Plexins, cell-surface receptors for semaphorins, are involved in cell adhesion and migration. In the previous work, we demonstrated that the loss of Plexin B1 expression is associated with poor outcome in breast cancer patients. The goal of the present study was a validation of Plexin B1 expression in a large scale microarray dataset from n=1086 breast cancer patients. Plexin B1 correlates with ER status (p<0.001) and is of prognostic significance only in ER positive (p=0.024) but not in ER negative samples (p=0.85). Among ER positive tumours, the loss of Plexin B1 expression is associated with a positive ErbB2 status (p=0.05) and a high Ki67 expression (p=0.016) in univariate analysis. Multivariate Cox regression including all standard parameters among ER positive tumours revealed that Plexin B1 (HR 1.59, 95% confidence interval (CI) 1.03-2.47, p=0.036) remains a significant prognostic marker besides tumour size (HR 2.27, 95% CI 1.33-3.89, p=0.0028) and Ki67 (HR 1.78, 95% CI 1.12-2.84, p=0.0149). Interestingly, the prognostic value of Plexin B1 was pronounced in low proliferating ER positive tumours otherwise characterised by a low risk of recurrence. In conclusion, this study confirms our previous observations suggesting Plexin B1 as a new prognostic marker in ER positive breast cancers.
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http://dx.doi.org/10.1016/j.ejca.2008.10.016 | DOI Listing |
Ageing Res Rev
December 2024
Department of Life Sciences and Public Health, Section of Histology and Embryology, Università Cattolica del Sacro Cuore, Rome, Italy; Fondazione Policlinico Universitario A. Gemelli, Rome, Italy. Electronic address:
The central nervous system (CNS) is wired by a complex network of integrated glial and neuronal signals, which is critical for its development and homeostasis. In this context, glia-glia communication is a complex and dynamic process that is essential for ensuring optimal CNS function. Semaphorins, which include secreted and transmembrane molecules, and their receptors, mainly found in the plexin and neuropilin families, are expressed in a wide range of cell types, including glia.
View Article and Find Full Text PDFDev Cell
December 2024
Institute of Aging & Tissue Regeneration, Stress and Cancer Research Unit of Chinese Academy of Medical Sciences (No.2019RU043), State Key Laboratory of Systems Medicine for Cancer, Ren-Ji Hospital, Shanghai Jiao Tong University School of Medicine (SJTU-SM), Shanghai 200127, China; Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, SJTU-SM, Shanghai 200025, China. Electronic address:
Loss of phosphatase and tensin homolog (PTEN) has been linked to an immunosuppressive tumor microenvironment, but its underlying mechanisms remain largely enigmatic. Here, we report that PTEN can be secreted by the transmembrane emp24 domain-containing protein 10 (TMED10)-channeled protein secretion pathway. Inhibiting PTEN secretion from tumor cells contributes to immunosuppression and impairs the tumor-suppressive role of PTEN, while intratumoral injection of PTEN protein promotes antitumor immunity and suppresses tumor growth in mice.
View Article and Find Full Text PDFBMC Cancer
August 2024
School of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences & Medicine, King's College London, Room 2.34B, New Hunts House, London, SE1 1UL, UK.
Background: Metastatic prostate cancer is a leading cause of cancer-related morbidity and mortality in men, yet the underlying molecular mechanisms are poorly understood. Plexins are transmembrane receptors for semaphorins with divergent roles in many forms of cancer. We recently found that a single clinically relevant specific amino acid change (Proline1597Leucine, (P1597L)), found in metastatic deposits of prostate cancer patients, converts PlexinB1 from a metastasis suppressor to a gene that drives prostate cancer metastasis in vivo.
View Article and Find Full Text PDFCancer Immunol Res
September 2024
Laboratory of Tumor Microenvironment, Candiolo Cancer Institute, FPO-IRCCS, Candiolo, Italy.
J Med Genet
June 2024
Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), INSERM U1258, CNRS-UMR7104, Université de Strasbourg, Strasbourg, France.
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