Author of

• 18272

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  P3.01 - Poster Session with Presenters Present (ID 469)

  • Event: WCLC 2016
  • Type: Poster Presenters Present
  • Track: Biology/Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 12/07/2016, 14:30 - 15:45, Hall B (Poster Area)

  • 18320

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    P3.01-048 - Cigarette Smoking is Associated with Epithelio-Mesenchymal Transition in Human Adenocarcinoma (ID 5531)

    14:30 - 14:30  |  Author(s): R. Miyata
    • Abstract

    Background:
    Cigarette smoking (CS) is well known to cause lung cancer. In addition to the mechanisms of tumorigenesis of lung cancer with CS, a lot of evidences are currently accumulating that CS induces epithelio-mesenchymal transition (EMT) in tumor cells. The correlation of CS with the malignant properties of lung cancer remained elusive in clinical settings. Here we examined the clinical significance of CS with regard to EMT and malignant progression in human lung adenocarcinoma.
    
    Methods:
    Clinical samples were obtained from the 239 cases of resected lung adenocarcinoma which were consecutively operated from January 2001 to December 2007 in our institution. Pathological stage distribution of the cases by TNM classification (WHO, 7th edition) was below: 1A: 118, 1B: 71, 2A: 22, 2B: 4, 3A: 23, 3B: 1. Smoking history was taken from all the patients, then their smoking status were classified into 3 groups according to the Brinkman Index (Non;0, n=109: Light;1~400, n=29: Heavy;401~, n=101). The samples were immunostained against E-cadherin and Vimentin using tissue microarrays of resected specimens to assess the activation level of EMT. Then, we classified into 3 groups: the group ‘N’, E-cadherin(E+) and Vimentin(V-), “null” EMT activation; the group ‘F’, E-/V+, ‘full’ EMT; the group ‘P’, E-/V- or E+/V+, ‘partial’ EMT. The numbers of the group F/ P/ N were 38/ 93/ 108, respectively. Furthermore, DNA samples were extracted from frozen surgical samples and the mutations for the hot-spot exons of EGFR, K-ras, and p53 were detected by SSCP or direct sequencing methods. The differences of survival duration, pathological invasive factors, DNA mutations and EMT activation level were statistically analysed among smoking groups.
    
    Results:
    Significant difference was found in 5-year survival rate among 3 smoking groups: Non, 89.1%; Light, 89.5%; Heavy, 61.7%. Smoking status was significantly associated with EMT activation, DNA mutation status, local invasive factors, and lymph-node metastasis. In the tumors harboring either wild-type K-ras or wild-type p53, heavy smoking was associated with EMT activation (p<0.0001, p=0.0002, respectively), whereas no correlation with regard to EGFR staus.
    
    Conclusion:
    Smoking amounts had a significant association with EMT activation level and malignant progression of human adenocarcinoma. Heavy smoking was related with EMT activation of the tumors either with wild-type K-ras or p53.