The progress of modern medicine in the understanding and diagnosis and treatment of central nervous system tumors has never left the impetus of basic research. After more than two decades of research accumulation, our understanding of molecular biology and molecular genetics, signal transduction pathways, cellular origin, malignant progression and biological characteristics of malignant brain tumors has been continuously advanced; in the past three decades, the WHO classification of CNS tumors has been updated in four editions, and the pathological characteristics of each tumor species, subtypes and their different histological manifestations have been precisely annotated, and additional descriptions of The epidemiology, clinical signs and symptoms, imaging, outcome and predictive factors of each type of tumor have been described; since four decades, the invention and application of imaging technologies represented by CT and MRI (also including PET-CT, SPECT and magnetoencephalography) have promoted the development of brain tumor diagnosis and treatment in leaps and bounds. The different research fields of brain tumor are even more continuously crossed and integrated with each other. Molecular neuropathology has summarized the geneticprofile of brain tumor occurrence and development; imaging diagnosis of brain tumors has advanced from the identification of tumor species to the diagnosis of tumor subtypes and the description of tumor biological characteristics; functional imaging technology has visualized the relationship between tumors and white matter conduction bundles, the localization of cortical functional areas, and the molecular and metabolic information of tumors. We identify problems from the clinical practice of CNS tumors, condense them into basic scientific questions for research, and then apply the research results to the diagnosis, treatment and prevention of brain tumors. This interactive cycle between basic research and clinical practice has bridged the gap between basic research and clinical application, creating a fast track between the laboratory and the bedside (B2B). In 2003, Elias A. Zerhouni of NIH published the “NIH Roadmap” in the journal Science, introducing the concept of translational medicine or translational research, which has made translational medicine a new starting point and focus of global medical research [1]. Translational medicine in CNS tumors is not only a concept, but also has been gaining practice in clinical work, which is reflected in genetic characterization and molecular typing of brain tumors, development of molecularly targeted drugs and individualized medicine. The diagnosis, treatment and prognosis of CNS tumors have been determined mainly based on the histopathological characteristics of the tumor for more than a hundred years [2]. However, clinical practice has taught us that tumors with the same histomorphologic features may have very different clinical outcomes. On the basis of light microscopy, pathological diagnostic techniques have been developed, and the introduction of electron microscopy, molecular biology, immunohistochemical staining, and quantitative RT-PCR is to refine or even replace the traditional pathological classification to form a more accurate classification system to reflect the cellular, genetic, and molecular changes in the development of gliomas. The molecular subtypes of CNS tumors and their unique responsiveness to specific adjuvant therapeutic measures are the prerequisites for individualized medical treatment of patients. The application of microarray technology in CNS tumor research has been an innovation in the field of translational medicine during the last decade. Although gene expression profiling based on DNA microallelepiped technology cannot completely replace the morphological classification of primary brain tumors, especially diffuse gliomas, it did reveal the presence of not only histological heterogeneity but also heterogeneity of gene expression within the tumor tissue in tumors diagnosed histomorphologically as gliomas [3]. Since 2000, the WHO classification of central nervous system tumors has classified glioblastoma as primary or secondary glioblastoma. Primary glioblastoma is more common, with an age of onset often above 50 years, a history of only weeks to months, and commonly amplification of EGFR or the presence of truncating mutations that do not require ligand activation, without mutations in the P53 gene; secondary glioblastoma has a younger age of onset, with some cases showing evidence of progression from lower grade tumors, and prominent changes at the molecular level with mutations in the P53 gene, without EGFR amplification [2]. In recent years, the molecular typing of gliomas is still being explored, such as the classification of glioblastomas into proneural, proliferative and mesenchymal based on molecularsignature. In proneural tumors, chromosome gain or loss is not evident, PTEN gene is intact, EGFR is not amplified, but the notch pathway is activated. In the proliferative and mesenchymal subtypes, there is loss of chromosome 7 or chromosome 10, normal or amplified EGFR but mutated PTEN. The main difference between the two types is the presence of a vasoproliferative phenotype in the mesenchymal subtype. The main difference between the two types is the