Ralf Küppers
University of Duisburg-Essen
308 Papers
2.3K Citations
Ralf Küppers is an academic researcher from University of Duisburg-Essen. The author has contributed to research in topics: Germinal center & Lymphoma. The author has an hindex of 77, co-authored 283 publications. Previous affiliations of Ralf Küppers include University of Cologne & Columbia University.
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Papers
Human splenic marginal zone B cells lack expression of activation-induced cytidine deaminase
TL;DR: The lack of AID‐positive MZ B’cells questions the recent speculation that B cell chronic lymphocytic leukemias with mutated V genes are derived from mutating MZB cells.
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High expression of several tyrosine kinases and activation of the PI3K/AKT pathway in mediastinal large B cell lymphoma reveals further similarities to Hodgkin lymphoma.
Christoph Renné,Klaus Willenbrock,José I. Martín-Subero,Nora Hinsch,Claudia Döring,Enrico Tiacci,Wolfram Klapper,Peter Möller,Ralf Küppers,M. L. Hansmann,Reiner Siebert,Andreas Bräuninger +11 more
TL;DR: Aberrant TK activities are a further shared pathogenic mechanism of MBL and HL and may be interesting targets for therapeutic intervention.
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B cells of chronic lymphatic leukemia express V genes in unmutated form.
TL;DR: This study confirms other published data on V gene expression in B-CLL in that the surface immunoglobulins in these tumors are unmutated.
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SAMHD1 is recurrently mutated in T-cell prolymphocytic leukemia.
Patricia Johansson,Ludger Klein-Hitpass,Axel Choidas,Peter Habenberger,Bijan Mahboubi,Baek Kim,Anke K. Bergmann,René Scholtysik,Martina Brauser,Anna Lollies,Reiner Siebert,Reiner Siebert,Thorsten Zenz,Ulrich Dührsen,Ralf Küppers,Jan Dürig +15 more
TL;DR: This study considerably extends the picture of pathways involved in molecular pathogenesis of T-PLL and identifies the tumor suppressor gene SAMHD1 with ~20% of T -PLL affected by destructive lesions likely as major player in T- PLL pathogenesis.
•Journal Article
Typing the histogenetic origin of the tumor cells of lymphocyte-rich classical Hodgkin's lymphoma in relation to tumor cells of classical and lymphocyte-predominance Hodgkin's lymphoma.
TL;DR: The mutation pattern of rearranged Ig genes of HRS cells in lrcHL is clearly different from those in lymphocytic and histiocytic cells of lpHL, and resembles the pattern in H RS cells of cHL, suggesting that HRS Cells in lRCHL derive from (preapoptotic) GC B cells that silenced hypermutation.
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