ArticleJournal of theoretical biology2011
Evolutionary dynamics of BRCA1 alterations in breast tumorigenesis.
Article in Journal of theoretical biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Oncogenic BRCA1,2 Mutations in the Human Lineage-A By-Product of Sexual Selection?Biomedicines · 2023Review
- Mathematical models of breast and ovarian cancers.Wiley interdisciplinary reviews. Systems biology and medicine · 2016Review
- Promoter methylation and expression changes ofOncology letters · 2015Article
- Evolution of pre-existing versus acquired resistance to platinum drugs and PARP inhibitors in BRCA-associated cancers.PloS one · 2014Article
- BRCA1-methylated sporadic breast cancers are BRCA-like in showing a basal phenotype and absence of ER expression.Virchows Archiv : an international journal of pathology · 2012Article
- Evolutionary pathways in BRCA1-associated breast tumors.Cancer discovery · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Cancer results from the accumulation of alterations in oncogenes and tumor suppressor genes. Tumor suppressors are classically defined as genes which contribute to tumorigenesis if their function is lost. Genetic or epigenetic alterations inactivating such genes may arise during somatic cell divisions or alternatively may be inherited from a parent. One notable exception to this rule is the BRCA1 tumor suppressor that predisposes to hereditary breast cancer when lost. Genetic alterations of this gene are hardly ever observed in sporadic breast cancer, while individuals harboring a germline mutation readily accumulate a second alteration inactivating the remaining allele--a finding which represents a conundrum in cancer genetics. In this paper, we present a novel mathematical framework of sporadic and hereditary breast tumorigenesis. We study the dynamics of genetic alterations driving breast tumorigenesis and explore those scenarios which can explain the absence of somatic BRCA1 alterations while replicating all other disease statistics. Our results support the existence of a heterozygous phenotype of BRCA1 and suggest that the loss of one BRCA1 allele may suppress the fitness advantage caused by the inactivation of other tumor suppressor genes. This paper contributes to the mathematical investigation of breast tumorigenesis.
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Registered trials
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