K
Karin Olsson
Researcher at Lund University
Publications - 54
Citations - 1860
Karin Olsson is an academic researcher from Lund University. The author has contributed to research in topics: Diamond–Blackfan anemia & Crayfish. The author has an hindex of 21, co-authored 43 publications receiving 1687 citations. Previous affiliations of Karin Olsson include University of Geneva.
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Lentiviral vector transduction of NOD/SCID repopulating cells results in multiple vector integrations per transduced cell: risk of insertional mutagenesis.
Niels-Bjarne Woods,Arne Muessig,Manfred G. Schmidt,Johan Flygare,Karin Olsson,Patrick Salmon,Didier Trono,Christof von Kalle,Stefan Karlsson +8 more
TL;DR: The ability of lentiviral vectors to transduce multiple copies into a subset of NOD/SCID repopulating cells, with a particular focus on the average number of vector copies integrating into these primitive progenitor cells, is demonstrated.
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Combination of pegylated IFN-α2b with imatinib increases molecular response rates in patients with low- or intermediate-risk chronic myeloid leukemia
Bengt Simonsson,Tobias Gedde-Dahl,Berit Markevärn,Kari Remes,Jesper Stentoft,Anders Almqvist,Mats Björeman,Max Flogegard,Perttu Koskenvesa,Anders Lindblom,Claes Malm,Satu Mustjoki,Kristina Myhr-Eriksson,Lotta Ohm,Anu Räsänen,Marjatta Sinisalo,Anders Själander,Ulla Strömberg,Ole Weiss Bjerrum,Hans Ehrencrona,Hans Ehrencrona,Franz Gruber,V Kairisto,Karin Olsson,Fredrik Sandin,Arnon Nagler,Johan Lanng Nielsen,Henrik Hjorth-Hansen,Kimmo Porkka +28 more
TL;DR: Lower doses of Peg-IFN-α2b may enhance tolerability while retaining efficacy and could be considered in future protocols with curative intent.
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Invasions and niche width: does niche width of an introduced crayfish differ from a native crayfish?
TL;DR: Assessing niche width in relation to invader success can be a useful tool trying to predict the impact of invasions on different scales, and suggests that signal crayfish has greater plasticity with respect to habitat utilisation and feeding than noblecrayfish.
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Mice with ribosomal protein S19 deficiency develop bone marrow failure and symptoms like patients with Diamond-Blackfan anemia.
Pekka Jaako,Johan Flygare,Johan Flygare,Karin Olsson,Ronan Quere,Mats Ehinger,Adrianna Henson,Steven R. Ellis,Axel Schambach,Christopher Baum,Johan Richter,Jonas Larsson,David Bryder,Stefan Karlsson +13 more
TL;DR: Both RPS19 gene transfer and the loss of p53 rescue the DBA phenotype implying the potential of the models for testing novel therapies, and the feasibility of transgenic RNA interference to generate mouse models for human diseases caused by haploinsufficient expression of a gene.
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Effective cell and gene therapy in a murine model of Gaucher disease.
Ida Berglin Enquist,Eva Nilsson,Andreas Ooka,Jan-Eric Månsson,Karin Olsson,Mats Ehinger,Roscoe O. Brady,Johan Richter,Stefan Karlsson +8 more
TL;DR: Both transplantation of WT bone marrow (BM) and gene therapy through retroviral transduction of BM from GD mice prevented development of disease and corrected an already established GD phenotype, demonstrating the feasibility of gene therapy for type 1 GD in vivo.