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Austen Worth

Researcher at Great Ormond Street Hospital for Children NHS Foundation Trust

Publications -  97
Citations -  3681

Austen Worth is an academic researcher from Great Ormond Street Hospital for Children NHS Foundation Trust. The author has contributed to research in topics: Transplantation & Hematopoietic stem cell transplantation. The author has an hindex of 30, co-authored 79 publications receiving 2694 citations. Previous affiliations of Austen Worth include John Radcliffe Hospital & University College London.

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Long-term follow-up of IPEX syndrome patients after different therapeutic strategies: An international multicenter retrospective study

Federica Barzaghi, +83 more
TL;DR: Patients receiving chronic IS were hampered by disease recurrence or complications, impacting long‐term disease‐free survival, and when performed in patients with a low OI score, HSCT resulted in disease resolution with better quality of life, independent of age, donor source, or conditioning regimen.
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Two novel activating mutations in the Wiskott-Aldrich syndrome protein result in congenital neutropenia

TL;DR: In vitro culture of bone marrow progenitors demonstrated a profound reduction in neutrophil production and increased levels of apoptosis, consistent with an intrinsic disturbance of normal myeloid differentiation as the cause of the neutropenia, suggesting a novel cause of myelodysplasia.
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Autoimmune lymphoproliferative syndrome: molecular basis of disease and clinical phenotype.

TL;DR: A detailed insight is provided into the pathophysiology of lymphocyte apoptosis and how this relates to the variable and complex clinical manifestations of ALPS.
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Loss-of-function nuclear factor κB subunit 1 (NFKB1) variants are the most common monogenic cause of common variable immunodeficiency in Europeans

Paul Tuijnenburg, +157 more
TL;DR: It is shown that heterozygous loss‐of‐function variants in NFKB1 are the most common known monogenic cause of CVID, which results in a temporally progressive defect in the formation of immunoglobulin‐producing B cells.