The causes and consequences of genetic heterogeneity in cancer evolution

By R. Burrell, Nicholas McGranahan, J. Bartek, Charles Swanton. Nature, 2013

2,128 citations recorded by the source corpus.

Subfields: Cancer Research, Cell Biology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/89892be3d3c37f34a5390706ffdb975ac32d3cd5

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Citations in the corpus

Cancer Evolution: Mathematical Models and Computational Inference (2014, background): “…implications have been reviewed recently and extensively (de Bruin et al. 2013; Bedard et al. 2013; Klein 2013; Junttila and de Sauvage 2013; Burrell et al. 2013; Meacham and Morrison 2013; Almendro et al. 2013; Aparicio and Caldas 2013; Greaves and Maley 2012; Marusyk et al. 2012; Caldas…”
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).”
The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, positive): “…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 (Greaves and Maley, 2012; Burrell et al., 2013) and seed different parts of a single tumor (Gerlinger et al., 2012).”
Biological and therapeutic impact of intratumor heterogeneity in cancer evolution. (2015, background): “This instability can contribute to intratumor heterogeneity by providing a pool of mutations upon which selection can act in a given microenvironmental context (Burrell et al., 2013a).”
Tumor cell-intrinsic factors underlie heterogeneity of immune cell infiltration and response to immunotherapy (2018, neutral): “Different tumors accumulate genetic and epigenetic alterations conferring diverse molecular, cellular, and clinical features, a phenomenon known as intertumoral heterogeneity (Burrell et al., 2013).”
Clonal status of actionable driver events and the timing of mutational processes in cancer evolution (2015, background): “Accumulating evidence suggests that tumors often evolve through a process of branched evolution, involving genetically distinct subclones (6, 7).”
Prospective derivation of a Living Organoid Biobank of colorectal cancer patients (2015, background): “This cellular heterogeneity and phenotypic variation allows the emergence of a complex clonal architecture, which underpins important features such as drug resistance and metastatic potential (Burrell et al., 2013).”