Met and c.414 T>C, p.Thr138Thr. The p.Lys130Met was found in one case diagnosed with Waldenstrom's disease with familial history of cancer. The enrolled in silico analysis, the functional study, and the absence of this variant in control population strengthen the hypothesis of its deleterious effect.From an extended number of candidate genes analyzed in familial hematological malignancies, IDH2 might be considerably involved since we reported a potential damaging effect.
MeSH term(s)	Adult ; Aged ; Female ; Hematologic Neoplasms/diagnosis ; Hematologic Neoplasms/genetics ; Humans ; Isocitrate Dehydrogenase/genetics ; Male ; Middle Aged ; Mutation/genetics
Chemical Substances	IDH2 protein, human (EC 1.1.1.41) ; Isocitrate Dehydrogenase (EC 1.1.1.41)
Language	English
Publishing date	2016-09-03
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1064950-5
ISSN	1432-0584 ; 0939-5555 ; 0945-8077
ISSN (online)	1432-0584
ISSN	0939-5555 ; 0945-8077
DOI	10.1007/s00277-016-2813-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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