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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\u2014or almost neutral\u2014with 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.<\/jats:p>","DOI":"10.1098\/rsif.2012.0810","type":"journal-article","created":{"date-parts":[[2012,12,5]],"date-time":"2012-12-05T16:40:11Z","timestamp":1354725611000},"update-policy":"https:\/\/doi.org\/10.1098\/crossmark-policy","source":"Crossref","is-referenced-by-count":30,"title":["On the dynamics of neutral mutations in a mathematical model for a homogeneous stem cell population"],"prefix":"10.1098","volume":"10","author":[{"given":"Arne","family":"Traulsen","sequence":"first","affiliation":[{"name":"1","department":["Evolutionary Theory Group, Max Planck Institute for Evolutionary Biology, August-Thienemann Strasse 2, 24306 Pl\u00f6n, Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tom","family":"Lenaerts","sequence":"additional","affiliation":[{"name":"2","department":["MLG, D\u00e9partement d'Informatique, Universit\u00e9 Libre de Bruxelles, Boulevard du Triomphe CP212, 1050 Brussels, Belgium"]},{"name":"3","department":["AI Laboratory, Computer Science Department, Vrije Universiteit Brussel, Pleinlaan 2, 1050 Brussels, Belgium"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge M.","family":"Pacheco","sequence":"additional","affiliation":[{"name":"4","department":["Departamento de Matem\u00e1tica e Aplica\u00e7\u00f5es, Universidade do Minho, 4710- 057 Braga, Portugal"]},{"name":"5","department":["ATP Group, CMAF, Instituto para a Investiga\u00e7\u00e3o Interdisciplinar, 1649-003 Lisboa Codex, Portugal"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Dingli","sequence":"additional","affiliation":[{"name":"6","department":["Division of Hematology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"175","reference":[{"key":"2026010519504079300_RSIF20120810C1","volume-title":"The statistical processes of evolutionary theory","author":"Moran,","year":"1962"},{"key":"2026010519504079300_RSIF20120810C2","doi-asserted-by":"publisher","first-page":"461","DOI":"10.4161\/cc.6.4.3853","article-title":"Stochastic dynamics of haematopoietic tumor stem cells","volume":"6","author":"Dingli,","year":"2007","journal-title":"Cell Cycle"},{"key":"2026010519504079300_RSIF20120810C3","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0028955","article-title":"Dynamics of resistance development to imatinib under increasing selection pressure: a combination of mathematical models and in vitro data","volume":"6","author":"Werner,","year":"2011","journal-title":"PLoS ONE"},{"key":"2026010519504079300_RSIF20120810C4","doi-asserted-by":"publisher","first-page":"433","DOI":"10.1016\/S0022-5193(03)00120-6","article-title":"Mutation\u2013selection networks of cancer initiation: tumor suppressor genes and chromosomal instability","volume":"223","author":"Komarova,","year":"2003","journal-title":"J. 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