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MiRNA profiling in relapsed or metastatic HNSCC patients treated with cetuximab and platinum therapy

ABSTRACT: By gene expression profiling (GEP) of head and neck squamous cell carcinomas (HNSCC) we were able to identify candidate biomarkers of progression free survival (PFS) in patients treated with cetuximab-based approaches (Bossi et al, Clinical Cancer Research 2016) . Here, the same samples were used for miRNA expression profiling. Integration of miRNA and gene expression data highlighted 16 miRNAs and 84 genes interconnected in a total of 245 interactions. After feature selection by smoothed t-statistic support vector machine, we identified a network 3 miRNAs and 5 genes that resulted the most relevant in predicting PFS (AUC=0.992). Overall, using a well defined clinical setting we gave the proof of principle that an integrative miRNA-mRNA expression could greatly contribute to refinement of the biology behind and to the potential identification of a predictive model.

ORGANISM(S): Homo sapiens

PROVIDER: GSE92595 | GEO | 2017/03/08

SECONDARY ACCESSION(S): PRJNA358220

REPOSITORIES: GEO

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Project description:KRAS mutation is a negative predictive factor for treatment with anti-epidermal growth factor receptor (EGFR) antibodies in metastatic colorectal cancer (mCRC). Novel predictive markers are required to further improve the selection of patients for this treatment. Here, we assessed the influence of modification of KRAS by gene copy number aberration (CNA) and microRNAs (miRNAs) in correlation to clinical outcome in mCRC patients treated with cetuximab in combination with chemotherapy and bevacizumab. Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 mCRC patients in a phase III trial, who were selected based upon their good (n=17) or poor (n=17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab. Gene copy number at the KRAS locus was assessed using high resolution genome-wide array CGH and the expression levels of 17 miRNAs targeting KRAS were determined by real-time PCR. Good response was associated with 12p12.1 copy number loss, even in patients with a KRAS mutation, while copy number gain in wild-type KRAS patients was correlated with a poor response. In KRAS mutated tumours increased miR-200b and decreased miR-143 expression were associated with a good response. In wild-type KRAS patients, miRNA expression did not predict response in a multivariate model. Thus, assessment of KRAS CNA and miRNAs targeting KRAS might further optimize the selection of patients eligible for anti-EGFR therapy. Copy number detection was performed using NimbleScan and Nexus software Formalin-fixed paraffin-embedded primary tumour tissue was used from 34 metastisized colorectal cancer patients in a phase III trial (CKTO 2005-02; ClinTrials.gov NCT00208546) of the Dutch Colorectal Cancer Group (DCCG), who were selected based upon their good (n=17) or poor (n=17) progression-free survival (PFS) upon treatment with cetuximab in combination with capecitabine, oxaliplatin, and bevacizumab.

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MiRNA profiling in relapsed or metastatic HNSCC patients treated with cetuximab and platinum therapy

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