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J. Chang



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    P2.06 - Poster Session 2 - Prognostic and Predictive Biomarkers (ID 165)

    • Event: WCLC 2013
    • Type: Poster Session
    • Track: Biology
    • Presentations: 1
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      P2.06-024 - Prognostic value of RALA and RALB overexpression in KRAS mutant lung cancer (ID 2050)

      09:30 - 09:30  |  Author(s): J. Chang

      • Abstract

      Background
      Oncogenic mutations of KRAS play important roles in cancer progression and resistance to chemotherapy in non-small cell lung cancer (NSCLC). Ras-related proteins, RALA and RALB, are members of the RAS superfamily of small GTPases and act as downstream effectors of KRAS. Therefore RAL proteins may be involved in cancer cell survival, invasion and metastasis. In this study, authors investigated the prognostic role of RALA and RALB overexpression in non-small cell lung cancer (NSCLC) patients with KRAS mutations.

      Methods
      Expression status of RALA and RALB in the tumor tissue of NSCLC patients whose tumor harbors KRAS mutations were evaluated by immunohistochemistry(n=12). In addition, we investigated 11 metastatic lung tumor tissue samples from KRAS mutant colorectal cancer patients. Predictive factors for survival were calculated using Kaplan-Meier estimator and Cox proportional hazards model.

      Results
      There was no statistically significant relation between RALA/RALB overexpression and KRAS mutation subtypes. However, RALB was frequently overexpressed in the tumor of advanced stageof NSCLC with KRAS mutation(p=0.015, χ[2]-test). Furthermore, the overall survival of the patients with RALB overexpression was significantly shorter than that of the patients without RALB overexpression (2.7 vs. 7.3 months, P<0.001; Mann-Whitney U test). In metastatic lung tumor tissues from KRAS mutant colorectal cancer patients, RALB protein overexpression showed only a trend toward shortened disease free survival.

      Conclusion
      RALB overexpression might be related to rapid disease progression and poor prognosis in NSCLC patients with KRAS mutations.