Integrated Analyses of Copy Number Variations and Gene Expression in Lung Adenocarcinoma
Author Information
Author(s): Lu Tzu-Pin, Lai Liang-Chuan, Tsai Mong-Hsun, Chen Pei-Chun, Hsu Chung-Ping, Lee Jang-Ming, Hsiao Chuhsing Kate, Chuang Eric Y.
Primary Institution: National Taiwan University
Hypothesis
Can concurrent genome-wide analyses of copy number variation and gene expression identify genes associated with tumorigenesis and survival in non-smoking female lung adenocarcinoma?
Conclusion
The study identified genes and pathways that may serve as prognostic biomarkers for lung tumorigenesis by integrating gene expression profiles and copy number variations.
Supporting Evidence
- 475 genes were identified as differentially expressed between tumor and normal tissues.
- Pathway analysis revealed two major dysregulated functions in lung tumorigenesis: survival regulation via AKT signaling and cytoskeleton reorganization.
- Validation of identified pathways using three independent cohorts demonstrated effective prediction of survival.
Takeaway
Researchers looked at changes in DNA and gene activity in lung cancer to find clues about how to predict survival and improve treatment.
Methodology
Concurrent genome-wide microarray analyses of CNVs and gene expression were performed on paired lung tumor and normal tissues.
Potential Biases
Potential biases may arise from the use of adjacent normal tissue as a reference, which could affect the identification of CNVs.
Limitations
The study focused only on non-smoking female patients, which may limit the generalizability of the findings.
Participant Demographics
The study included 42 non-smoking female patients with lung adenocarcinoma.
Statistical Information
P-Value
p=0.0034
Statistical Significance
p<10−5
Digital Object Identifier (DOI)
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