Researchers at King’s College London report that transposable elements (TEs), long‑dismissed "junk" DNA, can be reactivated in blood cancers with ASXL1 or EZH2 mutations. Reactivated TEs spread through cancer genomes and create stress that makes tumour cells reliant on PARP DNA‑repair enzymes. In mouse models and human cell lines, PARP inhibitors selectively killed myelodysplastic syndrome and chronic lymphocytic leukemia cells, suggesting a possible new treatment strategy pending clinical validation.
‘Junk’ DNA Recruited to Kill Cancer Cells: Reactivated Transposable Elements Expose Tumours to PARP Inhibitors
Researchers at King’s College London report that transposable elements (TEs), long‑dismissed "junk" DNA, can be reactivated in blood cancers with ASXL1 or EZH2 mutations. Reactivated TEs spread through cancer genomes and create stress that makes tumour cells reliant on PARP DNA‑repair enzymes. In mouse models and human cell lines, PARP inhibitors selectively killed myelodysplastic syndrome and chronic lymphocytic leukemia cells, suggesting a possible new treatment strategy pending clinical validation.
12:07, 03.11.2025Health
New research from King's College London suggests that sequences of non‑coding “junk” DNA can be reactivated in certain blood cancers and used against the cancer from within.
What the study found
Regions of the genome long labelled as "junk" do not code for proteins but can still influence cellular behavior. One such class, transposable elements (TEs), can move or copy themselves to new genomic locations. The international team led by King's College London reports that in some blood cancers, mutations in genes such as ASXL1 and EZH2 are associated with the reactivation and spread of TEs across cancer genomes.
Why that matters
Widespread TE activity creates genomic stress in malignant cells. To tolerate this stress and keep proliferating, the cancer cells become dependent on DNA‑repair enzymes called poly (ADP‑ribose) polymerases (PARPs). In mouse models and human cancer cell lines, the researchers showed that inhibiting PARP activity selectively killed cells from two blood cancers — myelodysplastic syndromes (MDS) and chronic lymphocytic leukemia (CLL) — while largely sparing healthy cells.
“This discovery offers new hope for patients with hard‑to‑treat cancers, by using existing drugs in a completely new way, turning what was once thought to be useless DNA into a powerful target for treatment,” says Chi Wai Eric So, KCL.
Implications and caveats
The study supports a form of synthetic lethality: exploiting a cancer’s new vulnerabilities (TE reactivation and PARP dependency) to selectively kill tumour cells. PARP inhibitors are already approved for some cancers, which may speed translation. However, these results are based on laboratory and mouse experiments; further clinical studies are needed to confirm safety and efficacy in patients and to identify which mutation profiles predict benefit.
Broader context
Transposable elements make up a large portion of the human genome and are increasingly recognised as regulators rather than inert junk. Recent work implicates TEs in immune regulation, neural function, and species barriers — and now potentially as a therapeutic vulnerability in cancer.
The study is published in the journal Blood.