Literature DB >> 17879119

Epithelial-mesenchymal transition (EMT) and activated extracellular signal-regulated kinase (p-Erk) in surgically resected pancreatic cancer.

M M Javle1, J F Gibbs, K K Iwata, Y Pak, P Rutledge, J Yu, J D Black, D Tan, T Khoury.   

Abstract

BACKGROUND: EMT or transformation to the mesenchymal phenotype plays an important role in tumor invasion and metastasis. In vitro data suggest that mesenchymal transformation may correlate with the activation of PI3 kinase and Ras/Erk pathways. We investigated the expression of EMT markers (low E-cadherin, high fibronectin, and vimentin) and their association with p-Erk in resected pancreatic cancer.
METHODS: Clinical data/surgical specimens from 34 consecutive pancreatic cancer patients (pts) who underwent pancreatectomy were included. Immunohistochemical staining was performed on formalin-fixed paraffin-embedded tissues using monoclonal antibodies against vimentin, fibronectin, E-cadherin, and p-Erk. The results were correlated with clinicopathological parameters and survival. Survival analysis (log-rank test, Cox proportional hazard model), categorical data analysis (Pearson's chi-square, Fisher's exact test) and Kendall's tau were performed at a significance level of 0.05.
RESULTS: The patient population was formed from 13 males and 21 females, with a median age of 66 years (range 38-84 years); American Joint Committee on Cancer (AJCC) stage 1 (n = 2), 2 (n = 27), 3 (n = 5); histological grade 1 (n = 4), 2 (n = 13), 3 (n = 16), 4 (n = 1). Median survival was 15 months (95% CI: 11-24 months). Fibronectin overexpression correlated with the presence of vimentin (p = 0.0048) and activated Erk (p = 0.0264). There was a borderline association of fibronectin with worsening grade (p = 0.06). A negative association between vimentin and E-cadherin was noted (p = 0.0024). Increased fibronectin or vimentin and decreased E-cadherin correlated with poor survival.
CONCLUSION: EMT is associated with poor survival in surgically resected pancreatic adenocarcinoma. A correlation between activated Erk and fibronectin was identified that may open avenues for targeted therapy for this subgroup.

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Year:  2007        PMID: 17879119     DOI: 10.1245/s10434-007-9540-3

Source DB:  PubMed          Journal:  Ann Surg Oncol        ISSN: 1068-9265            Impact factor:   5.344


  80 in total

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Review 3.  Translational research in pancreatic ductal adenocarcinoma: current evidence and future concepts.

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4.  Protein kinase Ciota is required for pancreatic cancer cell transformed growth and tumorigenesis.

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Review 5.  Pancreatic cancer stem cells: emerging target for designing novel therapy.

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7.  Inhibition of S-Adenosylmethionine-Dependent Methyltransferase Attenuates TGFβ1-Induced EMT and Metastasis in Pancreatic Cancer: Putative Roles of miR-663a and miR-4787-5p.

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8.  Glycogene expression alterations associated with pancreatic cancer epithelial-mesenchymal transition in complementary model systems.

Authors:  Kevin A Maupin; Arkadeep Sinha; Emily Eugster; Jeremy Miller; Julianna Ross; Vincent Paulino; Venkateshwar G Keshamouni; Nhan Tran; Michael Berens; Craig Webb; Brian B Haab
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9.  Overexpression of p42.3 promotes cell proliferation, migration, and invasion in human gastric cancer cells.

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Journal:  Tumour Biol       Date:  2016-07-23

Review 10.  Key players in pancreatic cancer-stroma interaction: Cancer-associated fibroblasts, endothelial and inflammatory cells.

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