A new driver of breast cancer emerges from the nucleus
A study published in *Cell Death & Disease* identifies LAP2α as a novel oncogenic driver in breast tumorigenesis. The research demonstrates that this nuclear protein promotes cancer development by mitigating replication stress, a key source of genomic instability in rapidly dividing tumor cells. By helping cancer cells cope with this internal pressure during DNA duplication, LAP2α enables tumor progression and survival, highlighting a previously underappreciated mechanism in cancer biology.
Why it might matter to you: This finding pinpoints a new potential target within the DNA damage response and replication stress pathways, areas of intense interest for precision oncology. For professionals focused on cancer genomics and targeted therapy, understanding LAP2α’s role could inform strategies to exploit replication stress as an Achilles’ heel in breast cancer and other malignancies. It underscores the ongoing need to map the full landscape of driver mutations and oncogenic signaling pathways that fuel tumorigenesis.
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