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Y. Ohtaki



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    P3.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 235)

    • Event: WCLC 2015
    • Type: Poster
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 1
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      P3.04-101 - Expression of the Endoplasmic Reticulum Stress Sensor BiP/GRP78 in Lung Adenocarcinoma: Correlations and Prognostic Significance (ID 2271)

      09:30 - 09:30  |  Author(s): Y. Ohtaki

      • Abstract
      • Slides

      Background:
      Endoplasmic Reticulum (ER) Stress Sensor, BiP/glucose-related protein 78 (GRP78) is an important member of the heat shock protein family 70 (HSPs70) that plays an essential role in the tumor growth and progression. It is localized to the endoplasmic reticulum. Although GRP78/BiP is highly expressed in various cancer cells, the clinicopathological significance of its expression in non-small cell lung cancer (NSCLC) remains unclear. The aim of the present study was to investigate the expression of the GRP78/BiP in patients with lung adenocarcinoma.

      Methods:
      Two hundred and twenty patients with surgically resected lung adenocarcinoma were evaluated as one institutional cohort. Tumor sections were stained by immunohistochemistry for GRP78/BiP, PERK, Ki-67, p-mTOR, and CD34 to assess the microvessel density. The correlation between GRP78/BiP and the other factors was assessed using the Spearman correlation analysis.

      Results:
      GRP78/BiP was highly expressed in 41% of patients, and was significantly associated with pleural invasion, lymphatic permeation, vascular invasion, cell proliferation, and p-mTOR phosphorylation. Multivaritate analysis confirmed that GRP78/BiP expression was an independent factor for predicting poor progression-free survival and overall survival in patients with stage I disease.

      Conclusion:
      The increased GRP78/BiP expression is an independent prognostic factor for early stage lung adenocarcinoma patients. Our study suggests that the expression of GRP78/BiP as ER stress marker plays a crucial role in the pathogenesis and development of lung adenocarcinoma.

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