Background: Male breast cancer (MBC) is a rare and aggressive disease. Thus, identification of new therapeutic targets is crucial.
Objective: Our objective was to evaluate the protein expression of MARCKS (Myristoylated Alanine-Rich C-Kinase Substrate) in MBC and to investigate its prognostic value.
Materials And Methods: MARCKS protein expression in tumor and stromal cells was analyzed by immunohistochemistry (IHC) in a retrospective series of 96 pre-chemotherapy MBC samples and 80 normal breast samples, from Tunisian patients treated at Salah Azaiez Institute. Correlations were searched between MARCKS expression and clinicopathological features including overall survival (OS).
Results: MARCKS was overexpressed in epithelial tumor cells in 66% of the MBC samples versus 26% of normal samples (p= 1.40 × 10-7). Such positive MARCKS expression in epithelial tumor cells was associated with positive HER2 status (p= 4.0 × 10-3). It was associated with shorter OS in uni-and multivariate analysis. By contrast, stromal IHC MARCKS expression was correlated only with tumor grade.
Conclusion: MARCKS tumor cell overexpression might in part explain the aggressiveness and the poor prognosis of MBC. MARCKS can represent a potential therapeutic target for MBC.
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http://dx.doi.org/10.3233/CBM-190637 | DOI Listing |
Front Biosci (Landmark Ed)
November 2024
Department of General Surgery, The First Affiliated Hospital of Anhui Medical University, 230022 Hefei, Anhui, China.
Background: Aneuploidy is crucial yet under-explored in cancer pathogenesis. Specifically, the involvement of brain expressed X-linked gene 4 () in microtubule formation has been identified as a potential aneuploidy mechanism. Nevertheless, 's comprehensive impact on aneuploidy incidence across different cancer types remains unexplored.
View Article and Find Full Text PDFCell Death Dis
December 2024
Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Regeneration of injured central nervous system (CNS) axons is highly restricted, leading to permanent neurological deficits. The myristoylated alanine-rich C-kinase substrate (MARCKS) is a membrane-associated protein kinase C (PKC) substrate ubiquitously expressed in eukaryotic cells, plays critical roles in development, brain plasticity, and tissues regeneration. However, little is known about the role of Marcks in CNS axon regeneration.
View Article and Find Full Text PDFIn vascular smooth muscle cells (VSMCs) and vascular endothelial cells (VECs), phosphatidylinositol 4,5-bisphosphate (PIP) acts as a substrate for phospholipase C (PLC)- and phosphoinositol 3-kinase (PI3K)-mediated signaling pathways and an unmodified ligand at ion channels and other macromolecules, which are key processes in the regulation of cell physiological and pathological phenotypes. It is envisaged that these distinct roles of PIP are achieved by PIP-binding proteins, which act as PIP buffers to produce discrete pools of PIP that permits targeted release within the cell. This review discusses evidence for the expression, cell distribution, and role of myristoylated alanine-rich C-kinase substrate (MARCKS), a PIP-binding protein, in cellular signaling and function of VSMCs.
View Article and Find Full Text PDFCells
November 2024
Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea.
J Thorac Dis
November 2024
Department of Thoracic Surgery, Sichuan Clinical Research Center for Cancer, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, Affiliated Cancer Hospital of University of Electronic Science and Technology of China, Chengdu, China.
Background: Traditional diagnostic methods have limited efficacy in predicting the prognosis of lung adenocarcinoma (LUAD), T cell immunoreceptor with immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) is a new biomarker. This study aimed to evaluate TIGIT expression as a LUAD biomarker and predict patient prognosis using a pathological feature model.
Methods: Clinical data and pathological images from The Cancer Genome Atlas (TCGA) were analyzed.
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