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Primary Phone: (520) 6264646
Arizona Cancer Center 3925
University of Arizona
Tucson AZ 85721
Primary Phone: (520) 6264646
PhD, Pharmacology and Toxicology
- College Of Pharmacy
Functional genomics; molecular biology of cancer; cancer pharmacology.
Environmental Health Research & Expertise:
Dr. Futscher is a member of the SWEHSC as an expert in epigenetics. Dr. Futscher is providing epigenetic analyses in many collaborative studies including developmental toxicity studies (Lantz-RFG2 - lung; Camenisch-RFG1-heart), genetic susceptibility (Klimecki-RFG1), and bladder cancer(Gandolfi-RFG1). He has been included in the recently renewed Superfund Program and currently has an NCI/NIEHS grant on "epigenetic remodeling following arsenical exposure" with both Klimecki and Gandolfi as Co-Is. He has also been able to translate his studies to exposed populations using the IHSFC Core for recruiting and sampling. In addition, Dr. Futscher was the founding director of the Genomics Shared Service and is currently its Scientific Director.
- Genetic and epigenetic inactivation of extracellular superoxide dismutase promotes an invasive phenotype in human lung cancer by disrupting ECM homeostasis.
- Epigenetic regulation of normal human mammary cell type-specific miRNAs.
- Hypomethylation of the 14-3-3σ promoter leads to increased expression in non-small cell lung cancer.
- Arsenic toxicology: translating between experimental models and human pathology.
- Monomethylarsonous acid produces irreversible events resulting in malignant transformation of a human bladder cell line following 12 weeks of low-level exposure.
- Role for DNA methylation in the regulation of miR-200c and miR-141 expression in normal and cancer cells.
- Arsenicals produce stable progressive changes in DNA methylation patterns that are linked to malignant transformation of immortalized urothelial cells.
- Stepwise DNA methylation changes are linked to escape from defined proliferation barriers and mammary epithelial cell immortalization.
- Epigenetic mediated transcriptional activation of WNT5A participates in arsenical-associated malignant transformation.
- p53 induces distinct epigenetic states at its direct target promoters.
- DNA methylation changes in ovarian cancer are cumulative with disease progression and identify tumor stage.
- Epigenetic remodeling during arsenical-induced malignant transformation.
- Epigenetic inactivation of the HOXA gene cluster in breast cancer.
- Epigenetic regulation of maspin expression in human ovarian carcinoma cells.
- Epigenetic silencing of DSC3 is a common event in human breast cancer.
- Role for DNA methylation in the control of cell type specific maspin expression. Previous years
- Epigenetic changes during cell transformation.
- Human Cell Surface Receptors as Molecular Imaging Candidates for Metastatic Prostate Cancer.
- Agglomerative epigenetic aberrations are a common event in human breast cancer.
- Optimal search-based gene subset selection for gene array cancer classification.
- MnSOD up-regulates maspin tumor suppressor gene expression in human breast and prostate cancer cells.
- Human pancreatic carcinoma cells activate maspin expression through loss of epigenetic control.
- Mutant p53 and aberrant cytosine methylation cooperate to silence gene expression.
- Editorial: maspin as a molecular target for cancer therapy.
- Development and molecular characterization of HCT-116 cell lines resistant to the tumor promoter and multiple stress-inducer, deoxycholate.
- The acetyltransferase p300/CBP-associated factor is a p53 target gene in breast tumor cells.
- Flipping the epigenetic switch.
- Pharmacogenomics of the polyamine analog 3,8,13,18-tetraaza-10,11-[(E)-1,2-cyclopropyl]eicosane tetrahydrochloride, CGC-11093, in the colon adenocarcinoma cell line HCT1161.
- Comparisons of PCR-based genome amplification systems using CpG island microarrays.
- Epigenetic regulation of the cell type-specific gene 14-3-3sigma.
- Aberrant methylation of the maspin promoter is an early event in human breast cancer.
- Different mutant/wild-type p53 combinations cause a spectrum of increased invasive potential in nonmalignant immortalized human mammary epithelial cells.