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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.
Intratumor clonal heterogeneity has been proposed as a major attribute underlying tumor evolution, progression, and resistance to chemotherapy and radiation.
Myeloid malignancies exist on a spectrum from asymptomatic clonal hematopoiesis to overt leukemia and exhibit substantial clonal heterogeneity.
Recent whole-genome sequencing (WGS) studies have demonstrated that tumors typically comprise a founding clone and multiple subclones (i.e., clonal heterogeneity is common).
In this article we review evidence for cancer clonal heterogeneity, evaluating the importance of tumour subclones and their growth through both Darwinian and neutral evolution.
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.
Clonal heterogeneity implies that expression can persist in different states through multiple cell divisions.
Melanoma cells show clonal heterogeneity.
Clonal heterogeneity was less common in glioblastomas.
HBEC clonal heterogeneity has also been reported by others [ 5].
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