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David A. Solomon

Researcher at University of California, San Francisco

Publications -  181
Citations -  7229

David A. Solomon is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 39, co-authored 149 publications receiving 5219 citations. Previous affiliations of David A. Solomon include University of Cincinnati Academic Health Center & Georgetown University.

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Mutational Inactivation of STAG2 Causes Aneuploidy in Human Cancer

TL;DR: Studying a near-diploid human cell line with a stable karyotype, it is found that targeted inactivation of STAG2 led to chromatid cohesion defects and aneuploidy, whereas in two aneuPLoid human glioblastoma cell lines, targeted correction of the endogenous mutant alleles of STAE led to enhanced chromosomal stability.
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Pharmacologic inhibition of histone demethylation as a therapy for pediatric brainstem glioma

TL;DR: It is shown that GSKJ4 pharmacologic inhibition of K27 demethylase JMJD3 increases cellular H3K27 methylation in K27M tumor cells and demonstrate potent antitumor activity both in vitro against K 27M cells and in vivo against K27m xenografts.
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cIMPACT-NOW update 6: new entity and diagnostic principle recommendations of the cIMPACT-Utrecht meeting on future CNS tumor classification and grading.

TL;DR: Working Committee 3 recommended that a substantial number of newly recognized types and subtypes should be considered for inclusion in future CNS tumor classifications.
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The genomic landscape of the Ewing Sarcoma family of tumors reveals recurrent STAG2 mutation

TL;DR: The largest genomic survey to date of 101 EFT (65 tumors and 36 cell lines) is reported, finding that EFT has a very low mutational burden but frequent deleterious mutations in the cohesin complex subunit STAG2 and that 11% of tumors pathologically diagnosed as EFT lack a typical EWSR1 fusion oncogene and these tumors do not have a characteristic Ewing sarcoma gene expression signature.
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Diffuse Midline Gliomas with Histone H3-K27M Mutation: A Series of 47 Cases Assessing the Spectrum of Morphologic Variation and Associated Genetic Alterations

TL;DR: A series of 47 diffuse midline gliomas with histone H3‐K27M mutation is described, involving 25 male and 22 female patients and centered not only in the pons, thalamus, and spinal cord, but also in the third ventricle, hypothalamus, pineal region and cerebellum.