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Correction to: CDKN2A/B deletion in IDH-mutant astrocytomas: An evaluation by Fluorescence in-situ hybridization.
J Neurooncol
March 2024
Department of Radiation Oncology, Tata Memorial Hospital & ACTREC, Tata Memorial Centre, Homi Bhabha National Institute, Mumbai, India.
Homophilic interaction of cell adhesion molecule 3 coordinates retina neuroepithelial cell proliferation.
J Cell Biol
June 2023
State Key Laboratory of Neuroscience, Institute of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, China.
Correct cell number generation is central to tissue development. However, in vivo roles of coordinated proliferation of individual neural progenitors in regulating cell numbers of developing neural tissues and the underlying molecular mechanism remain mostly elusive. Here, we showed that wild-type (WT) donor retinal progenitor cells (RPCs) generated significantly expanded clones in host retinae with G1-lengthening by p15 (cdkn2a/b) overexpression (p15+) in zebrafish.
View Article and Find Full Text PDFThe impact of heme biosynthesis regulation on glioma aggressiveness: Correlations with diagnostic molecular markers.
Front Mol Neurosci
September 2022
Department of Neurosurgery, Medical University of Vienna, Vienna, Austria.
Background: The prognosis of diffusely infiltrating glioma patients is dismal but varies greatly between individuals. While characterization of gliomas primarily relied on histopathological features, molecular markers increasingly gained importance and play a key role in the recently published 5 edition of the World Health Organization (WHO) classification. Heme biosynthesis represents a crucial pathway due to its paramount importance in oxygen transport, energy production and drug metabolism.
View Article and Find Full Text PDFComprehensive genomic profiling of EWSR1/FUS::CREB translocation-associated tumors uncovers prognostically significant recurrent genetic alterations and methylation-transcriptional correlates.
Mod Pathol
August 2022
Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
To elucidate the mechanisms underlying the divergent clinicopathologic spectrum of EWSR1/FUS::CREB translocation-associated tumors, we performed a comprehensive genomic analysis of fusion transcript variants, recurrent genetic alterations (mutations, copy number alterations), gene expression, and methylation profiles across a large cohort of tumor types. The distribution of the EWSR1/FUS fusion partners-ATF1, CREB1, and CREM-and exon involvement was significantly different across different tumor types. Our targeted sequencing showed that secondary genetic events are associated with tumor type rather than fusion type.
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