Heterogeneity in cancer: cancer stem cells versus clonal evolution.

By Mark Shackleton, E. Quintana, Eric R. Fearon, S. Morrison. Cell, 2009

1,225 citations recorded by the source corpus.

Subfields: Ecology, Evolution, Behavior and Systematics, Molecular Biology, Oceanography

View Paper: https://www.semanticscholar.org/paper/783dde29e63bb5545942cb888501c70d2b83cb13

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Ecology, Evolution, Behavior and Systematics

1. Ting Lu
2. Xiaona Fang
3. Jin Wang
4. Karsten Kruse

In Molecular Biology

1. J. Dick
2. Hans Clevers
3. M. Karin
4. Ting Lu
5. Xiaona Fang
6. Karsten Kruse
7. J. Chiche
8. S. Morrison

Citations in the corpus

• Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer (2009, background): “Yet a lot of interest has been paid recently to cancer stem cell research [247, 248], although the existence of such cells has been questioned [249].”
• Evolution of the cancer stem cell model. (2014, background): “As we have argued throughout this Review, both genetic and nongenetic determinants influence tumor heterogeneity and often these two views have been presented as mutually exclusive models, stimulating intense debate (Clevers, 2011 et al., 2012; Shackleton et al., 2009).”
• Breast cancer stem cell markers CD44, CD24 and ALDH1: expression distribution within intrinsic molecular subtype (2011, background): “Luminal and HER-OE breast cancer cell lines are mainly enriched in CD44 (cid:1) /low CD24 + tumour cells, whereas basal/ mesenchymal breast cancer cell lines are enriched in the CD44 + CD24 (cid:1) /low CSC phenotype; basal/epithelial breast cancer cells are mainly positive for both CD44 and CD24…”
• Cancer stem cells: impact, heterogeneity, and uncertainty. (2012, background): “Finally, some cancers follow a stem cell model in which tumorigenic cancer stem cells ‘‘differentiate’’ into nontumorigenic cancer cells, creating a hierarchical organization (Figure 1C; Table 1) (Dick, 2008; Reya et al., 2001; Shackleton et al., 2009).”
• Targeted drug delivery to tumors: Myths, reality and possibility (2011, neutral): “Both clonal evolution and cancer stem cell theories support intra-tumoral heterogeneity arising from genetic variation as well as epigenetic modification [81,82].”
• Phenotypic heterogeneity among tumorigenic melanoma cells from patients that is reversible and not hierarchically organized (2010, background): “We have found that both CD133+ and CD133 melanoma cells form tumors that exhibit similar heterogeneity in CD133 expression, suggesting that CD133 is reversibly expressed by tumorigenic melanoma cells rather than distinguishing cells at different levels of a hierarchy (Shackleton et al., 2009).”
• Tumor Metastasis: Molecular Insights and Evolving Paradigms (2011, neutral): “Indeed, xenograft serial transplantation studies involving several tumor types lend support to this model, although the applicability of these findings to all types of human malignancies continues to be debated (Shackleton et al., 2009; Clevers, 2011).”
• The Cancer Stem Cell Niche: How Essential is the Niche in Regulating Stemness of Tumor Cells? (2015, neutral): “Given that the major limitation of transplantation assays is that they cannot reveal the actual fate of the transplanted cell in its original tissue or tumor (Shackleton et al., 2009), it is of central importance to develop assays that can visualize and localize CSCs and their function within the pr”
• Inflammation meets cancer, with NF-κB as the matchmaker (2011, background): “Other tumors might arise from normal tissue stem cells or from tissue stem cells that were transformed to become cancer stem cell”
• Nonequilibrium physics in biology (2019, background): “primarily caused by epigenetic modifications (Shackleton et al., 2009).”
• Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “In contrast, a stochastic or clonal evolution model of tumor development suggests that the phenotypic heterogeneity of tumors is due to variations in the genetic or epigenetic composition of tumor subpopulations, but that these subpopulations are not hierarchically organized and have similar tumor-i”