CDI scientists identify key dynamic to boost cancer treatments while limiting stem cell transplant rejection
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Updates every hour. Last Updated: 23-Jun-2026 01:16 ET (23-Jun-2026 05:16 GMT/UTC)
Researchers revealed how zinc levels control the endoplasmic reticulum (ER), the cell’s primary protein factory, and how it fundamentally regulates cellular proteostasis. Using fluorescent probes, they found that the transporter ZIP7 keeps zinc levels in the ER low. When ZIP7 is disrupted, zinc level surges, inhibiting the enzyme Ero1 and disrupting the cell’s redox balance. This prevents proteins from folding correctly, leading to an array of pathologies including cancer.
Shi Yuankai’s team’s review on EGFR-TKIs for NSCLC (2000–2026) came out in the Chinese Medical Journal. Lung cancer leads in global cancer incidence/mortality, with NSCLC as the main subtype and EGFR a key driver. EGFR-TKIs are core for advanced EGFR-mutant NSCLC, with expanded clinical applications and prolonged patient survival. Yet EGFR-TKI resistance is a big challenge; the review summarizes its 2000–2025 development and future directions.
Researchers at Mass General Brigham behind FaceAge, an AI tool that estimates biological age from facial photographs, found that tracking changes in FaceAge over time provides added insight into cancer prognosis. In a study of more than 2,200 patients, a faster Face Aging Rate (FAR) was strongly associated with worse survival, supporting its potential as a non‑invasive biomarker to inform treatment planning and follow‑up.
The finding explains how the absence of a key protein in the structure of bile ducts promotes the onset of fibrosis.
If bile ducts let bile acids leak through, these will cause damage that liver tissue repairs by producing scars. The accumulation of these scars leads to fibrosis.
For the study’s authors, "this finding allows research to be steered towards safer therapies targeting liver fibrosis."
The paper is published in Nature Metabolism.
A study published in Science Bulletin identifies tRF-Glu-TTC-013, a tRNA-derived fragment, as a key driver of colorectal cancer liver metastasis. The researchers found that the molecule promotes tumour progression by enhancing glutamate metabolic reprogramming through a newly defined CREB3L1–AMDHD1 pathway.
Cancer treatment and other delicate medical procedures could one day be carried out using tiny microrobots guided precisely inside the body after scientists developed a new magnetic tool to control them.
Scientists have uncovered an unexpected way cells can generate cancer-driving proteins—by cutting RNA into shorter, functional fragments rather than following the standard blueprint. This process, newly termed as “RNA dicing,” enables the production of a truncated form of the JAK1 protein that remains highly active and can promote tumor growth, particularly when normal gene function is disrupted. The finding challenges conventional views of how genetic information is translated and points to a previously unrecognized mechanism that could influence cancer progression and response to targeted therapies.