# Whole-genome doubling (WGD)

Source: https://onco.cc/terms/whole-genome-doubling/  
OnCo record `whole-genome-doubling` (Term). Data CC BY-NC 4.0, attribute "Data from OnCo (onco.cc)"; commercial use needs a licence.

## TL;DR

Whole-genome doubling is a single event in which a cancer cell duplicates its entire genome, becoming tetraploid. It happens in about a third of cancers and buffers the chaos that follows.

## Summary

Whole-genome doubling (WGD) is a single event in which a cancer cell duplicates its entire genome and becomes tetraploid. It occurs in about a third of tumours, often early and with TP53 loss, and it buffers the chaos that follows: the doubled cell tolerates later chromosome loss and instability, evolves faster and carries a worse prognosis, as described in the Chromosomal instability & aneuploidy and p53 / RB / cell-cycle checkpoint pathways. WGD also creates dependencies on KIF18A and the spindle checkpoint that CIN-directed drugs are beginning to exploit, pursued in the idea Is aneuploidy itself a druggable vulnerability? Readers meet the term under Genome instability and mutation, in the TRACERx 100 and TRACERx 421 papers and in the spindle assembly checkpoint pathway.

## Fields

- Kind: Term
- Last checked: 2026-09-08

## Sources

- Wikipedia: https://en.wikipedia.org/wiki/Polyploidy
- Bielski et al., Genome doubling shapes the evolution and prognosis of advanced cancers (Nature Genetics 2018): https://doi.org/10.1038/s41588-018-0165-1

## Connected records

- targets: [TP53](https://onco.cc/targets/tp53/)
- pathways: [Chromosomal instability & aneuploidy](https://onco.cc/pathways/chromosomal-instability/), [Mitosis & the spindle assembly checkpoint](https://onco.cc/pathways/mitotic-spindle-checkpoint/), [p53 / RB / cell-cycle checkpoint](https://onco.cc/pathways/p53-cell-cycle/)
- terms: [Aneuploidy and chromosomal instability as the cause of cancer](https://onco.cc/terms/aneuploidy-theory-of-cancer/), [Enabling characteristic: genome instability and mutation](https://onco.cc/terms/genome-instability-mutation/), [KRAS allelic imbalance and mutant KRAS dosage in pancreatic cancer](https://onco.cc/terms/kras-allelic-imbalance/)
- key papers: [A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns](https://onco.cc/key-papers/paper-notta-punctuated-evolution-pancreatic-nature-2016/), [Genome doubling shapes the evolution and prognosis of advanced cancers](https://onco.cc/key-papers/paper-bielski-nat-genet/), [TRACERx 421: the full-cohort picture of how lung cancer evolves and which subclones drive relapse](https://onco.cc/key-papers/paper-tracerx-evolution-nature-2023/), [TRACERx first 100: tracking how lung cancers evolve, and how chromosomal chaos predicts relapse](https://onco.cc/key-papers/paper-tracerx-100-nejm-2017/), [Transcription phenotypes of pancreatic cancer are driven by genomic events during tumor evolution](https://onco.cc/key-papers/paper-chan-seng-yue-pancreatic-transcription-phenotypes-nat-genet-2020/)
- cancers: [Pancreatic ductal adenocarcinoma](https://onco.cc/cancers/pancreatic/)
- ideas: [Is aneuploidy itself a druggable vulnerability?](https://onco.cc/ideas/idea-targeting-aneuploidy/)

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