The three‐dimensional cancer nucleus

Abstract

Research into the three‐dimensional (3D) organization of the cancer cell genome started over 100 years ago. We follow an exciting avenue of research in this field, from Hansemann's early observations of aberrant mitoses and nuclei in cancer cells in the late 19th century to Boveri's theory of the cancer cell in the early 20th century, to current views of nuclear organization and its changes in cancer. Molecular and imaging methods go hand in hand with providing us with a better understanding of the spatial nature of the cancer cell genome. This has led to the concept that the structural order of the nucleus can be used as cancer cell biomarker.

Depletion of Trichoplein (TpMs) Causes Chromosome Mis-Segregation, DNA Damage and Chromosome Instability in Cancer Cells

“…In this scenario, the telomeres may have been critically shortened and/or uncapped, which enables end-to-end telomeric fusions that may happen between non-homologous or homologous chromosome pairs. End-to-end fusion chromosomes lead to breakage-fusion-bridge (B/F/B) cycles that increase the genetic diversity between tumor cells [28,29].…”

The mouse HP1 proteins are essential for preventing liver tumorigenesis

“…Chromatin dynamic organization is essential for the interpretation of genetic information 39 in a cell-type and tissue-specific manner (Prakash and Fournier, 2018). Alteration of this 40 organization can have devastating consequences, as evidenced by the large number of 41 diseases induced by mutations in chromatin-associated proteins (Koschmann et al, 2017;42 Mirabella et al, 2016), as well as by the dramatic changes in chromatin organization 43 observed in cancer cells (Mai, 2018). Although extensively studied in the past three decades, 44 it is still largely unknown how chromatin organization is regulated and involved in whole 45 organism homeostasis.…”

Assessment of the Utility of Gene Positioning Biomarkers in the Stratification of Prostate Cancers

“…We hypothesized that heterogeneity within a cancer type may reflect the 516 aggressiveness of a cancer and therefore be of prognostic value. Prognosis-related repositioning of 517 genomic regions in several types of cancer has previously been reported, with increased clustering of 518 telomeres linked to poorer patient outcomes (Mai, 2018). For example, at the time of diagnosis 519 telomeres were more likely to cluster in Hodgkin lymphoma patients whose disease later relapsed or 520 progressed compared to patients who responded well to treatment (Knecht et al, 2012).…”