Transcytosis across these cells followed by endocytosis into adjacent astrocytes. Astrocytes are known to provide cholesterol to neurons and are poised to exert significant control over cholesterol homeostasis in neuronal cells. Conceivably, normalization of cholesterol metabolism within diseased astrocytes could lead to an indirect normalization of cholesterol pools within neurons. Correction of the metabolic defect in astrocytes may then allow neurons to overcome their own metabolic defect, in turn leading to enhanced processing and trafficking of both cholesterol and GSLs. Consistent with this scenario, a recent study in which functional NPC1 protein was expressed in an astrocyte-specific manner in Npc12/2 mice was reported to lead to increased longevity and decreased neuronal storage of cholesterol. In this work, we report a fine mapping of chromosomal imbalances in a set of 27 BL primary tumors and cell lines. Whole-genome 44 K and 244 K Mepiroxol oligonucleotide arrays were 
used to analyze recurrent copy number alterations present in tumors and cell lines respectively. Comparison of the 15 dye-swap pairs from cell lines revealed identical aberrations. In most cases, the boundaries of the chromosomal aberrations were absolutely identical. The dye-swap helped to reduce the background level. Whole-genome oligonucleotide microarrays aCGH analysis allowed us to delineate the chromosomal imbalances at 15,20 Kb resolution in the 15 cell lines and at 70 Kb average resolution in the 13 primary tumors. Each sample was also investigated using conventional cytogenetics. Close agreement between karyotype data and wholegenome aCGH CNAs was observed. When discrepancies occurred, they were mostly explained, i) by a lack of detection due to karyotype resolution; ii) by aCGH locally blurred heterogeneous cell clones, or normal cell contamination in the sample; iii) by the presence of balanced chromosomal rearrangements. In addition to BL hallmark anomalies, 4 other apparently balanced translocations were detected exclusively by conventional cytogenetics, as expected. The karyotypes of the 11 Ginsenoside-F5 previously published cell lines were essentially identical to those reported elsewhere. Four cell lines have been karyotyped for the first time in the present paper. The BLMer cell line was established from a recurrent tumor. Karyotype analysis of BLMer showed the same anomalies as observed in the parental tumor.