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Mechanisms and clinical implications of tumor heterogeneity and convergence on recurrent phenotypes


Tumor heterogeneity has been identified at various -omic levels. The tumor genome, transcriptome, proteome, and phenome can vary widely across cells in patient tumors and are influenced by tumor cell interactions with heterogeneous physical conditions and cellular components of the tumor microenvironment. Here, we explore the concept that while variation exists at multiple -omic levels, changes at each of these levels converge on the same pathways and lead to convergent phenotypes in tumors that can provide common drug targets. These phenotypes include cellular growth and proliferation, sustained oncogenic signaling, and immune avoidance, among others. Tumor heterogeneity complicates treatment of patient cancers as it leads to varied response to therapies. Identification of convergent cellular phenotypes arising in patient cancers and targeted therapies that reverse them has the potential to transform the way clinicians treat these cancers and to improve patient outcome.

Type Journal
ISBN 1432-1440 (Electronic) 0946-2716 (Linking)
Authors McQuerry, J. A.; Chang, J. T.; Bowtell, D. D. L.; Cohen, A.; Bild, A. H.
Responsible Garvan Author (missing name)
Published Date 2017-11-14
Published Volume 95
Published Issue 11
Published Pages 1167-1178
Status Published in-print
DOI 10.1007/s00109-017-1587-4
URL link to publisher's version