The creation and characterization of permanent cell lines derived from primary human gliomas in the 1960s gave scientists access to unlimited, renewable material in which to study the development of brain tumors. These cells, however, were already tumorigenic and selected for growth in culture, limiting the amount of information that could be gathered about the events that led to the formation of their tumors of origin. In response to these limitations, investigators moved to the study of primary tumors to identify in a correlative fashion the lesions important in tumor formation, and to the use of animal models to gain information about the transformation process. While these approaches have been unarguably successful, they too are limited by their correlative nature (in the case of cytogenetic studies) and their potential lack of direct relevance to human cancer (in the case of mouse models). Recent developments in the isolation and manipulation of human cells have allowed investigators a fresh chance to address questions about brain tumors in a direct fashion. The present review serves as a summary of important recent findings derived from the use of defined human cells in the study of gliomas.
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http://dx.doi.org/10.2741/983 | DOI Listing |
JMIR Cancer
January 2025
Kulliyah of Nursing, International Islamic University Malaysia, Selangor, Malaysia.
Background: Many cancer survivors experience a wide range of symptoms closely linked to psychological problems, highlighting the need for psychological treatment, one of the most popular being mindfulness. The use of the internet has greatly increased in the last decade, and has encouraged the use of remote-based interventions to help people living with cancer access treatment remotely via devices.
Objective: The primary aim of this study was to explore the efficacy of internet-based mindfulness interventions on the physical symptoms of people living with cancer, where physical symptoms are defined as distressing somatic experiences (eg fatigue, insomnia, and pain) regardless of the underlying cause.
STAR Protoc
January 2025
Institute for Stem Cell Biology & Regenerative Medicine, Stanford University, Stanford, CA 94305, USA; Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA. Electronic address:
Hematopoietic stem cells (HSCs) generate blood and immune cells. Here, we present a protocol to differentiate human pluripotent stem cells (hPSCs) into hematopoietic progenitors that express the signature HSC transcription factors HLF, HOXA5, HOXA7, HOXA9, and HOXA10. hPSCs are dissociated, seeded, and then sequentially differentiated into posterior primitive streak, lateral mesoderm, artery endothelium, hemogenic endothelium, and hematopoietic progenitors through the sequential addition of defined, serum-free media.
View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Endocrinology Department, School of Medicine, Pontificia Universidad Católica de Chile, Av. Diagonal Paraguay 262, Cuarto Piso, Santiago, Chile.
X-linked hypophosphatemia (XLH) is a rare metabolic disorder characterized by elevated FGF23 and chronic hypophosphatemia, leading to impaired skeletal mineralization and enthesopathies that are associated with pain, stiffness, and diminished quality of life. The natural history of enthesopathies in XLH remains poorly defined, partly due to absence of a sensitive quantitative tool for assessment and monitoring. This study investigates the utility of 18F-NaF PET/CT scans in characterizing enthesopathies in XLH subjects.
View Article and Find Full Text PDFPediatr Surg Int
January 2025
Division of Pediatric Surgery, Department of Surgery, University of Florida College of Medicine, PO Box 100119, Gainesville, FL, 32610-0119, USA.
Purpose: Initial recommendations for ECMO had relative contraindications for low birth weight (BW) or low gestational age (GA) babies. However, more recent literature has demonstrated improved and acceptable outcomes of ECMO in smaller neonates. The purpose of this study was to understand both utilization and survival in patients with lower GA and BW.
View Article and Find Full Text PDFCancer Biol Ther
December 2025
Department of Pharmacology, Physiology, and Cancer Biology, Thomas Jefferson University, Philadelphia, PA, USA.
Adaptive immune resistance in cancer describes the various mechanisms by which tumors adapt to evade anti-tumor immune responses. IFN-γ induction of programmed death-ligand 1 (PD-L1) was the first defined and validated adaptive immune resistance mechanism. The endoplasmic reticulum (ER) is central to adaptive immune resistance as immune modulatory secreted and integral membrane proteins are dependent on ER.
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