presence of a vasoproliferative phenotype in the mesenchymal subtype. All proto-neurogenic glioblastomas are less aggressive than proliferative and mesenchymal ones, thus making this typing method prognostic. The purpose of the Tumor Genome Atlas Project is to apply genomic analysis techniques, using large-scale genome sequencing, to map tumor genomic variants and find all small variants of oncogenic and tumor suppressor genes through systematic analysis, so as to understand the mechanisms of tumor cell genesis and development, and ultimately to obtain breakthroughs in tumor diagnosis and treatment and to develop novel tumor prevention strategies [4]. Based on gene sequencing based on whole genome amplification, gene expression and methylation of 206 glioblastoma cases were analyzed, and mutations in gene sequences, such as mutations in ERBB2, NF1 and TP53 genes, were found in 91 specimens. The high frequency of mutations in PIK3R1 (PI3K regulatory subunit protein) gene in glioblastoma, combined with the inactivation of PTEN (a major negative regulator of PI3K), was found to demonstrate that the PI3K pathway is closely associated with the development of glioma. It is also noteworthy that mutations in the NF1 gene are frequently found in sporadic gliomas. IDH1 mutations in gliomas are probably the most meaningful finding in the genomic landscape of gliomas [5]. Interestingly, more than half of IDH1 mutations affect R172, with which IDH2 has an analogue.IDH1 mutations alter the activity of the encoded IDH enzyme, and thus disturb cellular homeostasis. IDH mutations are frequently seen in astrocytomas and oligodendroglial tumors. IDH mutations occur not only in tumors arising from astrocytes and oligodendrocytes, but also in tumors arising from precursor cells of the astrocyte and oligodendroglial cell lineage. In adult gliomas, IDH1 mutations are generally present in patients with young onset, and such patients have a better prognosis. Although IDH1 is an early event in the progression of malignant gliomas, hairy cell astrocytomas, which are WHO grade I, do not have this alteration. Hairy cell astrocytomas often show a tandem duplication of chromosome 7q34 resulting in a fusion between KIAA1549 and BRAF, and this alteration is not present in tumors with IDH1 mutations. Translational medicine research findings have become an engine for new drug development, with targeted therapies being examples and have transitioned from preclinical concepts to clinical trial therapies with the development of a range of targeted small molecule drugs and monoclonal antibodies, including tyrosine kinase inhibitors, angiogenesis inhibitors, and integrin inhibitors [6]. Among all malignant glioma targeted therapeutic strategies, bevacizumab (Bevac) is a landmark drug that has passed phase III trials for the clinical treatment of malignant glioma. Bevacizumab is a humanized anti-VEGF antibody (IgG1) consisting of a 93% human-derived structural domain and a 7% mouse-derived binding region that competitively inhibits the binding of VEGF to its cell membrane receptors. The combination of bevacizumab and topoisomerase-1 inhibitor irinotecan has been used as an important salvage therapy for malignant glioma. Cilengitide, a major inhibitor of integrins, competitively antagonizes integrin αvβ3 and αvβ5 receptors. In 51 patients with malignant glioma in a phase I clinical trial, cilengitide at different doses applied alone resulted in improved imaging performance in 10% of patients and stable disease in 31% of patients with well-tolerated drug. Preliminary results for patients with new-onset glioblastoma treated with a combination of cilengitide, temozolomide and radiation therapy showed improved 6-month progression-free survival and overall survival. A multi-center participatory phase III cilengitide clinical trial study in neoplastic glioblastoma is ongoing, with clinical trial results expected in 2013-2014.VEGF-Trap is a soluble receptor that binds VEGFR-1 and VEGFR-2 extracellular domain fusion proteins to the Fc fragment of IgG.VEGF-Trap can induce circulating VEGF-Trap can trick circulating VEGF to bind to it and achieve the goal of preventing VEGF from binding to its cell membrane receptor. A multicenter study of VEGF-TRAP in combination with temozolomide and radiation therapy is underway. The North American Brain Tumor Consortium is designing a phase II single-arm clinical trial of VEGF-TRAP alone in patients with recurrent malignant glioma who have failed temozolomide therapy. Sunitinib (a multi-tyrosine kinase target inhibitor of VEGFRs and PDGFRs) has initially shown good preclinical results in malignant glioma and is undergoing further validation at eight medical centers in Germany and Austria. Targeted therapy studies in malignant glioma have found that clinical trial results with small molecule selective inhibitors of VEGFR appear to be less effective than therapeutic strategies with VEGF as the inhibitory target. Imatinib (imatinid) has shown no effect in phase II clinical trials in recurrent glioma, and its combination with hydroxyurea has proven ineffective in phase II and III clinical trials. The results of vatalanib (VEGFR1-3 inhibitor) alone, in combination with temozolomide or lomustine, were not convincing because imaging results and progression-free survival were not significantly