This scientific commentary refers to ‘MCAM brain endothelial cells contribute to neuroinflammation by recruiting pathogenic CD4 T lymphocytes’ by Charabati . (https://doi.org/10.1093/brain/awac389).
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10115349 | PMC |
http://dx.doi.org/10.1093/brain/awad079 | DOI Listing |
Biology (Basel)
December 2024
Department of Medical Biology, Faculty of Medicine, Recep Tayyip Erdogan University, 53100 Rize, Turkey.
HER2-positive breast cancer has an aggressive tumour progression among breast cancers characterized by the overexpression of HER2. Trastuzumab is an FDA-approved drug and has significantly improved outcomes for patients; however, drug resistance remains a major challenge. Tumour heterogeneity, describing genetic, epigenetic, and phenotypic differences within and between tumours, complicates tumour treatment and contributes to drug resistance.
View Article and Find Full Text PDFMol Ther Oncol
December 2024
Department of Pediatrics, New York Medical College, Valhalla, NY 10595, USA.
Pediatric patients with recurrent metastatic neuroblastoma (NB) have a dismal 5-year survival. Novel therapeutic approaches are urgently needed. The melanoma cell adhesion molecule (MCAM/CD146/MUC18) is expressed in a variety of pediatric solid tumors, including NB, and constitutes a novel target for immunotherapy.
View Article and Find Full Text PDFSci Rep
October 2024
Oncoinvent ASA, 0484, Oslo, Norway.
Malignant mesothelioma, a highly aggressive cancer that primarily affects the serosal membranes, has limited therapeutic options, particularly for cavitary tumors, such as peritoneal and pleural malignant mesothelioma. Intracavitary administration of a radioimmunoconjugate to locally target mesothelioma cancer cells has been proposed as a treatment. CD146, upregulated in mesothelioma but not in healthy tissues, is a promising therapeutic target.
View Article and Find Full Text PDFBiomarkers
November 2024
Department of Biochemistry, School of Life Sciences, University of Sussex, Brighton, UK.
NPJ Breast Cancer
September 2024
Huntsman Cancer Institute, University of Utah, Salt Lake City, UT, 84112, USA.
Cell state control is crucial for normal tissue development and cancer cell mimicry of stem/progenitor states, contributing to tumor heterogeneity, therapy resistance, and progression. Here, we demonstrate that the cell surface glycoprotein Mcam maintains the tumorigenic luminal progenitor (LP)-like epithelial cell state, leading to Basal-like mammary cancers. In the Py230 mouse mammary carcinoma model, Mcam knockdown (KD) destabilized the LP state by deregulating the Ck2/Stat3 axis, causing a switch to alveolar and basal states, loss of an estrogen-sensing subpopulation, and resistance to tamoxifen-an effect reversed by Ck2 and Stat3 inhibitors.
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