Clonal competition with alternating dominance in multiple myeloma.
By J. Keats, M. Chesi, J. Egan, Victoria M Garbitt, Stephen E. Palmer, E. Braggio, S. V. Van Wier, P. Blackburn, A. Baker, A. Dispenzieri and 7 more. Blood, 2012
648 citations recorded by the source corpus.
Subfields: Hematology, Molecular Biology, Radiology, Nuclear Medicine and Imaging
View Paper: https://www.semanticscholar.org/paper/ce1de388daf88cf4333cbf34b9f1351940381383
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Hematology
In Molecular Biology
- Nicholas McGranahan
- Charles Swanton
- Elaine R. Mardis
- S. Nik-Zainal
- Richard K. Wilson
- D. Hoon
- Kevin J. Dawson
- P. van Loo
In Radiology, Nuclear Medicine and Imaging
Citations in the corpus
- Analytical and Clinical Validation of a Digital Sequencing Panel for Quantitative, Highly Accurate Evaluation of Cell-Free Circulating Tumor DNA (2015, background): “that the initial biopsy genomics did not reveal the tumor subclone that ultimately drove mortality (secondary plasma cell leukemia) [63].”
- Widespread genetic heterogeneity in multiple myeloma: implications for targeted therapy (2014, neutral): “…(e.g., cytogenetics, FISH, and array CGH) have pointed to the existence of clonal heterogeneity in MM, and recent studies using exome sequencing and copy number analyses in a small number of samples similarly documented clonal diversity (Egan et al., 2012; Keats et al., 2012; Walker et al., 2012).”
- SciClone: Inferring Clonal Architecture and Tracking the Spatial and Temporal Patterns of Tumor Evolution (2014, background): “For example, the alternate ‘‘waxing’’ and ‘‘waning’’ of subclonal CNAs has been observed in multiple myeloma [17,33].”
- Intratumor heterogeneity: evolution through space and time. (2012, neutral): “in cytogenetically high-risk multiple myeloma (24).”
- Biological and therapeutic impact of intratumor heterogeneity in cancer evolution. (2015, background): “Interestingly, in a series of 28 patients with MM, those with the highest cytogenetically defined clinical risk harbored disease that was most dynamic during the course of treatment (Keats et al., 2012).”
- Heterogeneity of genomic evolution and mutational profiles in multiple myeloma (2014, positive): “…single nucleotide polymorphism (SNP) arrays on serial samples showed that molecular events necessary for MM progression are not attained in a linear fashion but rather through branching, nonlinear pathways 9,10 , a pattern typical of a complex ecosystem of clones competing for evolution.”
- Cancer heterogeneity: implications for targeted therapeutics (2013, background): “There are intriguing clinical examples of variation in temporal patterns of tumour genomic architectures within multiple myeloma patients, and in some patients a distinct pattern of complex clonal competition was observed (Keats et al, 2012).”