improved. Clinical trials of vatalanib in combination with temozolomide and radiation therapy are ongoing. Clinical studies with cediranib (cediranib) (VEGFR-2/PDGFRβ, c-kit tyrosine kinase inhibitor) and vandetanib (vandetanib) (VEGFR-2, EGFR; RET tyrosine kinase inhibitor) have also failed to significantly prolong progression-free survival or overall survival of patients. Individualized targeted therapy guided by geneticprofile and molecular markers will become a new theme in the treatment of malignant glioma, and individually designed targeted therapy regimens will evolve from single-target inhibition to multi-target therapy. Individualized medical treatment of malignant glioma will be a difficult journey. Previous empirical chemotherapy and radiotherapy approaches may delay the optimal treatment of patients with malignant glioma and cause financial losses to patients. The core of individualized chemotherapy and radiotherapy regimens is to anticipate the patient’s sensitivity to treatment [7]. Individualization of chemotherapy regimens is the inevitable direction of pharmacological treatment of malignant gliomas. Until the ability to examine the genetic characteristics of all malignant glioma patients’ own tumors and find a correspondence with the effect of adjuvant therapy is available, there are still molecular markers that can be used to guide clinical treatment. The first molecular marker of therapeutic relevance is the heterozygous deletion of chromosomes 1p and 19q. In oligodendroglioma, such patients are sensitive to PCV (combination of methylbenzylhydrazine, CCNU and vincristine) chemotherapy regimens if they have a combined deletion of chromosomes 1p and 19q. O6-methylguanine-DNA-methyltransferase (MGMT) is another Defective promoter methylation and DNA mismatch repair of MGMT is a hypermutated phenotype in brain tumors. If the MGMT promoter is found in a non-methylated state or MGMT is highly active in the genome of glioblastoma cells, it predicts that the tumor is resistant to alkylating agents such as temozolomide [8]. Translational medicine in CNS tumors is a never-ending research process in a continuous cycle of upward mobility. The bidirectional and open linkage between basic research and clinical practice will allow the results of laboratory research to be rapidly and effectively applied to clinical practice, while the timely feedback of problems identified in the clinic to the laboratory will initiate more in-depth research. Brain tumor stem cells, also known as brain tumor-initiating cells or stem cell-like brain tumor cells, are the most important discoveries in terms of cells of brain tumor origin in the last decade [5]. These cells, like neural stem cells, can form cell spheres and exhibit self-renewal capacity in growth factor-rich cell culture media; and express differentiation markers of astrocytes, oligodendrocytes and neurons in differentiation media. Brain tumor stem cells express not only CD133 but also proteins that play a key role in maintaining neural stem cell self-renewal, such as Sox2, Nanog and Oct4. It has been found that if mice are inoculated with brain tumor stem cells, the transplanted tumors resemble primary glioblastoma more than if they are inoculated with human glioma cell lines. Because brain tumor stem cells are highly proliferative and infiltrative migrating and highly resistant to radiotherapy and chemotherapy, improving the understanding of brain tumor stem cells will be of great importance for the treatment of malignant brain tumors. Brain tumor stem cells will remain an important bridging point for the interaction between basic research and clinical practice. Some new phenomena have also been identified in the targeted anti-angiogenic therapy of malignant glioma that deserve to be explored in depth by basic research. For example, when bevacizumab or other inhibitors of endothelial growth factor are used, the MRIT1 contrast enhancement is reduced due to the reduction of abnormal vascular leakage, showing a pseudo treatment response, which makes it difficult to determine the efficacy and adjust the treatment regimen; malignant glioma treated with bevacizumab will show an enhanced ability of tumor cells to invade and migrate, ultimately leading to a treatment failure response. The reciprocal interaction between clinical and basic research on targeted therapies will promote further rationalization and improvement of targeted treatment regimens. More and more neurosurgeons and neuro-oncologists, who have been studied and trained in basic research, can keenly capture the progress of basic research and at the same time can provide the urgent problems in the clinic to basic research, and are important reserve talents for clinical translational medicine. Medical practitioners engaged in CNS tumor diagnosis and treatment should pay attention to the establishment of tumor specimen repository and database, build a network of clinical trial bases and application platform of translational medicine, and take the initiative to apply the results of basic research to the screening of interferable diseases, pre-clinical or early patient diagnosis, so that brain tumor patients can really benefit from the flourishing basic research. Translational medicine of brain tumor is not far from us, it is not only a concept but also a practice.