Breast cancer cells, when disseminated to other secondary organs such as the lungs, may stay in a dormant state for years, even decades. But the mechanisms that limit their expansion are not well understood. This is what researchers call a dormant mesenchymal-like phenotype (M-like) before metastasis to the lungs. Now, scientists have shown in a study published Oct. 7, 2024, in Cell, that the limiting of disseminated breast cancer cells (DCCs) to metastasize in the lungs is due to alveolar macrophages (AMs), which activate signals that make DCCs stay dormant.
Zymedi Co. Ltd. has disclosed lysyl-tRNA synthetase (KARS)/laminin receptor (LR) interaction inhibitors reported to be useful for the treatment of cancer metastasis, autoimmune disease, inflammatory disorders, fibrosis and cardiovascular disorders.
Researchers at Rockefeller University have identified a signaling loop between breast cancer cells and sensory neurons that promoted tumor metastasis, and showed that in animal models, treatment with the approved anti-nausea medication aprepitant could disrupt that loop.
Researchers from Northeast Normal University in Changchun demonstrated that compound AW-01178 reversed the abnormal regulation of E-cadherin by inhibiting the class I HDAC enzyme.
Not all cancer cells that detach from the primary tumor and embark on a journey to another organ colonize it. To establish themselves, cells need specific conditions. Scientists at the Federal Institute of Technology Zurich (ETH Zurich) explored this hypothesis in the liver and identified a protein involved in metastatic transformation. Blocking it prevented liver metastasis. Their findings may have applications in other organs and various types of cancers.
Breast cancer is the leading cancer malignancy in women and triple-negative breast cancer (TNBC) is among the most aggressive types as it is insensitive to endocrine and HER2-targeted therapy because it lacks all three hormonal receptors.
Previous studies have demonstrated that the natural product isotoosendanin (ITSN) inhibited triple-negative breast cancer (TNBC) metastasis by preventing epithelial-mesenchymal transition (EMT) and lamellipodia formation regulated by the TGF-β–Smad2/3 signaling pathway in TNBC cells through directly binding to TGF-β receptor type 1 (TGF-βR1).
Breast cancer is a common cause of brain metastases and new research has shown that metastatic cells can invade the meninges not by entering the circulation and crossing the blood-brain barrier, but by traveling along the outer surface of the blood vessels that connect the vertebral bone marrow and the skull.
RNA-binding proteins (RBPs) have emerged as interesting targets for cancer therapy. There is growing evidence that RBPs are dysregulated in cancer, usually with abnormal expression and/or with the presence of mutations.
