Editorial: Cancer Models

Cancer ModelsCancer is still a major concern for public health and is a cause of death while being psychologically the most dreaded disease.Until recent times, the diagnosis of a progressed form of cancer invariably meant that there was little chance for long-term survival.This notion has changed recently thanks to the tremendous efforts in cancer research and development (compared to other diseases) supported by enormous public and private financing.To illustrate this, just consider the "moonshot initiative" announced by US President Obama in 2016 (1).Cancer research, like research in other diseases, highly depends on representative and reliable model systems.However, cancer is not the single molecule-defined tumor, but rather a heterogenic and highly variable complex of different individual diseases.This makes research on cancer highly difficult, expensive, and explains the enormous resources needed.Looking back on more than 100 years of cancer research, the models used have changed constantly and extended permanently to all the new stages of drug discovery including target identification, lead structure optimization, tolerability, toxicity, biomarker discovery, and individual patient prediction.Today, the selection of the most appropriate model to best reflect the given tumor entity is one of the major challenges for the cancer researchers.From the available volumes on the research topic "Cancer Models, " we collected original papers and review articles that addressed the topic of tumor modeling from perspectives such as molecular biology, biochemistry, microorganisms, cells, and organoids, fishes, animals, and xenografts, up to computational cancer models and patient data analysis.Next-generation sequencing-based methods have recently revealed complex patterns of chromosomal aberrations, which are beyond explanation by classical models of karyotypic evolution.The term chromothripsis has been introduced to describe the phenomenon of temporarily and spatially confined genomic instability.This results in dramatic chromosomal rearrangements of segments of one or a few chromosomes.Simultaneously, misrepaired DNA double-strand breaks are causing another phenomenon called chromoplexy, which is characterized by the presence of chained translocations and interlinking deletion bridges in chromosomes.Steininger et al. have been new models for the molecular biology underlying tumorigenesis.They developed a technology for genome-wide identification of chromosomal translocations based on the analysis of translocation-associated changes in spatial proximities of chromosome territories.Using the sequence data from a cutaneous T-cell lymphoma for genome-wide chromosome conformation capture (Hi-C), they fine-mapped chromosomal breakpoints and correlated them with gene-associated biological processes like transcription.As identification and functional analysis of chromosomal aberrations are basic for cancer research, such genome-wide highresolution analyses of structural chromosomal aberrations will gain increasing importance.