In the February 22nd online edition of Stem Cells, C. H. Stuelten et al from the National Cancer Institute reported the results of their study on analyzing a tumor cell line (NC160) that may express cell surface marker reflecting tumor stem cells or cancer-initiating cells (CIC). With FACS analysis, the investigators determined if the putative CIC surface markers, CD15, CD24, CD44, CD133, CD166, CD326, PGP) and aldehyde dehydrogenase activity are found in various NC160 cell line panels. The experimental data did not reveal a single marker or combination of marker that could be correlated to the ability to form cell colonies. The researcher noted certain expression patterns correlated with tumor types such as breast and lung cancers that were of a more mesenchymal phenotype. The authors concluded from their observation that the "complexity and tumor type specificity of marker display creates challenges for the application of cell sorting and other approaches to isolation of putative tumor stem cell populations and suggests that therapeutic targeting strategies will need to take this into account."

In the February 9th issue of PNAS, D. Xie et al. from the Univ. of Texas Southwestern Medical Center reported their experimental results on the role of the DAB2IP gene in modulating the epithelial-to-mesenchyal transition (EMT) in prostate cancer (PCa). The study was based on the observation that a single nucleotide polymorphism/loss in expression of the gene can result in either an aggressive or metastatic form of PCa. The experimental data revealed that a loss in expression of DAB2IP can initiate EMT in PCa. This transition is confirmed histologically by downregulation of E-cadherin and upregulation of vimentin. On the other hand, restoring DAB2IP expression in metastatic PCa cells reversed EMT. With a xenograft mouse model, knocking down endogenous DAB2IP expression in human carcinoma cells resulted in metastatic lesions in distant organs concomitant with lymph node involvement. The authors also demonstrated that DAB2IP regulates EMT by modulating the activity of β-catenin/T cell factor.