Recently, a few case reports of thymoma-associated panencephalitis (TAPE) have brought to light a disease entity that has not been fully characterized. Literature review of TAPE reveals an array of associated neuronal antibodies, with varied responses to thymomectomy with or without immunotherapy. This report describes a case of TAPE and proposes that the GABAA receptor antibody is a potential target antigen driving the immune process in this disease entity. Treatment-wise, early thymomectomy consistently improves the overall course of disease. Further study of such cases will be critical in clarifying the mechanisms of disease, improving early diagnosis, and developing targeted approaches to treatment.
Human cytomegalovirus (HCMV) was reported in glioblastoma multiforme (GBM) over a decade ago and this finding has the potential to increase our understanding of the disease and it offers an alternative tumor-specific therapeutic target. Due of this promise, there is a fair amount of time, energy and money being directed towards understanding and utilizing this connection for eventual therapeutic purposes. Nevertheless, the association between GBM and HCMV remains controversial. Several studies have reported conflicting results, further undermining the potential clinical value of this association. In this review, the authors will discuss the latest developments on this evolving issue. Specifically, the results of the latest studies, both positive and negative, will be discussed. Furthermore, potential theories to explain discrepancies reported in the literature will be proposed. Clinical implications including potential targets for anti-HCMV therapy and the latest developments in anti-HCMV therapy will be presented. Finally, solutions to remedy this controversial issue in neuro-oncology will be offered.
Aim: The pathogenesis of central nervous system infections (CNSI) has not been fully understood; some studies indicated that reactive oxygen species may induce brain damage. The aim of our study was to investigate serum antioxidant status in patients with CNSI.
Methods: The serum levels of uric acid (UA), bilirubin and albumin of 548 individuals were enrolled in our study, comprising of 114 healthy controls (HC) and 434 patients with five different kinds of CNSI, which including viral meningitis and/or meningoencephalitis, cysticercosis of brain, tuberculous meningitis and/or meningoencephalitis, cryptococcus meningitis and/or meningoencephalitis, and bacterial meningitis and/or meningoencephalitis.
Results: The data suggested that there were reducing levels of oxidation state (serum UA, bilirubin and albumin) in CNSI patients when compared with HC. Likewise, similar results were observed when cohorts were divided into male and female subgroups.
Conclusion: The authors demonstrated that serum antioxidant status in patients with CNSI was lower; the reason may be due to exhaustion of antioxidant capacity. Therefore, enhancing antioxidant power and keeping oxidative stress and antioxidants in balance may be beneficial to the patients with CNSI.
The last fifteen years have seen the application of the cancer stem cell hypothesis to tumors of the central nervous system, in particular to high grade glioma (HGG), the most aggressive and common brain cancer in adults. Seminal studies have shown that cancer stem cells (alternatively named tumor-initiating cells) are capable of self-renew and multipotency, similar to their normal counterpart. More importantly they give rise to tumors that closely mimic the phenotype and genotype of human HGG. The identification of neurogenic niches in adult rodent and human brain has further reinforced the hypothesis that HGG might derive from the malignant transformation occurring in these areas, especially in the sub-ventricular zone (SVZ), the largest and most well characterised stem cell niche. Following from evidence of animal model studies supporting this hypothesis, recently we investigated the role of the SVZ in neuro-oncogenesis using tissue material derived from HGG patients. We also described response to conventional chemo-therapies of cancer stem cells isolated from the SVZ and the tumor mass (T) of the same patients and reconstructed tumor evolution. In this review, such findings will be discussed in the context of the current literature on the biology of the SVZ in the normal and disease brain.
This review examines glioma disease initiation, promotion, and progression with a focus on the cell types present within the tumor mass and the molecules responsible for the immunosuppressive microenvironment that are present at each step of the disease. The cell types and molecules present also correlate with the grade of malignancy. An overall “type 2” chronic inflammatory microenvironment develops that facilitates glioma promotion and contributes to the neo‑vascularization characteristic of gliomas. An immunosuppressive microenvironment shields the tumor mass from clearance by the patient’s own immune system. Here, we provide suggestions to deal with a chronically‑inflamed tumor microenvironment and provide recommendations to help optimize adjuvant immune and gene therapies currently offered to glioma patients.