Is cancer returning to a unicellular past?
Some tumours express older evolutionary gene programmes more strongly and multicellular programmes less strongly. That observation is real; the proposed “atavism” explanation remains a contested research hypothesis.
Written retrospectively and published on August 3, 2026.
Background reading, not clinical guidance. This describes published research; it is not a recommendation for any individual case, and the cited studies may have been superseded.
Cancer is sometimes described as a return to an ancient, unicellular mode of life. The phrase comes from the atavism hypothesis: the idea that a tumour reactivates programmes that pre-date multicellular animals while losing programmes needed for tissue cooperation.
A 2017 analysis compared tumour and matched normal tissue across seven TCGA cohorts. Genes with very old evolutionary origins were more often up-regulated in the tumours, while genes that arose with animal multicellularity were more often down-regulated. The pattern is interesting, and the authors explicitly discussed it in atavism terms.
Why that is not a settled account of cancer
Old genes include much of the cell-cycle, DNA-replication and basic metabolic machinery. Genes associated with multicellularity include differentiation, adhesion and tissue signalling. Rapidly dividing, poorly differentiated cells can therefore show this pattern without literally retracing evolution.
Critical reviews also point to a methodological question: estimating the evolutionary age of genes is difficult, and different methods can change the apparent pattern. The careful conclusion is narrower than the headline: tumours often disrupt the balance between ancient core functions and multicellular tissue functions; why they do so remains open.
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