Amoureux et al. BMC Cancer 2010, 10:91 http://www.biomedcentral.com/1471-2407/10/91 of contact mediated inhibition of proliferation as exerted in astrocytes [47] or neuroblastoma cell lines [48]. Importantly, we also found olig2 expression to be regulated by PSA-NCAM expression in the GBM9 cell line or to be activated in C6 after PSA-NCAM expres- sion. The mechanisms underlying olig2 regulation could be related to PSA-NCAM mediated alterations of cell proliferation, survival or differentiation [19,41-44,48] and remain to be elucidated. Olig2 has been described as a negative regulator of astrocytic differentiation path- way [49], to be required for gliomagenesis and to be coupled to an inhibition of the antiproliferative p21 pathway [12]. Olig2 is also known to play an important role in proliferation and fate determination in the devel- opment of the nervous system and adulthood [50]. Therefore, one of the consequences of PSA-NCAM up regulation in GBM could be olig2 increase and its downstream growth and differentiation consequences. Further investigations of the impact of olig2 levels in relation to GBM patients’ survival appear compelling. In conclusion, PSA-NCAM is another example of molecules having a dual role, during development as fundamental regulators of pattern formation and differ- entiation, and in cancer. Moreover, the role of an adhe- sion molecule of the immunoglobulin family in cancer stem cell is not unprecedented since L1CAM was recently shown to be required to suppress glioma growth of CD133+ cells in vitro and in vivo [7]. These findings constitute the first evidence that PSA-NCAM expression correlates with GBM patient survival. This novel biomarker for GBM may represent an interesting molecular tool for diagnosis and prognosis in clinical use. This may also have important clinical implications for the treatment of GBM patients as previously sug- gested with chemicals that alter PSA expression with the goal to modulate polysialylation in tumors [51]. This study warrants further investigation of PSA-NCAM with regard to response to treatment in future prospective studies on a larger number of GBM patients. Conclusions We present PSA-NCAM as a new candidate prognosis biomarker for GBM. It represents immediate valuable information to improve life conditions of patients and clinical decisions, and represents a prospective therapeu- tic target and stratifying factor for clinical trials. This novel finding, next to the negative impact of PSA- NCAM on survival and metastasis in other cancers, emphasizes a critical and general role of PSA-NCAM in cancer evolution. The new ELISA test described in the current study was characterized as an accurate and spe- cific quantitative mean to measure PSA-NCAM from a small amount of biopsy, and therefore is a powerful tool, notably for validation in a larger patient cohort, Page 10 of 12 but also to investigate PSA-NCAM with regard to response to treatment. In addition, this new ELISA test can be applied to all tumors expressing PSA-NCAM. Acknowledgements We are grateful to A. Tchoghandjian from providing the GBM9 cell line. This work was supported by INCA grants to DF-B and GR (projet structurant RS019 and Gliother project). Written consent for publication was obtained from the patient or their relative. Author details 1Université de la Méditerranée CNRS UMR6216, Institut de Biologie du Développement de Marseille Luminy, Marseille, France. 2Abcys SA, 5, rue Pierre Chausson, Paris, France. 3Université de la Méditerranée, CRO2 UMR911, Marseille, France. 4Service d’Anatomie Pathologique et de Neuropathologie, Hôpital de la Timone, Marseille, France. 5Unité de Neurooncologie, Hôpital de la Timone, Marseille, France. 6Unité d’Aide méthodologique à la Recherche Clinique et Epidémiologique, DRRC, AP-HM, Marseille, France. 7Service de Neurochirurgie, Hôpital de la Timone, Marseille, France. Authors’ contributions MCA performed the PSA-NCAM ELISA measurements, the olig2/PSA-NCAM immunocytochemistry and Western blot experiments, designed the in vitro experiments, performed the analysis of the data and wrote the manuscript. GR made substantial intellectual contribution to the study and the drafting of the manuscript. BC performed the PSA-NCAM immmunohistochemistry and scoring. AL performed the statistical analysis. PM and OC recruited the patients in a non-selective, consecutive manner, established the diagnosis, performed the surgery and defined the inclusion criteria for the study. DFB participated in study conception, design and establishment of the patients’ diagnosis, interpretation of data and drafting of the manuscript. All authors read and approved the manuscript. Competing interests M-C. Amoureux receives her salary from Abcys SA. Study design, analysis and manuscript writing was entirely overseen by IBDML and Hôpital de la Timone. Received: 30 July 2009 Accepted: 10 March 2010 Published: 10 March 2010 References 1. 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