Intra-tumoral Heterogeneity—Experimental Models, Molecular Mechanisms and Clinical Relevance

Dear Colleagues,

Intratumoral heterogeneity (ITH) has increasingly been recognized as a key contributing factor to chemoresistance and cancer relapse. Thus, improved understanding of the molecular mechanisms underlying ITH is highly important and relevant in the quest against cancers. ITH can be generally categorized into two groups, namely, clonal and nonclonal. Clonal ITH, which is linked to the intrinsic genetic instability of cancer cells, is characterized by the accumulation of genetic and epigenetic aberrations that commonly accompany tumor progression. Nonclonal ITH, which is closely linked to the interactions between cancer cells and microenvironment, is characterized by phenotypic plasticity. One of the most characterized mechanisms to generate nonclonal ITH is epithelial–mesenchymal transition, in which relatively mature-appearing epithelial cells de-differentiate into immature-appearing, stem-like mesenchymal cells. Chemotherapeutic agents and various hostile microenvironments (e.g., hypoxia and oxidative stress) are known to promote this type of phenotypic conversion, which is often associated with increased chemoresistance. Using tumor samples from patients, studies have found a significant correlation between the acquisition of stem-like features in cancer cells and a worse clinical outcome. In recent years, various technical advances have greatly facilitated the detection and molecular characterization of ITH, such as the use of next-generation sequencing of single cells, CRISPR barcoding, and various transcription factor reporter systems. Both research and review articles pertaining to these topics are welcome. 

Prof. Dr. Raymond Lai
Guest Editor

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