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R. Li



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    P1.05 - Poster Session with Presenters Present (ID 457)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Early Stage NSCLC
    • Presentations: 1
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      P1.05-019 - Two Inflammatory Biomarkers MDC/CCL22 and BLC/CXCL13 Are Independently Associated with the Significant Risk of Early Stage Lung Adenocarcinoma (ID 3966)

      14:30 - 14:30  |  Author(s): R. Li

      • Abstract
      • Slides

      Background:
      This prospective study was designed to investigate the association between multiple inflammatory biomarkers in circulation and the risk for early stage lung adenocarcinoma.

      Methods:
      We measured 10 inflammatory biomarkers in 228 early stage lung adenocarcinoma patients and 228 age, sex and smoking matched healthy controls by using the Luminex bead-based assay.

      Results:
      Only two biomarkers were significantly associated with early stage lung adenocarcinoma risk after Bonferroni correction: the multivariate odd ratio or OR (95% confidence interval or CI) was 0.29 (0.16-0.53) for MDC/CCL22 (P<0.0001) and 4.17 (2.23-7.79) for BLC /CXCL13 (P<0.0001) for the comparison of 4[th] quartile with 1[st] quartile. When analysis was restricted to never smokers (196 patients/196 controls), MDC/CCL22 and BLC/CXCL13 were still significantly associated with early stage lung adenocarcinoma risk (OR; 95% CI; P: 0.37; 0.21-0.66; P<0.0001 for MDC/CCL22 and 2.78; 1.48-5.22; P =0.001 for BLC/CXCL13). Additionally, significance persisted after restricting analysis to 159 stage IA lung adenocarcinoma patients and 159 matched controls for MDC/CCL22 (OR; 95% CI; P: 0.37; 0.21-0.66; <0.0001) and BLC/CXCL13 (2.78; 1.48-5.22). Furthermore, elevated BLC/CXCL13 was associated with a 2.90-fold (95% CI: 1.03-8.17; P=0.037) increased risk of subcentimeter lung adenocarcinoma, and there was an increasing trend for BLC/CXCL13 with the progression of subcentimeter lung adenocarcinoma.

      Conclusion:
      Our findings demonstrated that MDC/CCL22 and BLC/CXCL13 were independently associated with the significant risk of early stage lung adenocarcinoma, and this association persisted even in non-smokers and in stage IA patients. Moreover, BLC/CXCL13 was identified to play a carcinogenic role in the progression of lung adenocarcinoma.

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    P2.01 - Poster Session with Presenters Present (ID 461)

    • Event: WCLC 2016
    • Type: Poster Presenters Present
    • Track: Biology/Pathology
    • Presentations: 1
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      P2.01-082 - Transcriptional Profiling Identified the Anti-Proliferative Effect of Mitofusin-2 Deficiency and Its Risk in Lung Adenocarcinoma (ID 6011)

      14:30 - 14:30  |  Author(s): R. Li

      • Abstract

      Background:
      Mitofusin-2(MFN2) was initially identified as a hyperplasia suppressor in hyper-proliferative vascular smooth muscle cells of hypertensive rat arteries, which has also been implicated in various cancers. There exists a controversy in whether it is an oncogene or exerting anti-proliferative effect on tumor cells. Our previous cell cycle analysis and MTT assay showed that cell proliferation was inhibited in MFN2 deficient A549 human lung adenocarcinoma cells, without investigating the changes in regulatory network or addressing the underlying mechanisms.

      Methods:
      We performed expression profiling in MFN2 knock-down A549 cells. Furthermore, we compared the expression profiling of a cohort consisting of 61 pairs of tumor-normal match samples from The Cancer Genome Atlas(TCGA).

      Results:
      The expression profiling in MFN2 knock-down cells suggested that cancer related pathways were among the most susceptible pathways to MFN2 deficiency. Next, we teased out the specific pathways to address the impact that MFN2 ablation had on A549 cells, as well as identified a few genes whose expression level associated with clinicopathologic parameters. In addition, transcriptional factor target enrichment analysis identified E2F as a potential transcription factor that was deregulated in response to MFN2 deficiency. Figure 1 Figure 2





      Conclusion:
      The anti-proliferative effect of MFN2 deficiency and its risk in lung adenocarcinoma were found by transcriptional profiling.