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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.
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.
In plain words · TP53 is the 'guardian of the genome', broken in half of all cancers. Fixing it directly has so far defeated every attempt, so drugs exploit what its loss makes cancers depend on.
Showing the target this term concerns: TP53.
Relapse after surgery is driven by particular subclones that can be identified in the primary tumour and tracked in blood, which argues for evolution-aware adjuvant strategies. The pollution finding reframes carcinogenesis: some agents promote already-mutant cells rather than causing mutations.
It explains why single-sample classifiers disagree on about one tumour in eight and why KRAS allelic imbalance and GATA6 copy number are being read alongside expression.
One term page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
Lung cancers keep evolving after they form, and it is ongoing chromosomal instability rather than the number of mutations that best predicts who will relapse. This gives a rationale for targeting the earliest (clonal) drivers and neoantigens and for tracking evolution in blood after surgery.
The textbook PanIN-to-cancer ladder is only part of the story, and a screening programme cannot assume years of orderly progression in every patient.
Shares KRAS allelic imbalance and mutant KRAS dosage in pancreatic cancer, Transcription phenotypes of pancreatic cancer are driven by genomic events during tumor evolution, Pancreatic ductal adenocarcinoma.
Shares KRAS allelic imbalance and mutant KRAS dosage in pancreatic cancer, Transcription phenotypes of pancreatic cancer are driven by genomic events during tumor evolution, Pancreatic ductal adenocarcinoma.
Shares p53 / RB / cell-cycle checkpoint, TP53.
Shares KRAS allelic imbalance and mutant KRAS dosage in pancreatic cancer, Transcription phenotypes of pancreatic cancer are driven by genomic events during tumor evolution, Pancreatic ductal adenocarcinoma.
Shares TRACERx 421: the full-cohort picture of how lung cancer evolves and which subclones drive relapse, Aneuploidy and chromosomal instability as the cause of cancer, TRACERx first 100: tracking how lung cancers evolve, and how chromosomal chaos predicts relapse.
Shares A renewed model of pancreatic cancer evolution based on genomic rearrangement patterns, Transcription phenotypes of pancreatic cancer are driven by genomic events during tumor evolution, Pancreatic ductal adenocarcinoma.
Shares KRAS allelic imbalance and mutant KRAS dosage in pancreatic cancer, TP53, Pancreatic ductal adenocarcinoma.
Shares Is aneuploidy itself a druggable vulnerability?, Aneuploidy and chromosomal instability as the cause of cancer, Chromosomal instability & aneuploidy.