PERSPECTIVE article
Front. Epigenet. Epigenom.
Sec. Chromatin Epigenomics
Volume 3 - 2025 | doi: 10.3389/freae.2025.1607433
This article is part of the Research TopicEpigenetic Trailblazers: Pioneers and Perspectives in Cellular Memory and DifferentiationView all articles
Hansemann's anaplastic theory of cancer after 135 years
Provisionally accepted
Steven Henikoff1,2*
Kami Ahmad1- 1Fred Hutchinson Cancer Center, Seattle, United States
- 2Howard Hughes Medical Institute (HHMI), Chevy Chase, Maryland, United States
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The term “anaplasia” was coined in 1890 to describe chromosomal changes common to primordial cancer cells, but ever since the mechanisms whereby a cell becomes anaplastic has been the subject of much speculation. Recent results based on genomic and epigenomic profiles of cancer patient samples provide a glimpse into early events that lead to aneuploidy, the original defining feature of an anaplastic cell. We propose that the anaplastic cell is one in which RNA Polymerase II hypertranscribes S-phase-dependent histone genes, and the resulting histone excess facilitates DNA replication while competing for CENP-A, causing centromere breaks that initiate whole-arm aneuploidy.
Keywords: chromosome, Centromere, Anaplasia, Aneuploidy, Histones, CENP-A
Received: 07 Apr 2025; Accepted: 24 Apr 2025.
Copyright: © 2025 Henikoff and Ahmad. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Steven Henikoff, Fred Hutchinson Cancer Center, Seattle, United States
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