Functional microarray analysis suggests repressed cell-cell signaling and cell survival-related modules inhibit progression of XXXX .

@entity5 @entity1 @entity213 @entity3
BACKGROUND: @entity5 shows a great diversity in its clinical behavior which cannot be easily predicted using the currently available clinical or pathological markers. The identification of pathways associated with lymph node @entity3 (N+) and recurrent @entity213 ( @entity213 ) may increase our understanding of the complex biology of this disease. METHODS: Tumor samples were obtained from untreated @entity213 @entity1 undergoing surgery. @entity1 were classified according to pathologic lymph node status (positive or negative) or @entity5 recurrence (recurrent or non-recurrent @entity5 ) after treatment (surgery with neck dissection followed by radiotherapy). Using microarray gene expression, we screened @entity5 samples according to modules comprised by genes in the same pathway or functional category. RESULTS: The most frequent alterations were the repression of modules in negative lymph node (N0) and in non-recurrent @entity5 rather than induction of modules in N+ or in recurrent @entity5 . N0 @entity5 showed repression of modules that contain cell survival genes and in non-recurrent @entity5 cell-cell signaling and extracellular region modules were repressed. CONCLUSIONS: The repression of modules that contain cell survival genes in N0 @entity5 reinforces the important role that apoptosis plays in the regulation of @entity3 . In addition, because @entity5 samples used here were not microdissected, @entity5 gene expression data are represented together with the stroma, which may reveal signaling between the microenvironment and @entity5 cells. For instance, in non-recurrent @entity5 , extracellular region module was repressed, indicating that the stroma and @entity5 cells may have fewer interactions, which disable @entity3 development. Finally, the genes highlighted in our analysis can be implicated in more than one pathway or characteristic, suggesting that therapeutic approaches to prevent @entity5 progression should target more than one gene or pathway, specially apoptosis and interactions between @entity5 cells and the stroma.
