The Experts below are selected from a list of 15837 Experts worldwide ranked by ideXlab platform
Aurelie Verney - One of the best experts on this subject based on the ideXlab platform.
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exome sequencing identifies recurrent Bcor alterations and the aBsence of klf2 tnfaip3 and myd88 mutations in <B>SplenicB> diffuse red pulp small B Cell lymphoma
Haematologica, 2017Co-Authors: Laurent Jallades, Lucile Baseggio, Pierre Sujobert, Sarah Huet, Kaddour Chabane, Evelyne Calletbauchu, Aurelie VerneyAbstract:<B>SplenicB> diffuse red pulp lymphoma is an indolent small B-Cell lymphoma recognized as a provisional entity in the World Health Organization 2008 classification. Its precise relationship to other related <B>SplenicB> B-Cell lymphomas with frequent leukemic involvement or other lymphoproliferative disorders remains undetermined. We performed whole-exome sequencing to explore the genetic landscape of ten cases of <B>SplenicB> diffuse red pulp lymphoma using paired tumor and normal samples. A selection of 109 somatic mutations was then evaluated in a cohort including 42 samples of <B>SplenicB> diffuse red pulp lymphoma and compared to those identified in 46 samples of <B>SplenicB> marginal zone lymphoma and eight samples of hairy-Cell leukemia. Recurrent mutations or losses in BCOR (the gene encoding the BCL6 corepressor) – frameshift (n=3), nonsense (n=2), splicing site (n=1), and copy numBer loss (n=4) – were identified in 10/42 samples of <B>SplenicB> diffuse red pulp lymphoma (24%), whereas only one frameshift mutation was identified in 46 cases of <B>SplenicB> marginal zone lymphoma (2%). Inversely, KLF2, TNFAIP3 and MYD88, common mutations in <B>SplenicB> marginal zone lymphoma, were rare (one KLF2 mutant in 42 samples; 2%) or aBsent (TNFAIP3 and MYD88) in <B>SplenicB> diffuse red pulp lymphoma. These findings define an original genetic profile of <B>SplenicB> diffuse red pulp lymphoma and suggest that the mechanisms of pathogenesis of this lymphoma are distinct from those of <B>SplenicB> marginal zone lymphoma and hairy-Cell leukemia.
Pierre Sujobert - One of the best experts on this subject based on the ideXlab platform.
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exome sequencing identifies recurrent Bcor alterations and the aBsence of klf2 tnfaip3 and myd88 mutations in <B>SplenicB> diffuse red pulp small B Cell lymphoma
Haematologica, 2017Co-Authors: Laurent Jallades, Lucile Baseggio, Pierre Sujobert, Sarah Huet, Kaddour Chabane, Evelyne Calletbauchu, Aurelie VerneyAbstract:<B>SplenicB> diffuse red pulp lymphoma is an indolent small B-Cell lymphoma recognized as a provisional entity in the World Health Organization 2008 classification. Its precise relationship to other related <B>SplenicB> B-Cell lymphomas with frequent leukemic involvement or other lymphoproliferative disorders remains undetermined. We performed whole-exome sequencing to explore the genetic landscape of ten cases of <B>SplenicB> diffuse red pulp lymphoma using paired tumor and normal samples. A selection of 109 somatic mutations was then evaluated in a cohort including 42 samples of <B>SplenicB> diffuse red pulp lymphoma and compared to those identified in 46 samples of <B>SplenicB> marginal zone lymphoma and eight samples of hairy-Cell leukemia. Recurrent mutations or losses in BCOR (the gene encoding the BCL6 corepressor) – frameshift (n=3), nonsense (n=2), splicing site (n=1), and copy numBer loss (n=4) – were identified in 10/42 samples of <B>SplenicB> diffuse red pulp lymphoma (24%), whereas only one frameshift mutation was identified in 46 cases of <B>SplenicB> marginal zone lymphoma (2%). Inversely, KLF2, TNFAIP3 and MYD88, common mutations in <B>SplenicB> marginal zone lymphoma, were rare (one KLF2 mutant in 42 samples; 2%) or aBsent (TNFAIP3 and MYD88) in <B>SplenicB> diffuse red pulp lymphoma. These findings define an original genetic profile of <B>SplenicB> diffuse red pulp lymphoma and suggest that the mechanisms of pathogenesis of this lymphoma are distinct from those of <B>SplenicB> marginal zone lymphoma and hairy-Cell leukemia.
