The main limitation of the present study is the relatively low sample size of 87 in relation to the large number of parameters that was analyzed. The sample size allowed the inclusion of only 5 covariates in the regression model to minimize the risk of overfitting. In addition, we only included early stage NSCLC patients. Thus, additional studies using larger patient groups and also including later stages of NSCLC, i.e. stage III/IV, might provide more insight in the prognostic value of galectin mRNA expression profiling. In summary, extensive galectin expression profiling confirmed the prognostic value of galectin-1 and identified gal-9D5 as a potential novel prognostic markers in early stage NSCLC. Identification of such markers is important to identify patients that will benefit from adjuvant chemotherapy. In addition, our findings exemplify the relevance of profiling individual splice variants of galectin-9. It remains to be determined whether splice variant-specific profiling has a similar benefit in other cancer types, including those in which overall galectin-9 expression is a prognostic marker. The cell cycle consists in four phases: G1, S, G2 and M. In addition, in response to some situations, cells can exit reach the G0 phase primarily encountered in two cases: in quiescent stem cells, which can usually enter the cell cycle upon appropriate stimulations, or in terminally differentiated cells, generally irreversibly withdrawn from the cell cycle. Positioning cells within cell cycle at single cell or population level is the basis of cell cycle studies. However, the procedures dedicated to this aim are often time consuming, and generally destructive thereby precluding studies on live cells. Indeed, detection of markers used in cell cycle studies usually needs the fixation/permeabilization of the cells. While the staining of nucleic acids with some vital dyes is yet possible, it gives relatively imprecise information and is not suitable for all cell types. Recently, several groups have designed new tools to conveniently define the position of fixed or living cells within the cell cycle. These new indicators are based on the constitutive expression of a gene encoding a chimeric marker, which consists in a fusion between a fluorescent protein and a cellular protein that undergoes cell cycle regulation of its stability or distribution. Several new cell cycle indicators have thus emerged, using either proteins involved in DNA replication or in LY2109761 700874-71-1 mitosis. The cell cycle of the pancreatic beta cells has been thoroughly investigated. However, despite these efforts, our knowledge of its regulation, especially in human, remains far from being complete. For instance, the mechanisms underlying the very slow turnover of beta cells after a perinatal wave of proliferation are poorly understood although age-dependent loss of responsiveness to PDGF probably partly accounts for this evolution. In adult rodents, new beta cells arise primarily by duplication of preexisting beta cells while neogenesis mainly occurs before birth. In human, adult beta cells appear even more deeply resting, being probably mostly postmitotic and evidence for neogenesis is scarce.