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Gene expression profiling classifies lung squamous cell carcinomas with N1 positive lymph nodes

ABSTRACT: Using gene expression microarrays, we tested whether lung SCCs that have metastasised to loco-regional lymph nodes (N1/2m) are different to those that directly invade and involve local nodes (N1d). Using 22,323 element microarrays, a non-parametric test identified 126 genes/transcripts that discriminated between N0 (n=35) and N1/2m (n=16) tumours (Wilcoxon-Mann-Whitney U test, P<0.01). Hiearchical clustering of all 59 tumours (including 8 N1d tumours) demonstrated the N1d tumours clustered with the N0 tumours rather than the N1/2m tumours. Next, we built class prediction models from the 35 N0 tumours and 16 N1/2m tumours to predict the class of N1d tumours. All models consistently classified N1d tumours as similar to N0 tumours. This could explain some of the variable response of some N1 tumours to adjuvant chemotherapy, and suggest refinement of the TNM "N" stage nomenclature to adjust for this biological observation to ensure appropriate patients benefit from treatment. Keywords: non-small cell lung carcinoma, squamous cell, nodal metastasis, TNM staging, expression profiling Expression profiling using 22K element microarrays of 59 primary lung squamous cell carcinomas.

ORGANISM(S): Homo sapiens

SUBMITTER: Larsen JE

PROVIDER: S-ECPF-GEOD-5828 | biostudies-other | 2007 Jul

REPOSITORIES: biostudies-other

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Project description:BACKGROUND: Prion diseases are characterized by the accumulation of the pathogenic PrPSc protein, mainly in the brain and the lymphoreticular system. Although prions multiply/accumulate in the lymph nodes without any detectable pathology, transcriptional changes in this tissue may reflect biological processes that contribute to the molecular pathogenesis of prion diseases. Little is known about the molecular processes that occur in the lymphoreticular system in early and late stages of prion disease. We performed a microarray-based study to identify genes that are differentially expressed at different disease stages in the mesenteric lymph node of sheep naturally infected with scrapie. Oligo DNA microarrays were used to identify gene-expression profiles in the early/middle (preclinical) and late (clinical) stages of the disease. RESULTS: In the clinical stage of the disease, we detected 105 genes that were differentially expressed (?2-fold change in expression). Of these, 43 were upregulated and 62 downregulated as compared with age-matched negative controls. Fewer genes (50) were differentially expressed in the preclinical stage of the disease. Gene Ontology enrichment analysis revealed that the differentially expressed genes were largely associated with the following terms: glycoprotein, extracellular region, disulfide bond, cell cycle and extracellular matrix. Moreover, some of the annotated genes could be grouped into 3 specific signaling pathways: focal adhesion, PPAR signaling and ECM-receptor interaction. We discuss the relationship between the observed gene expression profiles and PrPSc deposition and the potential involvement in the pathogenesis of scrapie of 7 specific differentially expressed genes whose expression levels were confirmed by real time-PCR. CONCLUSIONS: The present findings identify new genes that may be involved in the pathogenesis of natural scrapie infection in the lymphoreticular system, and confirm previous reports describing scrapie-induced alterations in the expression of genes involved in protein misfolding, angiogenesis and the oxidative stress response. Further studies will be necessary to determine the role of these genes in prion replication, dissemination and in the response of the organism to this disease.

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Gene expression profiling classifies lung squamous cell carcinomas with N1 positive lymph nodes

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