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Nina F. Øbro
Researcher at University of Cambridge
Publications - 11
Citations - 649
Nina F. Øbro is an academic researcher from University of Cambridge. The author has contributed to research in topics: Stem cell & Biology. The author has an hindex of 3, co-authored 6 publications receiving 310 citations. Previous affiliations of Nina F. Øbro include Copenhagen University Hospital.
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Journal ArticleDOI
Population dynamics of normal human blood inferred from somatic mutations.
Henry Lee-Six,Nina F. Øbro,Mairi Shepherd,Sebastian Grossmann,Kevin J. Dawson,Miriam Belmonte,Robert J. Osborne,Brian J. P. Huntly,Inigo Martincorena,Elizabeth Anderson,Laura O’Neill,Michael R. Stratton,Elisa Laurenti,Anthony R. Green,David G. Kent,Peter J. Campbell +15 more
TL;DR: Analysis of blood from a healthy human show that haematopoietic stem cells increase rapidly in numbers through early life, reaching a stable plateau in adulthood, and contribute to myeloid and B lymphocyte populations throughout life.
Journal ArticleDOI
Somatic mutation landscapes at single-molecule resolution
Federico Abascal,Luke M. R. Harvey,Emily G. Mitchell,Emily G. Mitchell,Andrew R. J. Lawson,Stefanie V Lensing,Peter R. Ellis,Andrew Russell,Raul E. Alcantara,Adrian Baez-Ortega,Yichen Wang,Eugene Jing Kwa,Henry Lee-Six,Alex Cagan,Tim H. H. Coorens,Michael Spencer Chapman,Sigurgeir Olafsson,Steven Leonard,David T. Jones,Heather E. Machado,Megan Davies,Nina F. Øbro,Krishnaa T. Mahubani,Kieren Allinson,Moritz Gerstung,Kourosh Saeb-Parsy,David G. Kent,David G. Kent,Elisa Laurenti,Michael R. Stratton,Raheleh Rahbari,Peter J. Campbell,Peter J. Campbell,Robert J. Osborne,Inigo Martincorena +34 more
TL;DR: NanoSeq as discussed by the authors is a duplex sequencing protocol with error rates of less than five errors per billion base pairs in single DNA molecules from cell populations, enabling the study of somatic mutations in any tissue independently of clonality.
Journal ArticleDOI
Longitudinal Cytokine Profiling Identifies GRO-α and EGF as Potential Biomarkers of Disease Progression in Essential Thrombocythemia.
Nina F. Øbro,Jacob Grinfeld,Jacob Grinfeld,Miriam Belmonte,Miriam Belmonte,Melissa Irvine,Mairi Shepherd,Tata Nageswara Rao,Axel Karow,Axel Karow,Lisa M Riedel,Oliva B Harris,E. Joanna Baxter,Jyoti Nangalia,Anna L. Godfrey,Claire N. Harrison,Juan Li,Radek C. Skoda,Peter J. Campbell,Anthony R. Green,Anthony R. Green,David G. Kent,David G. Kent +22 more
TL;DR: Data implicate the immune cell microenvironment as a significant player in ET disease evolution and illustrate the utility of cytokines as potential biomarkers for reaching beyond genomic classification for disease stratification and monitoring.
Journal ArticleDOI
Life-threatening viral disease in a novel form of autosomal recessive IFNAR2 deficiency in the Arctic
C. Duncan,Morten K Skouboe,Sophie Howarth,Anne Kruse Hollensen,Rui Chen,Malene Børresen,Benjamin J. Thompson,Jarmila Stremenova Spegarova,Catherine F Hatton,Frederik Filip Stæger,Mette K. Andersen,John C. Whittaker,Søren R. Paludan,Sofie E. Jørgensen,Martin K. Thomsen,Jacob Giehm Mikkelsen,Carsten Heilmann,Daniela Buhas,Nina F. Øbro,Jakob T. Bay,Hanne Vibeke Marquart,M. Teresa de la Morena,Joseph Klejka,Matthew Hirschfeld,Lise Borgwardt,Isabel Forss,Tania N. Masmas,Anja Poulsen,Francisco Noya,Guy A. Rouleau,Torben Hansen,Sirui Zhou,Anders Albrechtsen,Reza Alizadehfar,Eric J. Allenspach,Sophie Hambleton,Trine H. Mogensen +36 more
TL;DR: A novel form of autosomal recessive IFNAR2 deficiency due to a null and common allele in Arctic populations is reported, broadening its clinical phenotype from diseases caused by live-attenuated viral vaccines to include life-threatening influenza and SARS-CoV-2.
Journal ArticleDOI
Diverse mutational landscapes in human lymphocytes
Heather E. Machado,Emily G. Mitchell,Nina F. Øbro,Kirsten Kübler,Megan Davies,Daniel Leongamornlert,Alyssa Cull,Francesco Lauria,Mathijs A. Sanders,Alex Cagan,Craig M. McDonald,Miriam Belmonte,Mairi Shepherd,Felipe A. Vieira Braga,Robert Osborne,Krishnaa T. Mahbubani,Inigo Martincorena,Elisa Laurenti,Anthony R. Green,Gad Getz,Paz Polak,Kourosh Saeb-Parsy,Daniel J. Hodson,David G. Kent,Peter J. Campbell +24 more
TL;DR: In this paper , the authors sequenced whole genomes from 717 normal naive and memory B and T cells and haematopoietic stem cells and found that all lymphocyte subsets carried more point mutations and structural variants than stem cells, with higher burdens in memory cells than in naive cells and with T cells accumulating mutations at a higher rate throughout life.