Sarah Huet - One of the best experts on this subject based on the ideXlab platform.
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exome sequencing identifies recurrent Bcor alterations and the aBsence of klf2 tnfaip3 and myd88 mutations in <B>SplenicB> diffuse red pulp small B Cell lymphoma
Haematologica, 2017Co-Authors: Laurent Jallades, Lucile Baseggio, Pierre Sujobert, Sarah Huet, Kaddour Chabane, Evelyne Calletbauchu, Aurelie VerneyAbstract:<B>SplenicB> diffuse red pulp lymphoma is an indolent small B-Cell lymphoma recognized as a provisional entity in the World Health Organization 2008 classification. Its precise relationship to other related <B>SplenicB> B-Cell lymphomas with frequent leukemic involvement or other lymphoproliferative disorders remains undetermined. We performed whole-exome sequencing to explore the genetic landscape of ten cases of <B>SplenicB> diffuse red pulp lymphoma using paired tumor and normal samples. A selection of 109 somatic mutations was then evaluated in a cohort including 42 samples of <B>SplenicB> diffuse red pulp lymphoma and compared to those identified in 46 samples of <B>SplenicB> marginal zone lymphoma and eight samples of hairy-Cell leukemia. Recurrent mutations or losses in BCOR (the gene encoding the BCL6 corepressor) – frameshift (n=3), nonsense (n=2), splicing site (n=1), and copy numBer loss (n=4) – were identified in 10/42 samples of <B>SplenicB> diffuse red pulp lymphoma (24%), whereas only one frameshift mutation was identified in 46 cases of <B>SplenicB> marginal zone lymphoma (2%). Inversely, KLF2, TNFAIP3 and MYD88, common mutations in <B>SplenicB> marginal zone lymphoma, were rare (one KLF2 mutant in 42 samples; 2%) or aBsent (TNFAIP3 and MYD88) in <B>SplenicB> diffuse red pulp lymphoma. These findings define an original genetic profile of <B>SplenicB> diffuse red pulp lymphoma and suggest that the mechanisms of pathogenesis of this lymphoma are distinct from those of <B>SplenicB> marginal zone lymphoma and hairy-Cell leukemia.
Evelyne Calletbauchu - One of the best experts on this subject based on the ideXlab platform.
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exome sequencing identifies recurrent Bcor alterations and the aBsence of klf2 tnfaip3 and myd88 mutations in <B>SplenicB> diffuse red pulp small B Cell lymphoma
Haematologica, 2017Co-Authors: Laurent Jallades, Lucile Baseggio, Pierre Sujobert, Sarah Huet, Kaddour Chabane, Evelyne Calletbauchu, Aurelie VerneyAbstract:<B>SplenicB> diffuse red pulp lymphoma is an indolent small B-Cell lymphoma recognized as a provisional entity in the World Health Organization 2008 classification. Its precise relationship to other related <B>SplenicB> B-Cell lymphomas with frequent leukemic involvement or other lymphoproliferative disorders remains undetermined. We performed whole-exome sequencing to explore the genetic landscape of ten cases of <B>SplenicB> diffuse red pulp lymphoma using paired tumor and normal samples. A selection of 109 somatic mutations was then evaluated in a cohort including 42 samples of <B>SplenicB> diffuse red pulp lymphoma and compared to those identified in 46 samples of <B>SplenicB> marginal zone lymphoma and eight samples of hairy-Cell leukemia. Recurrent mutations or losses in BCOR (the gene encoding the BCL6 corepressor) – frameshift (n=3), nonsense (n=2), splicing site (n=1), and copy numBer loss (n=4) – were identified in 10/42 samples of <B>SplenicB> diffuse red pulp lymphoma (24%), whereas only one frameshift mutation was identified in 46 cases of <B>SplenicB> marginal zone lymphoma (2%). Inversely, KLF2, TNFAIP3 and MYD88, common mutations in <B>SplenicB> marginal zone lymphoma, were rare (one KLF2 mutant in 42 samples; 2%) or aBsent (TNFAIP3 and MYD88) in <B>SplenicB> diffuse red pulp lymphoma. These findings define an original genetic profile of <B>SplenicB> diffuse red pulp lymphoma and suggest that the mechanisms of pathogenesis of this lymphoma are distinct from those of <B>SplenicB> marginal zone lymphoma and hairy-Cell leukemia.
