Author of

• 12812

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  P3.20 - Poster Session 3 - Early Detection and Screening (ID 174)

  • Event: WCLC 2013
  • Type: Poster Session
  • Track: Imaging, Staging & Screening
  • Presentations: 1
  • Moderators:
  • Coordinates: 10/30/2013, 09:30 - 16:30, Exhibit Hall, Ground Level

  • 12818

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    P3.20-006 - Proteomic analysis of the bronchial epithelium to develop a molecular signature of risk for lung cancer (ID 2008)

    09:30 - 09:30  |  Author(s): M. Li
    • Abstract

    Background
    A small percentage of at-risk individuals ultimately develop lung cancer. This warrants a search for a strategy to identify individuals who will be developing lung cancer. The bronchial epithelium represents the field of carcinogenesis and may serve as surrogate tissue for biomarker of risk. Therefore we hypothesized that proteomic alterations in the histologically normal airway epithelium from risk stratified individuals allow us to derive a signature of risk of developing lung cancer.

    Methods
    We have collected bronchial brushings specimens from risk stratified individuals (Bach PB et al. 2003) and categorized them as Control (group 1), low (group 2) and high (group 3) risk groups. We collected three bronchial brushings specimens from each individual in a single session for acquiring shotgun proteomics (n=30). We also collected brushings from cancer patients whose risk criteria are similar to low (group 5) and high (group 6) risk groups as well as a group of never smoker lung cancer patients (group 4). Shotgun proteomics data were acquired from 3 technical replicates of pooled specimens from 5 individuals. Candidate biomarkers were selected based on group comparison and trend analysis.

    Results
    We have acquired shotgun proteomics data from bronchial brushings specimen from individuals at-risk for lung cancer development. A total of 4973 proteins have been identified. Jonchere-Terpestra trend test was performed among control, low risk and high risk groups (Groups 1, 2, and 3). Expression level of 316 proteins were altered (trend p <0.05) with 238 proteins demonstrating upward and 78 proteins downward trends. DNA repair and oxidative stress and the galactose metabolic enzyme pathway were enriched in the upward trend analysis.

    Conclusion
    We identified a proteomic candidate signature of risk of developing lung cancer from histologically normal bronchial epithelial cells. Integration of these results with those upcoming from two other molecular platforms will allow us to narrow down the molecular aberrations most predictive of risk. This signature will be validated in an independent cohort. Such signature of risk for lung cancer may serve as a powerful tool for lung cancer risk assessment and may provide the basis of patient selection for surveillance programs and chemoprevention. This work is funded by RO1 CA102353to PPM.