ArticleJournal of the Royal Society, Interface2013
On the dynamics of neutral mutations in a mathematical model for a homogeneous stem cell population.
Article in Journal of the Royal Society, Interface, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Stem cell graft dose and composition could impact on the expansion of donor-derived clones after allogeneic hematopoietic stem cell transplantation - a virtual clinical trial.Frontiers in immunology · 2024Article
- Stem cell mutations, associated cancer risk, and consequences for regenerative medicine.Cell stem cell · 2023Review
- Article
- Stem Cell DNA Damage and Genome Mutation in the Context of Aging and Cancer Initiation.Cold Spring Harbor perspectives in biology · 2020Review
- Clonal hematopoiesis of indeterminate potential and its impact on patient trajectories after stem cell transplantation.PLoS computational biology · 2019Article
- Long-term treatment-free remission of chronic myeloid leukemia with falling levels of residual leukemic cells.Leukemia · 2018Article
- Evolutionary dynamics of paroxysmal nocturnal hemoglobinuria.PLoS computational biology · 2018Article
- Optimizing homeostatic cell renewal in hierarchical tissues.PLoS computational biology · 2018Article
- Clonal dominance and transplantation dynamics in hematopoietic stem cell compartments.PLoS computational biology · 2017Article
- Mathematical Modeling Links Pregnancy-Associated Changes and Breast Cancer Risk.Cancer research · 2017Article
- Model-Based Evaluation of Spontaneous Tumor Regression in Pilocytic Astrocytoma.PLoS computational biology · 2015Article
- Cellular population dynamics control the robustness of the stem cell niche.Biology open · 2015Article
- Dynamics of leukemia stem-like cell extinction in acute promyelocytic leukemia.Cancer research · 2014Article
- Robustness of differentiation cascades with symmetric stem cell division.Journal of the Royal Society, Interface · 2014Article
- Interactions and tradeoffs between cell recruitment, proliferation, and differentiation affect CNS regeneration.Biophysical journal · 2014Article
- Mathematical model of adult stem cell regeneration with cross-talk between genetic and epigenetic regulation.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- A deterministic model for the occurrence and dynamics of multiple mutations in hierarchically organized tissues.Journal of the Royal Society, Interface · 2013Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The theory of the clonal origin of cancer states that a tumour arises from one cell that acquires mutation(s) leading to the malignant phenotype. It is the current belief that many of these mutations give a fitness advantage to the mutant population allowing it to expand, eventually leading to disease. However, mutations that lead to such a clonal expansion need not give a fitness advantage and may in fact be neutral--or almost neutral--with respect to fitness. Such mutant clones can be eliminated or expand stochastically, leading to a malignant phenotype (disease). Mutations in haematopoietic stem cells give rise to diseases such as chronic myeloid leukaemia (CML) and paroxysmal nocturnal haemoglobinuria (PNH). Although neutral drift often leads to clonal extinction, disease is still possible, and in this case, it has important implications both for the incidence of disease and for therapy, as it may be more difficult to eliminate neutral mutations with therapy. We illustrate the consequences of such dynamics, using CML and PNH as examples. These considerations have implications for many other tumours as well.
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.