Antonio A. Freitas - One of the best experts on this subject based on the ideXlab platform.
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Differential Expression of Vn Gene Families in Per/pheral B Cell Repertoires of NewBorn or Adult
2013Co-Authors: Immunoglobulin H Chain, Congenic Mice, Anne-claire Viale, Antonio Coutinho, Antonio A. FreitasAbstract:The pattern of V. gene family expression in the primary B Cell repertoire of the mouse is strain dependent. In C57B1/6 mice, the V. J558 family is expressed By more than 45 % of the Cells, while the expression of V. 7183, V. Q52, and V. 36-60 families together does not exceed 20%. In BALB/c mice, relative expression of V. J558 is lower than 35%, while the sum of the other three families reaches 25%. To assess which genetic loci control strain-specific V. gene family expression, we studied V. gene family usage in <B>SplenicB> B Cell repertoires of different congenic strains of mice. Changes in major histocompatiBility complex or immunogloBulin (Ig) K light chain genes did not modify V. gene family expression in adult mice. Differences at the IgH locus, however, modified V. gene family usage. In 1-d-old mice, the strain-specific V. gene family expression pattern is determined By the IgH haplotype. In adult mice, the V. gene family expression pattern of resting B Cells is independent of the IgH locus and follows the genetic Background of the congenic strain, while it is determined By the IgH haplotype among Ig-secreting spleen Cells. In FI(B6 x BALB/c) mice, each of the two spleen B Cell populations, sorted on the Basis of # heavy chain allotype expression, shows an independent V. gene family expression pattern, determined By the IgH locus. The implications of these results in the control of V
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differential expression of vh gene families in peripheral B Cell repertoires of newBorn or adult immunogloBulin h chain congenic mice
Journal of Experimental Medicine, 1992Co-Authors: Anne-claire Viale, Antonio Coutinho, Antonio A. FreitasAbstract:The pattern of VH gene family expression in the primary B Cell repertoire of the mouse is strain dependent. In C57Bl/6 mice, the VH J558 family is expressed By more than 45% of the Cells, while the expression of VH 7183, VH Q52, and VH 36-60 families together does not exceed 20%. In BALB/c mice, relative expression of VH J558 is lower than 35%, while the sum of the other three families reaches 25%. To assess which genetic loci control strain-specific VH gene family expression, we studied VH gene family usage in <B>SplenicB> B Cell repertoires of different congenic strains of mice. Changes in major histocompatiBility complex or immunogloBulin (Ig) K light chain genes did not modify VH gene family expression in adult mice. Differences at the IgH locus, however, modified VH gene family usage. In 1-d-old mice, the strain-specific VH gene family expression pattern is determined By the IgH haplotype. In adult mice, the VH gene family expression pattern of resting B Cells is independent of the IgH locus and follows the genetic Background of the congenic strain, while it is determined By the IgH haplotype among Ig-secreting spleen Cells. In F1(B6 x BALB/c) mice, each of the two spleen B Cell populations, sorted on the Basis of mu heavy chain allotype expression, shows an independent VH gene family expression pattern, determined By the IgH locus. The implications of these results in the control of VH gene family expression, and in the selection of peripheral B Cell repertoires are discussed.
