The study, led by IRB Barcelona, shows that tumours with chromosomal instability can promote their own growth by damaging the surrounding healthy tissues.

Senescent tumour cells release signals that block the proliferation of neighbouring cells, ultimately inducing their death.

Published in EMBO Reports, the study identifies a new interaction mechanism between the tumour and its environment, which could open new avenues for researching targeted therapies against senescent cells.

BUFFALO, NY — June 4, 2026 — A new case report was published in Volume 13 of Oncoscience on April 2, 2026, titled “Sebaceous adenoma of the eyelid: A clinical, histopathological, and immunohistochemical perspective.”

Researchers at The University of Texas MD Anderson Cancer Center have discovered a molecular pathway that drives certain stressed or aging cells to become abnormally active, causing inflammation inside blood vessel plaques. This results in disturbed blood flow and high-risk lesions that can lead to blood clots that cause heart attacks or strokes.

Breast cancer can remain dormant in the bone marrow for decades before reactivating, resulting in cancer relapse. A study published in Bone Research unveils the critical role of Notch2 signaling pathway in promoting this dormant state. The study explains how dormant cancer cells mimic healthy stem cells and activate stress pathways to survive in the bone marrow—paving the way for innovative targeted therapies against dormant cancer cells.

DNA is the blueprint of the human body. However, tens of thousands of DNA lesions occur in our bodies every day. In particular, if “apurinic/apyrimidinic sites” (AP sites, damaged sites where one letter of DNA information has been erased) are not properly repaired, they can lead to cancer and aging. Finding these tiny damaged sites within the vast genome is as difficult as “finding a single needle in Seoul.” Korean researchers have uncovered the secret of how a DNA repair enzyme rapidly searches for damaged sites by sliding along DNA.