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Cover Image
Paclitaxel is an antimicrotubule agent that is known to target β-tubulin subunits. Ferlini and colleagues have demonstrated that paclitaxel also interacts with Bcl-2, and is able to convert its function from antiapoptotic to proapoptotic. The direct interaction was proven with surface plasmon resonance technology (biosensogram, bottom panel ). Using bioinformatics, modeling of the interaction was obtained (top panel ) and, through this approach, the authors discovered an extraordinary homology between the binding site in both paclitaxel targets (Bcl-2 and β-tubulin). This finding suggests the possibility that paclitaxel is a peptide-mimicking drug. The authors assessed this possibility and discovered that the mimicked protein is Nur77, a factor known for its ability to convert Bcl-2 from a protector to a cell killer. This discovery could lead to the development of better clinical use of paclitaxel, as well as a novel generation of anticancer agents sharing this mechanism of action. For additional information, please see the article by Ferlini and colleagues on page 6906 of this issue. - PDF Icon PDF LinkTable of Contents
Cancer Research
Table of Contents
Point-Counterpoint Reviews
Meeting Report
Cell, Tumor, and Stem Cell Biology
Ectopic Runx2 Expression in Mammary Epithelial Cells Disrupts Formation of Normal Acini Structure: Implications for Breast Cancer Progression
Clinical Research
Endocrinology
Epidemiology
The CHRNA5-CHRNA3-CHRNB4 Nicotinic Receptor Subunit Gene Cluster Affects Risk for Nicotine Dependence in African-Americans and in European-Americans
Polymorphisms in DNA Repair Genes, Smoking, and Bladder Cancer Risk: Findings from the International Consortium of Bladder Cancer
Experimental Therapeutics, Molecular Targets, and Chemical Biology
Fyn and Src Are Effectors of Oncogenic Epidermal Growth Factor Receptor Signaling in Glioblastoma Patients
Targeting Sphingosine Kinase 1 Inhibits Akt Signaling, Induces Apoptosis, and Suppresses Growth of Human Glioblastoma Cells and Xenografts
c-Jun NH2-Terminal Kinase Activation Is Essential for DRAM-Dependent Induction of Autophagy and Apoptosis in 2-Methoxyestradiol–Treated Ewing Sarcoma Cells
Preclinical Evaluation of Novel Glutamate-Urea-Lysine Analogues That Target Prostate-Specific Membrane Antigen as Molecular Imaging Pharmaceuticals for Prostate Cancer
Inhibitors of Deacetylases Suppress Oncogenic KIT Signaling, Acetylate HSP90, and Induce Apoptosis in Gastrointestinal Stromal Tumors
Distinct Concentration-Dependent Effects of the Polo-like Kinase 1–Specific Inhibitor GSK461364A, Including Differential Effect on Apoptosis
Immunology
Molecular Biology, Pathobiology, and Genetics
MicroRNA Expression, Chromosomal Alterations, and Immunoglobulin Variable Heavy Chain Hypermutations in Mantle Cell Lymphomas
Chromobox Protein Homologue 7 Protein, with Decreased Expression in Human Carcinomas, Positively Regulates E-Cadherin Expression by Interacting with the Histone Deacetylase 2 Protein
Prevention
Chemopreventive Effects of Gefitinib on Nonsmoking-Related Lung Tumorigenesis in Activating Epidermal Growth Factor Receptor Transgenic Mice
Systems Biology and Emerging Technologies
Tumor Microenvironment
Corrections
Journal Archive
Cancer Research
(1941-Present; volumes 1-current)Published twice monthly since 1987. From 1941-1986, published monthly.
(ISSN 0008-5472)
The American Journal of Cancer
(1931-1940; volumes 15-40)Published quarterly in 1931, bimonthly in 1932, and monthly from 1933 to 1940. The journal changed title to Cancer Research in 1941.
(ISSN 0099-7374)
The Journal of Cancer Research
(1916-1930); volumes 1-14)Published quarterly from 1916 through 1930 (publication was suspended from November 1922 to March 1924). The journal changed title to The American Journal of Cancer in 1931.
(ISSN 0099-7013)
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