ArticleProceedings of the National Academy of Sciences of the United States of America2008
Neutral evolution in paroxysmal nocturnal hemoglobinuria.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 56 citations in OpenAlex.
- Mathematical modeling ofProceedings of the National Academy of Sciences of the United States of America · 2026Article
- Paroxysmal Nocturnal Hemoglobinuria: Biology and Treatment.Medicina (Kaunas, Lithuania) · 2023Review
- Significance of paroxysmal nocturnal hemoglobinuria clone in immunosuppressive therapy for children with severe aplastic anemia.Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2022Article
- The importance of terminal complement inhibition in paroxysmal nocturnal hemoglobinuria.Therapeutic advances in hematology · 2022Review
- Is nature truly healing itself? Spontaneous remissions in Paroxysmal Nocturnal Hemoglobinuria.Blood cancer journal · 2021Article
- Clonal hematopoiesis and bone marrow failure syndromes.Best practice & research. Clinical haematology · 2021Review
- Insights Into the Emergence of Paroxysmal Nocturnal Hemoglobinuria.Frontiers in immunology · 2021Review
- Evolutionary dynamics of paroxysmal nocturnal hemoglobinuria.PLoS computational biology · 2018Article
- Article
- Paroxysmal nocturnal haemoglobinuria.Nature reviews. Disease primers · 2017Review
- Clonal Replacement Underlies Spontaneous Remission in Paroxysmal Nocturnal Haemoglobinuria.British journal of haematology · 2017Article
- Recent advances in the pathogenesis and treatment of paroxysmal nocturnal hemoglobinuria.F1000Research · 2016Review
- Dynamics of leukemia stem-like cell extinction in acute promyelocytic leukemia.Cancer research · 2014Article
- Effect of dedifferentiation on time to mutation acquisition in stem cell-driven cancers.PLoS computational biology · 2014Article
- Article
- On the dynamics of neutral mutations in a mathematical model for a homogeneous stem cell population.Journal of the Royal Society, Interface · 2013Article
- Last marrow standing: bone marrow transplantation for acquired bone marrow failure conditions.Current hematologic malignancy reports · 2012Review
- The small population of PIG-A mutant cells in myelodysplastic syndromes do not arise from multipotent hematopoietic stem cells.Haematologica · 2012Article
- Dynamics of mutant cells in hierarchical organized tissues.PLoS computational biology · 2011Article
- Natural history of paroxysmal nocturnal hemoglobinuria clones in patients presenting as aplastic anemia.European journal of haematology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paroxysmal nocturnal hemoglobinuria is an acquired hematopoietic stem cell (HSC) disorder characterized by the partial or complete deficiency of glycosyl-phosphatidylinositol (GPI)-linked membrane proteins, which leads to intravascular hemolysis. A loss of function mutation in the PIG-A gene, required for GPI biosynthesis, explains how the deficiency of many membrane proteins can result from a single genetic event. However, to date the mechanism of expansion of the GPI(-) clone has not been fully understood. Two hypotheses have been proposed: A selective advantage of GPI(-) cells because of a second mutation or a conditional growth advantage of GPI(-) cells in the presence of an immune attack on normal (GPI(+)) HSCs. Here, we explore a third possibility, whereby the PNH clone does not have a selective advantage. Simulations in a large virtual population accurately reproduce the known incidence of the disease; and the fit is optimized when the number of stem cells is decreased, reflecting a component of bone marrow failure in PNH. The model also accounts for the occurrence of spontaneous cure in PNH, consequent on clonal extinction. Thus, a clonal advantage may not be always necessary to explain clonal expansion in PNH.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.