11 results match your criteria: "Arizona Cancer Center and BIO5 Institute[Affiliation]"
Anticancer Res
February 2017
Cardiff China Medical Research Collaborative, Cardiff University School of Medicine, Cardiff, U.K.
Unlabelled: More men die with prostate cancer (PCa) than from it. However, once PCa is no longer organ-confined, it is associated with significant mortality. Epithelial-to-mesenchymal transition (EMT) is one mechanism facilitating progression in cancer.
View Article and Find Full Text PDFJ Am Chem Soc
August 2016
Biodesign Center for BioEnergetics, and School of Molecular Sciences, Arizona State University, Tempe, Arizona 85287, United States.
The recently discovered role of the BCL2 (B-cell lymphoma 2 gene) promoter i-motif DNA in modulation of gene expression via interaction with the ribonucleoprotein hnRNP L-like (hnRNP LL) has prompted a more detailed study of the nature of this protein-DNA interaction. The RNA recognition motifs (RRMs) of hnRNP LL were expressed individually, and both RRM1 and RRM2 were found to bind efficiently to the BCL2 i-motif DNA, as well as being critical for transcriptional activation, whereas RRM3-4 bound only weakly to this DNA. Binding was followed by unfolding of the DNA as monitored by changes in the CD spectrum.
View Article and Find Full Text PDFBMJ
May 2016
Atomic Oncology, Newport, NSW 2106, Australia.
Curr Med Chem
October 2014
Department of Pathology, University of Arizona College of Medicine, The Arizona Cancer Center and BIO5 Institute, Tucson, AZ 85724-5043 USA.
Unlabelled: Neuroendocrine prostate carcinoma (NE-PCa) is a heterogeneous disease. Due to a high prevalence of NE (neuroendocrine) differentiation in patients who receive prolonged androgen deprivation treatment, the real incidence of NE-PCa remains unknown. Similarly, the biological steps from prostate carcinoma (PCa) toward NE differentiation are far less than definitive and, consequently, there is a lack of evidence to support any of the treatments as the "gold standard".
View Article and Find Full Text PDFCell Adh Migr
August 2013
Department of Molecular and Cellular Biology, Arizona Cancer Center and BIO5 Institute, University of Arizona, Tucson, AZ, USA.
MUC1 is a transmembrane mucin that is often overexpressed in metastatic cancers and often used as a diagnostic marker for metastatic progression. The extracellular domain of MUC1 can serve as a ligand for stromal and endothelial cell adhesion receptors, and the cytoplasmic domain engages in several interactions that can result in increased migration and invasion, as well as survival. In this review, we address the role of MUC1 in metastatic progression by assessing clinical studies reporting MUC1 levels at various disease stages, reviewing mouse models utilized to study the role of MUC1 in metastatic progression, discuss mechanisms of MUC1 upregulation, and detail MUC1 protein interactions and signaling events.
View Article and Find Full Text PDFCancer Epidemiol Biomarkers Prev
March 2012
Department of Pathology, University of Arizona College of Medicine, The Arizona Cancer Center and BIO5 Institute, Tucson, Arizona 85724, USA.
Curr Oncol
October 2011
Department of Pathology, University of Arizona College of Medicine, Arizona Cancer Center and BIO5 Institute, Tucson, AZ, U.S.A.
J Transl Med
April 2011
Department of Pathology, University of Arizona College of Medicine, Arizona Cancer Center and BIO5 Institute, Tucson, Arizona, AZ 85724-5043 USA.
Background: Transglutamiase-4 (TGase-4), also known as prostate transglutaminase, belongs to the TGase family and is uniquely expressed in the prostate gland. The functions of this interesting protein are not clearly defined. In the present study, we have investigated an unexpected link between TGase-4 and the melanoma differentiation-associated gene-7/interleukin-24 (MDA-7/IL-24), a cytokine known to regulate the growth and apoptosis of certain cancer and immune cells.
View Article and Find Full Text PDFJ Transl Med
October 2010
Department of Pathology, University of Arizona College of Medicine, Arizona Cancer Center and BIO5 Institute, Tucson, AZ 85724, USA.
Oncogene
March 2007
Department of Molecular and Cellular Biology, Arizona Cancer Center and Bio5 Institute, University of Arizona, Tucson, AZ 85724, USA.
ErbB receptors are key regulators of cell survival and growth in normal and transformed tissues. The oncogenic glycoprotein MUC1 is a binding partner and substrate for erbB1 and MUC1 expression can potentiate erbB-dependent signal transduction. After receptor activation, erbB1 is typically downregulated via an endocytic pathway that results in receptor degradation or recycling.
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