Why Cancer Drugs Leave the Same Mark on DNA ✎ bioRxiv

Original: "Chromosomal mutational signatures of DNA damaging agents at single cell resolution"
b42w:2609.90045 · the paper's page · 2026-09-07 · All rights reserved · independent analysis · 1 min
Different drugs that damage DNA leave the same large mark in cells, right at the ends of chromosomes, and that mark can be measured.

Chromosomes inside a cell are like long strings of beads, and cancer drugs act like scissors that cut those strings. Until now it was hard to see exactly where the cut landed, because the damage is scattered across a multitude of cells. Now scientists have come up with a way to do it: they read the DNA of each cell separately and compare how the ends of chromosomes changed after the drug.

Five different drugs, even though they cut DNA in different ways, leave the same mark: large losses of pieces right at the very ends of chromosomes. Scientists called this a telomere-restricted signature.

This mark persists in cells for up to eight weeks after the drug is removed. And if a tumor becomes resistant to treatment, the mark disappears. That means the mark can tell you whether a drug is working. Today this approach can already be used in labs to test new compounds and monitor treatment.

Telomere-bounded events arise within 2.5 megabases of the chromosome end, but short reads cannot resolve the telomeric repeats themselves, so the authors call them "telomere-bounded" rather than "telomeric."

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Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.

Concepts
dna damage dna repair mutation telomere