Abstract
Cancer Catherine M. Worsley a,b , Elizabeth S. Mayne a,b , Rob B. Veale c . a Department of Molecular Medicine and Haematology, Faculty of Health Science, University of the Witwatersrand, Johannesburg. b Department of Molecular Medicine and Haematology, Charlotte Maxeke Johannesburg Academic Hospital, National Health Laboratory Service. c School of Molecular and Cell Biology, Faculty of Science, University of the Witwatersrand, Johannesburg.
Highlights
Tumours contain a host of cancer clones that are genetically and epigenetically different from one another [1]
Evolutionary principles describe the process of clonal evolution and aid in formulating novel strategies for disease management and prognosis [4]
An understanding of tumour heterogeneity and clone fitness is key to developing better treatment options
Summary
Cancer chemotherapy kills some tumour cells, leaving behind resistant clones with less competition for space and resources. These clones, groups of cells that share common ancestry, proliferate without restriction causing disease relapse. Tumours contain a host of cancer clones that are genetically and epigenetically different from one another [1]. These clones follow a Darwinian process of somatic selection where they compete for space and resources within their microenvironments [2]. Chemotherapy itself is a selective pressure that influences tumour heterogeneity and clonal evolution. Evolutionary principles describe the process of clonal evolution and aid in formulating novel strategies for disease management and prognosis [4]
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