Amplifications and Metabolic Rewiring in Neuroblastoma.

Cancer is a disease caused by (epi)genomic and gene expression abnormalities and characterized by metabolic phenotypes that are substantially different from the normal phenotypes of the tissues of origin. Metabolic reprogramming is one of the key features of tumors, including those established in the human nervous system. In this work, we emphasize a well-known cancerous genomic alteration: the amplification of and its downstream effects in neuroblastoma phenotype evolution.

Histone H3K9 methyltransferase SETDB1 overexpression correlates with pediatric high-grade gliomas progression and prognosis.

Pediatric high-grade gliomas (pHGGs) are heterogeneous, diffuse, and highly infiltrative tumors with dismal prognosis. Aberrant post-translational histone modifications with elevated histone 3 lysine trimethylation (H3K9me3) have been recently implicated in pHGGs' pathology, conferring to tumor heterogeneity. The present study investigates the potential involvement of H3K9me3 methyltransferase SETDB1 in the cellular function, progression, and clinical significance of pHGG.

Emerging Roles of TRIM Family Proteins in Gliomas Pathogenesis.

Gliomas encompass a vast category of CNS tumors affecting both adults and children. Treatment and diagnosis are often impeded due to intratumor heterogeneity and the aggressive nature of the more malignant forms. It is therefore essential to elucidate the molecular mechanisms and explore the intracellular signaling pathways underlying tumor pathology to provide more promising diagnostic, prognostic, and therapeutic tools for gliomas.

Typical Enhancers, Super-Enhancers, and Cancers.

Non-coding segments of the human genome are enriched in -regulatory modules that constitute functional elements, such as transcriptional enhancers and Super-enhancers. A hallmark of cancer pathogenesis is the dramatic dysregulation of the "archetype" gene expression profiles of normal human cells. Genomic variations can promote such deficiencies when occurring across enhancers and Super-enhancers, since they affect their mechanistic principles, their functional capacity and specificity, and the epigenomic features of the chromatin microenvironment across which these regulatory elements reside.

Insights into the multi-faceted role of Pioneer transcription factors in glioma formation and progression with targeting options.

Pioneer transcription factors (TFs) present an important subtype of transcription factors which are vital for cell programming during embryonic development and cellular memory during mitotic growth, as well as cell fate reprogramming. Pioneer TFs can engage specific target binding sites on nucleosomal DNA to attract chromatin remodeling complexes, cofactors, and other transcription factors, ultimately controlling gene expression by shaping locally the epigenome. The priority of binding that they exhibit in contrast to other transcription factors and their involvement in crucial events regarding cell fate, has implicated their aberrant function in the pathogenesis of several disorders including carcinogenesis.

Transcription Factors with Targeting Potential in Gliomas.

Gliomas portray a large and heterogeneous group of CNS tumors, encompassing a wide range of low- to high-grade tumors, as defined by histological and molecular characteristics. The identification of signature mutations and other molecular abnormalities has largely impacted tumor classification, diagnosis, and therapy. Transcription factors (TFs) are master regulators of gene expression programs, which ultimately shape cell fate and homeostasis.