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Lance D. Miller

Researcher at Wake Forest University

Publications -  208
Citations -  16169

Lance D. Miller is an academic researcher from Wake Forest University. The author has contributed to research in topics: Cancer & Breast cancer. The author has an hindex of 58, co-authored 195 publications receiving 14459 citations. Previous affiliations of Lance D. Miller include University of Texas MD Anderson Cancer Center & East Carolina University.

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Discovery of estrogen receptor α target genes and response elements in breast tumor cells

TL;DR: Only a small core set of human genes appear to be sufficient to induce ER effects in breast cancer cells, and that cis-regulatory regions of these core ER target genes are poorly conserved suggests that different evolutionary mechanisms are operative at transcriptional control elements than at coding regions.
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Conservation of gene expression signatures between zebrafish and human liver tumors and tumor progression

TL;DR: Comparative analysis of microarray data from zebrafish liver tumors with those from four human tumor types revealed molecular conservation at various levels between fish and human tumors, providing a useful strategy for identifying an expression signature that is strongly associated with a disease phenotype.
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Intrinsic molecular signature of breast cancer in a population-based cohort of 412 patients.

TL;DR: The intrinsic gene set, originally selected to reveal stable tumor characteristics, was shown to have a strong correlation with progression-related properties such as grade, p53 mutation and genomic instability.
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Prospective Molecular Profiling of Melanoma Metastases Suggests Classifiers of Immune Responsiveness

TL;DR: Ranking of gene expression data from pretreatment samples identified approximately 30 genes predictive of clinical response, suggesting that immune responsiveness might be predetermined by a tumor microenvironment conducive to immune recognition.
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Iron addiction: a novel therapeutic target in ovarian cancer

TL;DR: The iron dependence of ovarian cancer TICs renders them exquisitely sensitive in vivo to agents that induce iron-dependent cell death (ferroptosis) as well as iron chelators, and thus creates a metabolic vulnerability that can be exploited therapeutically.