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Clonal heterogeneity is defined as the presence of several subclones possessing different genomic alterations within a tumor.
Universal threshold cut-off values for defining gain/loss were not applied because of subpopulation clonal heterogeneity, ploidy, and percentage of neuroblastic cells, which varied from one sample to another.
We defined a case having different log2 ratios in one sample as a sample with clonal heterogeneity (Fig. 1a).
We defined a case indicating the same log2 ratio for all CNA as a sample without clonal heterogeneity (Fig. 1a) because the single tumor cell population was calculated from the log2 ratio(s) of all CNA in this sample.
We defined such a case with different log2 ratios showing one tumor cell population as a sample without clonal heterogeneity.
In this review, we address how tumor clonality is measured using next-generation sequencing (NGS) data, highlight that clonal heterogeneity is common across multiple tumor types, and discuss the potential clinical implications of tumor clonal heterogeneity.
The ultimate hope is that identifying mutations associated with clonal heterogeneity and disease progression will lead to new personalized medicine approaches in which treatments will be tailored to the unique spectrum of mutations that define the individual clones within a patient's tumor.
Myeloid malignancies exist on a spectrum from asymptomatic clonal hematopoiesis to overt leukemia and exhibit substantial clonal heterogeneity.
Intratumor clonal heterogeneity has been proposed as a major attribute underlying tumor evolution, progression, and resistance to chemotherapy and radiation.
Inasmuch as cells switch from one state to another, clonal heterogeneity must contribute to cellular heterogeneity.
The ELISA measurements of secreted IgM from independent replacements did not reveal evidence of clonal heterogeneity.
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