β-Glucan, a complex polysaccharide derived from fungal and yeast cell walls, plays a crucial role in modulating immune responses through their interaction with receptors such as Dectin-1 and Complement receptor 3 (CR-3). This review provides an in-depth analysis of the molecular mechanisms by which β-glucans activate receptor-mediated signalling pathways, focusing particularly on the LC3-associated phagocytosis (LAP) and autophagy pathways. Hence, we explore how β-glucan receptor engagement stimulates NADPH oxidase 2 (NOX-2), leading to the intracellular production of significant level of reactive oxygen species (ROS) essential for both conventional autophagy and LAP. While significant progress has been made in elucidation of downstream signaling by glucans, the regulation of phago-lysosomal maturation and antigen presentation during LAP induction still remains less explored. This review aims to provide a comprehensive overview of these pathways and their regulation by β-glucans. By consolidating the current knowledge, we seek to highlight how these mechanisms can be leveraged for therapeutic applications, particularly in the context of tuberculosis (TB) management, where β-glucans could serve as host-directed adjuvant therapies to combat drug-resistant strains. Despite major advancements in this field, currently key research gaps still persist, including detailed molecular interactions between β-glucan receptors and NOX-2 and the translation of these findings to in-vivo models and clinical investigations. This review underscores the need for further research to explore the therapeutic potential of β-glucans in managing not only tuberculosis but also other diseases such as cancer, cardiovascular conditions, and metabolic disorders.

Background: The World Health Organization (WHO) classification of central nervous system (CNS) tumors necessitates testing of isocitrate dehydrogenase (IDH) 1/2 gene mutation in patients with adult-type diffuse glioma (ADG) for better disease management. In clinical practice, the testing of IDH1 is primarily achieved using immunohistochemistry (IHC) specific to IDH1-R132, which carries a sensitivity of 80% and specificity of 100%. However, in some cases, non-specific background staining or regional heterogeneity in the protein expression of IDH1 may necessitate confirmatory genetic analysis. Robust and reliable assays are needed for IDH1/2 mutation testing. The aim of the current study was to detect IDH1 mutation in cfDNA and tissue of adult-type diffuse glioma with allele-specific qPCR. Materials and Methods: In the current study, IDH1-R132H mutation was analyzed in tumor tissue with paired cell-free DNA (cfDNA) in patients with ADG (n = 45) using IHC and competitive allele-specific Taqman PCR (CAST-PCR). Genomic DNA was extracted from formalin-fixed paraffin-embedded (FFPE) tissue and matched serum for cfDNA using commercially available kits. CAST-PCR with IHC for the detection of IDH1-R132H mutation was also compared. Results: The IDH1-R132H mutation was detected in 46.67% (21/45) cases and 57.78% (26/45) cases using IHC and allele-specific CAST-PCR. In cfDNA of matched IDH1-mutant FFPE tissue DNA, IDH1-R132H mutation was detected in 11.54% (3/26) using CAST-PCR. The concordance rate for IDH1-R132Hmutation between IHC and CAST-PCR was 80.77% (21/26). Conclusion: The CAST-PCR assay is more precise and sensitive for IDH1-R132Hdetection than traditional IHC, and IDH1-R132H mutation detection using cfDNA may add to the current methods of glioma genomic characterization.

Precise classification of central nervous system (CNS) malignancies is vital for the treatment and prognostication. Identification of noninvasive markers can be of importance to guide treatment decisions and in monitoring treatment response. CNS tumors are classified based on morphology with an essential complement of molecular changes, including mutations, amplifications, and methylation. Neuroimaging is the mainstay for initial diagnosis and monitoring tumor response with obvious limitations of imprecise tumor typing and no information on diagnostic, predictive and prognostic markers. Liquid biopsy has evolved as a diagnostic tool in body fluids and is being investigated as a surrogate for tissue biopsy in managing primary and metastatic brain tumors. Liquid biopsy refers to analyzing biological fluids such as peripheral blood, urine, pleural effusion, ascites, and cerebrospinal fluid (CSF); however, peripheral blood remains the primary source of fluid biopsy. The analytes include cell-free DNA (cfDNA) circulating tumor cells (CTCs), circulating micro RNAs (miRNAs), circulating proteins and extracellular vesicles (EVs). Analysis of these components is actively used for early cancer detection, auxiliary staging, prognosis assessment, detection of minimal residual disease (MRD), and monitoring drug resistance in various solid tumors. In recent years, liquid biopsy has been studied in CNS tumors, and analysis of CTCs and cfDNA have become relevant research topics. In the current review, we have explained the clinical potential of liquid biopsy in CNS tumors to assist in diagnosing and predicting prognosis and response to treatment.