The DOI matches its Crossref record; 102 of the 102 references it cites were found in a registry or an index.
Cancer stem cells versus phenotype‐switching in melanoma
Open accessAbstract
Summary: Tumours comprise multiple phenotypically distinct subpopulations of cells, some of which are proposed to possess stem cell‐like properties, being able to self‐renew, seed and maintain tumours, and provide a reservoir of therapeutically resistant cells. Here, we use melanoma as a model to explore the validity of the cancer stem cell hypothesis in the light of accumulating evidence that melanoma progression may instead be driven by phenotype‐switching triggered by genetic lesions that impose an increased sensitivity to changes in the tumour microenvironment. Although at any given moment cells within a tumour may exhibit differentiated, proliferative or invasive phenotypes, an ability to switch phenotypes implies that most cells will have the potential to adopt a stem cell‐like identity. Insights into the molecular events underpinning phenotype‐switching in melanoma highlight the close relationship between signalling pathways that generate, maintain and activate melanocyte stem cells as well as the inverse correlation between proliferation and invasive potentials. An understanding of phenotype‐switching in melanoma, and in particular the signalling events that regulate the expression of the microphthalmia‐associated transcription factor Mitf, points to new therapeutic opportunities aimed at eradicating therapeutically resistant stem cell‐like melanoma cells.
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Mutations of the BRAF gene in human cancer
Davies, H., Bignell, G. R., Cox, C., Stephens, P., Edkins, S., Clegg, S., Teague, J., Woffendin, H., Garnett, M. J., Bottomley, W., et al. (2002) · Nature · doi:10.1038/nature00766 · Cited by 10,674
A cell initiating human acute myeloid leukaemia after transplantation into SCID mice
Lapidot, T., Sirard, C., Vormoor, J., Murdoch, B., Hoang, T., Caceres-Cortes, J., Minden, M., Paterson, B., Caligiuri, M. A., & Dick, J. E. (1994) · Nature · doi:10.1038/367645a0 · Cited by 4,783
Clarke, M. F., Dick, J. E., Dirks, P. B., Eaves, C. J., Jamieson, C. H. M., Jones, D. L., Visvader, J., Weissman, I. L., & Wahl, G. M. (2006) · Cancer Research · doi:10.1158/0008-5472.can-06-3126 · Cited by 3,051
A Chromatin-Mediated Reversible Drug-Tolerant State in Cancer Cell Subpopulations
Sharma, S. V., Lee, D. Y., Li, B., Quinlan, M. P., Takahashi, F., Maheswaran, S., McDermott, U., Azizian, N., Zou, L., Fischbach, M. A., et al. (2010) · Cell · doi:10.1016/j.cell.2010.02.027 · Cited by 2,770
BRAFE600-associated senescence-like cell cycle arrest of human naevi
Michaloglou, C., Vredeveld, L. C. W., Soengas, M. S., Denoyelle, C., Kuilman, T., van der Horst, C. M. A. M., Majoor, D. M., Shay, J. W., Mooi, W. J., & Peeper, D. S. (2005) · Nature · doi:10.1038/nature03890 · Cited by 2,160
RAF inhibitors transactivate RAF dimers and ERK signalling in cells with wild-type BRAF
Poulikakos, P. I., Zhang, C., Bollag, G., Shokat, K. M., & Rosen, N. (2010) · Nature · doi:10.1038/nature08902 · Cited by 1,811
Efficient tumour formation by single human melanoma cells
Quintana, E., Shackleton, M., Sabel, M. S., Fullen, D. R., Johnson, T. M., & Morrison, S. J. (2008) · Nature · doi:10.1038/nature07567 · Cited by 1,796
Garraway, L. A., Widlund, H. R., Rubin, M. A., Getz, G., Berger, A. J., Ramaswamy, S., Beroukhim, R., Milner, D. A., Granter, S. R., Du, J., et al. (2005) · Nature · doi:10.1038/nature03664 · Cited by 1,548
Kinase-Dead BRAF and Oncogenic RAS Cooperate to Drive Tumor Progression through CRAF
Heidorn, S. J., Milagre, C., Whittaker, S., Nourry, A., Niculescu-Duvas, I., Dhomen, N., Hussain, J., Reis-Filho, J. S., Springer, C. J., Pritchard, C., et al. (2010) · Cell · doi:10.1016/j.cell.2009.12.040 · Cited by 1,465
Blanpain, C., Lowry, W. E., Geoghegan, A., Polak, L., & Fuchs, E. (2004) · Cell · doi:10.1016/j.cell.2004.08.012 · Cited by 1,428
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Oncogenic roles of EMT-inducing transcription factors
Puisieux, A., Brabletz, T., & Caramel, J. (2014) · Nature Cell Biology · doi:10.1038/ncb2976 · Cited by 1,040
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Bravo González-Blas, C., De Winter, S., Hulselmans, G., Hecker, N., Matetovici, I., Christiaens, V., Poovathingal, S., Wouters, J., Aibar, S., & Aerts, S. (2023) · Nature Methods · doi:10.1038/s41592-023-01938-4 · Cited by 778
Low MITF/AXL ratio predicts early resistance to multiple targeted drugs in melanoma
Müller, J., Krijgsman, O., Tsoi, J., Robert, L., Hugo, W., Song, C., Kong, X., Possik, P. A., Cornelissen-Steijger, P. D. M., Foppen, M. H. G., et al. (2014) · Nature Communications · doi:10.1038/ncomms6712 · Cited by 639
Self-citationA SUMOylation-defective MITF germline mutation predisposes to melanoma and renal carcinoma
Bertolotto, C., Lesueur, F., Giuliano, S., Strub, T., de Lichy, M., Bille, K., Dessen, P., d’Hayer, B., Mohamdi, H., Remenieras, A., et al. (2011) · Nature · doi:10.1038/nature10539 · Cited by 526
A Switch in the Expression of Embryonic EMT-Inducers Drives the Development of Malignant Melanoma
Caramel, J., Papadogeorgakis, E., Hill, L., Browne, G. J., Richard, G., Wierinckx, A., Saldanha, G., Osborne, J., Hutchinson, P., Tse, G., et al. (2013) · Cancer Cell · doi:10.1016/j.ccr.2013.08.018 · Cited by 517
Metadata
- Authors
- Hoek, K. S., & Goding, C. R.
- Venue
- Pigment Cell & Melanoma Research
- Publisher
- Wiley
- Published
- 2010-09-24
- Volume
- 23
- Issue
- 6
- Pages
- 746-759
- ISSN
- 1755-1471 (ISSN-L)
- 1755-148X
- OpenAlex
- W1590243782
- Cited by
- 506
- References
- 102
- FWCI
- 15.24
- Type
- journal article
- Language
- en
- Open access
- green
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- Hoek, K. S., & Goding, C. R. (2010). Cancer stem cells versus phenotype‐switching in melanoma. Pigment Cell & Melanoma Research. https://doi.org/10.1111/j.1755-148x.2010.00757.x
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
