Human glioblastoma-associated microglia/monocytes express a distinct RNA profile compared to human control and murine samples

Ion Channel Expression Patterns in Glioblastoma Stem Cells with Functional and Therapeutic Implications for Malignancy

ZNF131 suppresses centrosome fragmentation in Glioblastoma stem-like cells through regulation of HAUS5

N6-methyladenosine mRNA marking promotes selective translation of regulons required for human erythropoiesis [RNA-Seq]

Pseudouridylation of tRNA-derived fragments steers translation control in stem cells [Polysome-Seq]

N6-methyladenosine mRNA marking promotes selective translation of regulons required for human erythropoiesis[Ribosome Profiling]

N6-methyladenosine mRNA marking promotes selective translation of regulons required for human erythropoiesis

CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors [Bulk RNA-seq]

CRISPR-Cas9 Screens Reveal Genes Regulating a G0-like State in Human Neural Progenitors

Multiplexed functional genomic analysis of somatic 5' untranslated region mutations across the spectrum of human prostate cancer (Ribosome Profiling)

NTRK2 splice variant, TrkB.T1, is the predominant isoform in gliomas and enhances gliomagenesis via PI3K signaling

Comparison of tumor-associated YAP1 fusions identifies a recurrent set of functions critical for oncogenesis[RNASeq]

Comparison of tumor-associated YAP1 fusions identifies a recurrent set of functions critical for oncogenesis

A simple and highly efficient method for multi-allelic CRISPR-Cas9 editing in primary cell cultures

Multiplexed functional genomic analysis of somatic 5' untranslated region mutations across the spectrum of human prostate cancer (PLUMAGE)

Multiplexed functional genomic analysis of somatic 5’ untranslated region mutations across the spectrum of human prostate cancer

A bladder cancer patient-derived xenograft reflects aggressive growth dynamics in vivo and in organoids

KAT5 activity regulates quiescent-like states in human gliomas.

Both YAP1-MAML2 and constitutively active YAP1 drive the formation of tumors that resemble NF2 mutant meningiomas in mice [human]

Both YAP1-MAML2 and constitutively active YAP1 drive the formation of tumors that resemble NF2 mutant meningiomas in mice