Tumors of epithelial origin, i.e., carcinomas, are defined by aneuploidy, chromosomal instability, and intratumor heterogeneity (ITH). These characteristics, which are commonly, but incorrectly, interpreted as a chromosomal chaos, result in patterns of genomic imbalances that are maintained during cancer progression and are specific for different tumor entities. For instance, almost all cervical carcinomas have extra copies of the long arm of chromosome 3, and the majority of aneuploid colorectal carcinomas have gains of chromosomes and chromosome arms 7, 8q, 13, 20q and losses of 17p and 18q1. Conserved genomic imbalances occur in premalignant lesions, are maintained throughout tumor progression, in metastases, and in cell lines derived from primary tumors. They are invariably associated with disease progression and must therefore be considered drivers and hallmarks of tumorigenesis2. A systematic understanding of the biology of carcinomas requires analyzing how these genomic imbalances affect the higher order structure of the interphase nucleus and, with that, the transcriptional equilibrium of cancer cells.
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