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Topics {✒️}

hrp-conjugated rabbit/mouse anti-igg wnt/β-catenin/tcf survival pathways wnt/β-catenin pathway- e-cadherin wnt/β-catenin signaling upregulation canonical wnt/β-catenin pathway active wnt/β-catenin pathway active wnt/β-catenin signaling wnt/β-catenin signaling pathway e-cadherin-β-catenin complexes open access article wnt/β-catenin pathway activation 1309/fdhx-l92r-batq-2ge0 regulating cell-cell adhesion β-catenin mediated pathway stabilized β-catenin enters epithelial mesenchymal transition epithelial-mesenchymal transition wnt/β-catenin signaling [17 wnt/β-catenin signaling tumour necrosis factor-alpha cell surface β-catenin wnt/beta-catenin pathway article download pdf antibody-based therapies targeting central transcription mediator β-catenin mediated regulation pre-publication history glycogen synthase kinase-3 anti-e-cadherin antibody related subjects enhanced chemiluminescence system invasive ductal carcinoma similar e-cadherin loss e-cadherin membrane loss epithelial-mesenchymal transitions e-cadherin/catenin complex completely e-cadherin-negative [9–12] cd44+/cd24- cells e-cadherin immunostaining examined full size image e-cadherin monoclonal antibody e-cadherin membranous localization normal breast tissue invasive lobular carcinomas e-cadherin immunohistochemical expression infiltrating ductal carcinoma membranous e-cadherin expression canonical wnt signaling tcf/lef transcription factors e-cadherin promoter methylation

Schema {🗺️}

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         headline:Expression analysis of E-cadherin, Slug and GSK3β in invasive ductal carcinoma of breast
         description:Cancer progression is linked to a partially dedifferentiated epithelial cell phenotype. The signaling pathways Wnt, Hedgehog, TGF-β and Notch have been implicated in experimental and developmental epithelial mesenchymal transition (EMT). Recent findings from our laboratory confirm that active Wnt/β-catenin signaling is critically involved in invasive ductal carcinomas (IDCs) of breast. In the current study, we analyzed the expression patterns and relationships between the key Wnt/β-catenin signaling components- E-cadherin, Slug and GSK3β in IDCs of breast. Of the 98 IDCs analyzed, 53 (54%) showed loss/or reduced membranous staining of E-cadherin in tumor cells. Nuclear accumulation of Slug was observed in 33 (34%) IDCs examined. Loss or reduced level of cytoplasmic GSK3β expression was observed in 52/98 (53%) cases; while 34/98 (35%) tumors showed nuclear accumulation of GSK3β. Statistical analysis revealed associations of nuclear Slug expression with loss of membranous E-cadherin (p = 0.001); nuclear β-catenin (p = 0.001), and cytoplasmic β-catenin (p = 0.005), suggesting Slug mediated E-cadherin suppression via the activation of Wnt/β-catenin signaling pathway in IDCs. Our study also demonstrated significant correlation between GSK3β nuclear localization and tumor grade (p = 0.02), suggesting its association with tumor progression. The present study for the first time provided the clinical evidence in support of Wnt/β-catenin signaling upregulation in IDCs and key components of this pathway - E-cadherin, Slug and GSK3β with β-catenin in implementing EMT in these cells.
         datePublished:2009-09-14T00:00:00Z
         dateModified:2009-09-14T00:00:00Z
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            Epithelial Mesenchymal Transition
            Invasive Ductal Carcinoma
            Normal Breast Tissue
            Invasive Lobular Carcinoma
            Nuclear Accumulation
            Cancer Research
            Oncology
            Surgical Oncology
            Health Promotion and Disease Prevention
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      headline:Expression analysis of E-cadherin, Slug and GSK3β in invasive ductal carcinoma of breast
      description:Cancer progression is linked to a partially dedifferentiated epithelial cell phenotype. The signaling pathways Wnt, Hedgehog, TGF-β and Notch have been implicated in experimental and developmental epithelial mesenchymal transition (EMT). Recent findings from our laboratory confirm that active Wnt/β-catenin signaling is critically involved in invasive ductal carcinomas (IDCs) of breast. In the current study, we analyzed the expression patterns and relationships between the key Wnt/β-catenin signaling components- E-cadherin, Slug and GSK3β in IDCs of breast. Of the 98 IDCs analyzed, 53 (54%) showed loss/or reduced membranous staining of E-cadherin in tumor cells. Nuclear accumulation of Slug was observed in 33 (34%) IDCs examined. Loss or reduced level of cytoplasmic GSK3β expression was observed in 52/98 (53%) cases; while 34/98 (35%) tumors showed nuclear accumulation of GSK3β. Statistical analysis revealed associations of nuclear Slug expression with loss of membranous E-cadherin (p = 0.001); nuclear β-catenin (p = 0.001), and cytoplasmic β-catenin (p = 0.005), suggesting Slug mediated E-cadherin suppression via the activation of Wnt/β-catenin signaling pathway in IDCs. Our study also demonstrated significant correlation between GSK3β nuclear localization and tumor grade (p = 0.02), suggesting its association with tumor progression. The present study for the first time provided the clinical evidence in support of Wnt/β-catenin signaling upregulation in IDCs and key components of this pathway - E-cadherin, Slug and GSK3β with β-catenin in implementing EMT in these cells.
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      dateModified:2009-09-14T00:00:00Z
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         Epithelial Mesenchymal Transition
         Invasive Ductal Carcinoma
         Normal Breast Tissue
         Invasive Lobular Carcinoma
         Nuclear Accumulation
         Cancer Research
         Oncology
         Surgical Oncology
         Health Promotion and Disease Prevention
         Biomedicine
         general
         Medicine/Public Health
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      name:Department of Anatomy, Vardhman Mahavir Medical College and Safdarjung Hospital, New Delhi, India
      name:Department of Pathology, All India Institute of Medical Sciences, New Delhi, India
      name:Department of Surgery, Vardhman Mahavir Medical College and Safdarjung Hospital, New Dehi, India
      name:Department of Surgery, All India Institute of Medical Sciences, New Delhi, India
      name:Department of Biochemistry, All India Institute of Medical Sciences, New Delhi, India
      name:Sonshine Family Centre for Head & Neck Disease, Mount Sinai Hospital, Toronto, Canada
      name:Department of Otolaryngology-Head and Neck Surgery, Mount Sinai Hospital, Toronto, Canada
      name:Department of Pathology and Laboratory Medicine, Mount Sinai Hospital, Toronto, Canada
      name:Department of Otolaryngology-Head and Neck Surgery, University of Toronto, Toronto, Canada

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