CLONAL EVOLUTION IN CANCER

By M. Greaves, Carlo C. Maley. Nature, 2012

1,692 citations recorded by the source corpus.

Cancers evolve by a reiterative process of clonal expansion, genetic diversification and clonal selection within the adaptive landscapes of tissue ecosystems. The dynamics are complex, with highly variable patterns of genetic diversity and resulting clonal architecture. Therapeutic intervention may destroy cancer clones and erode their habitats, but it can also inadvertently provide a potent selective pressure for the expansion of resistant variants. The inherently Darwinian character of cancer is the primary reason for this therapeutic failure, but it may also hold the key to more effective control.

Subfields: Cancer Research, Cell Biology, Genetics

View Paper: https://www.semanticscholar.org/paper/b24898f8df57f0d24aab358af227b2920e4b4500

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Citations in the corpus

Evolution of the cancer stem cell model. (2014, background): “Advanced genome sequencing has demonstrated that cancer within a single patient is a heterogeneous mixture of genetically distinct sub-clones that arise through branching evolution (Burrell et al., 2013; Greaves and Maley, 2012).”
Cancer therapy shapes the fitness landscape of clonal hematopoiesis (2020, neutral): “Among individuals with CH, 69% (n = 4,952) had one mutation and 31% (2,264) had two or more.”
TITAN: inference of copy number architectures in clonal cell populations from tumor whole-genome sequence data (2014, background): “We estimate the cellular prevalence of the CNA/LOH with the assumption that co-occurring events will be represented in the same clones, resulting from ‘‘punctuated’’ clonal expansions (Navin et al. 2011; Greaves and Maley 2012).”
Clonal Evolution in Breast Cancer Revealed by Single Nucleus Genome Sequencing (2014, background): “These rare mutations may play an important role in diversifying the phenotypes of cancer cells, allowing them to surive selective pressures in the tumor microenvironment, including the immune system, hypoxia and chemotherapy 35,36 .”
Cancer epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance (2014, background): “This would be a factor in countering the strictly hierarchical theory for existence of CSCs as a stable population, with unrestricted tumor initiating potential that always give rise to progeny cells lacking or reduced for the tumor-initiating property (Greaves and Maley, 2012; Gupta et al., 2011).”
Mutational Analysis Reveals the Origin and Therapy-driven Evolution of Recurrent Glioma (2013, neutral): “The genetic landscape of tumors is continually evolving, which can be an impediment to the clinical management of cancer patients with recurrent disease (1, 2).”
Breast cancer development and progression: Risk factors, cancer stem cells, signaling pathways, genomics, and molecular pathogenesis (2018, background): “The clonal evolution of genetically heterogeneous tumor initiating cells or cancer stem cells may contribute significantly to intratumor heterogeneity of breast cancer, even though the establishment of tumor heterogeneity has been traditionally explained by the cancer stem cell hypothesis(23,305,321”
Cancer heterogeneity—a multifaceted view (2013, positive): “When a selective pressure is applied, such as therapy, the fittest—most resistant—subclones are invariably selected to survive and expand to manifest clinically as a tumour relapse [5,6].”