Despite advances in neuroscience cancer research during the past decades, the survival of cancer patients has only marginally improved and the cure remains unlikely. The blood-brain barrier (BBB) is a major obstacle protecting the entry of therapeutic agents to central nervous system, especially for primary central nervous system lymphoma (PCNSL). Thus, the use of small nanoparticle as a drug carrier may be new strategies to overcome this problem. In this study, we fabricated liposome consisting of superparamagnetic iron oxide nanoparticles (SPIONs) functionalized with anti-CD20 (Rituximab; RTX). The designed nanoparticles have a theranostic property which is not only to improve drug delivery, but also to offer diagnostic and monitoring capabilities. TEM images revealed the spherical shape of liposome with the approximately average diameters about 140-190nm with slightly negatively charge surfaces. Superparamagnetic property of SPIONs-loaded liposomes was confirmed by VSM. Liposome colloidal could be prolonged at 4°C and 25°C storages. RTX conjugated liposome induced cell internalization and apoptosis effect in B-lymphoma cells. Drug targeting and therapeutic effect was investigated in BBB model. The result confirmed that liposome nanocarrier is required as a drug carrier for effectively RTX across the BBB.

The 2021 WHO Classification of Central Nervous System Tumors recommended evaluation of cyclin‐dependent kinase inhibitor 2A/B (CDKN2A/B) deletion in addition to codeletion of 1p/19q to characterize IDH‐mutant gliomas. Here, we demonstrated the use of a nanopore‐based copy‐number variation sequencing (nCNV‐seq) approach to simultaneously identify deletions of CDKN2A/B and 1p/19q. The nCNV‐seq approach was initially evaluated on three distinct glioma cell lines and then applied to 19 IDH‐mutant gliomas (8 astrocytomas and 11 oligodendrogliomas) from patients. The whole‐arm 1p/19q codeletion was detected in all oligodendrogliomas with high concordance among nCNV‐seq, FISH, DNA methylation profiling, and whole‐genome sequencing. For the CDKN2A/B deletion, nCNV‐seq detected the loss in both astrocytoma and oligodendroglioma, with strong correlation with the CNV profiles derived from whole‐genome sequencing (Pearson correlation (r) = 0.95, P < 2.2 × 10−16 to r = 0.99, P < 2.2 × 10−16) and methylome profiling. Furthermore, nCNV‐seq can differentiate between homozygous and hemizygous deletions of CDKN2A/B. Taken together, nCNV‐seq holds promise as a new, alternative approach for a rapid and simultaneous detection of the molecular signatures of IDH‐mutant gliomas without capital expenditure for a sequencer.