H. Artee Luchman

Elevated mutant frequencies and predominance of G:C to A:T transition mutations in Msh6(-/-) small intestinal epithelium.

Mutational-reporter transgenes rescued from mice lacking either Mgmt, or both Mgmt and Msh6 suggest that O6-alkylguanine-induced miscoding does not contribute to the spontaneous mutational spectrum.

Mgmt deficiency alters the in vivo mutational spectrum of tissues exposed to the tobacco carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).

Temporally controlled prostate epithelium-specific gene alterations.

The pace of prostatic intraepithelial neoplasia development is determined by the timing of Pten tumor suppressor gene excision.

An in vivo patient-derived model of endogenous IDH1-mutant glioma.

DNA hypermethylation and 1p Loss silence NHE-1 in oligodendroglioma.

On-target JAK2/STAT3 inhibition slows disease progression in orthotopic xenografts of human glioblastoma brain tumor stem cells.

Spontaneous loss of heterozygosity leading to homozygous R132H in a patient-derived IDH1 mutant cell line.

Prostate epithelium-specific deletion of the selenocysteine tRNA gene Trsp leads to early onset intraepithelial neoplasia.

Potent Targeting of the STAT3 Protein in Brain Cancer Stem Cells: A Promising Route for Treating Glioblastoma.

Novel MSH6 mutations in treatment-naïve glioblastoma and anaplastic oligodendroglioma contribute to temozolomide resistance independently of MGMT promoter methylation.

Dual mTORC1/2 blockade inhibits glioblastoma brain tumor initiating cells in vitro and in vivo and synergizes with temozolomide to increase orthotopic xenograft survival.

IDH1 Mutation Induces Reprogramming of Pyruvate Metabolism.

Precursor States of Brain Tumor Initiating Cell Lines Are Predictive of Survival in Xenografts and Associated with Glioblastoma Subtypes.

Comparative genomic and genetic analysis of glioblastoma-derived brain tumor-initiating cells and their parent tumors.

Control of glioblastoma tumorigenesis by feed-forward cytokine signaling.

Clonal expansion and epigenetic reprogramming following deletion or amplification of mutant .