What's Happening?
Researchers from King's College London have discovered that sections of DNA, previously considered 'junk', could be used to fight drug-resistant blood cancers. These non-coding DNA segments, known as transposable
elements (TEs), can move within the genome and have been found to play roles in gene regulation. The study focused on two blood cancers, myelodysplastic syndrome and chronic lymphocytic leukemia, where mutations in genes ASXL1 and EXH2 lead to uncontrolled cell growth. The researchers found that these mutations cause TEs to reactivate, stressing cancer cells and making them reliant on PARP repair proteins. Drugs that inhibit PARPs were effective in killing the cancer cells while sparing healthy ones.
Why It's Important?
This discovery offers a new approach to treating hard-to-treat blood cancers by targeting the reactivated 'junk' DNA. The findings suggest that existing drugs could be repurposed to exploit this vulnerability in cancer cells, potentially leading to more effective treatments with fewer side effects. The research highlights the importance of non-coding DNA in disease development and opens new avenues for cancer therapy. The use of PARP inhibitors, already employed in other cancer treatments, could be expanded to include these blood cancers, providing new hope for patients.
What's Next?
Further research is needed to validate these findings in clinical settings and explore their applicability to other cancer types. The study sets the stage for developing new therapeutic strategies that leverage the reactivation of TEs to induce synthetic lethality in cancer cells. Researchers will likely investigate the broader implications of these findings for other cancers and refine the use of PARP inhibitors in treatment protocols.
