L'AQUILA — Professor Anna Teti, from the University of L'Aquila and the National Council of Research, led a study on breast cancer cell dormancy. The findings were published online on May 14, 2026, in Volume 14 of Bone Research.

Breast cancer cells can transfer to the bone marrow and enter a dormant state for years or decades before causing a relapse. These cancer cells mimic properties of healthy stem cells to survive within protective bone marrow environments. "We discovered that breast cancer cells can exploit the same protective systems that normally maintain healthy stem cells in bone marrow," said Professor Anna Teti. "This allows cancer cells to remain hidden and potentially reactivate years later."

The research team investigated the signaling proteins Notch1 and Notch2 to understand the mechanism behind this dormancy. They found that Notch2 plays a dominant role in breast cancer cell dormancy, unlike Notch1 which does not exhibit similar dormant behavior. Breast cancer cells with high Notch2 levels divided more slowly when interacting with specialized osteoblasts located in the endosteal niche.

RNA sequencing further revealed that cells with high Notch2 expression displayed lower activity in genes associated with cell growth and division. Notch2-rich cells activated genes linked to hematopoietic stem cells, including CXCR4, CD34, and TIE2. Cells exhibiting high levels of CXCR4 or TIE2 formed fewer and smaller bone tumors in mice. "This was a particularly interesting finding because it suggests that cancer cells can acquire stem cell-like properties to evade treatment and survive in the body for very long periods," said Professor Anna Teti.

Additionally, cells with high Notch2 expression activated stress-response pathways known as the unfolded protein response. These cells showed elevated levels of molecules including PERK, ATF4, CHOP, and CD177. CD177-high cells specifically showed high Notch2 and CXCR4 expression, reduced cell proliferation, and were associated with improved patient survival outcomes. The study identifies Notch2, CXCR4, CD177, and stress-response pathways as key regulators of cellular dormancy.

No independent assessment of Professor Anna Teti’s claims was available.