Issues
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One of the visionary ideas of the late Dr. Judah Folkman was to treat cancer based on discovery of ultra-early biomarkers long before tumors become symptomatic or determination of their anatomical location is feasible. This idea was based on the hypothesis that most tumors remain dormant as microscopic lesions for a long period of time, until they gain the ability to recruit vessels in a process called tumor angiogenesis. Dormant tumors that switch to the angiogenic phenotype grow exponentially and ultimately become clinically apparent, which is referred to as the disease state of cancer. A major limitation in investigating the tumor dormancy process is the lack of suitable experimental models and the limited clinical accessibility of dormant tumors. In this report, Almog and colleagues identified the molecular determinants of tumor dormancy by characterizing the consensus transcriptome signature of dormant versus fast-growing experimental human osteosarcoma, liposarcoma, breast carcinoma, and glioblastoma multiforme tumor models. Differential regulation and activation of several signaling pathways not previously associated with the dormancy process are also reported and validated based on protein expression and activation levels. The molecular signature of tumor dormancy was further used to test the feasibility of selected proteins as blood (plasma)-based biomarkers in mice and in human specimens. The enhanced sensitivity of dormant tumors to angiostatin, compared with that of fast-growing angiogenic tumors, was correlated with selective uptake of angiostatin (green) in angiomotin (red)-positive dormant osteosarcoma cells (blue, cell nucleus). This work may provide molecular instructions for discovery of ultra-early tumor biomarkers and possible therapeutic targets for the blockage of early tumor development. For details, see the article by Almog and colleagues on page 836 of this issue. - PDF Icon PDF LinkTable of Contents
Cancer Research
Table of Contents
Reviews
Priority Reports
p34SEI-1 Inhibits Apoptosis through the Stabilization of the X-Linked Inhibitor of Apoptosis Protein: p34SEI-1 as a Novel Target for Anti–Breast Cancer Strategies
Faciogenital Dysplasia Protein Fgd1 Regulates Invadopodia Biogenesis and Extracellular Matrix Degradation and Is Up-regulated in Prostate and Breast Cancer
Large-Scale Profiling of Archival Lymph Nodes Reveals Pervasive Remodeling of the Follicular Lymphoma Methylome
Cell, Tumor, and Stem Cell Biology
Antitumor Effects of a Combined 5-Aza-2′Deoxycytidine and Valproic Acid Treatment on Rhabdomyosarcoma and Medulloblastoma in Ptch Mutant Mice
Endocrinology
Steroid Sulfatase and Estrogen Sulfotransferase in Colon Carcinoma: Regulators of Intratumoral Estrogen Concentrations and Potent Prognostic Factors
Epidemiology
Experimental Therapeutics, Molecular Targets, and Chemical Biology
Limits to Thymidylate Synthase and TP53 Genes as Predictive Determinants for Fluoropyrimidine Sensitivity and Further Evidence for RNA-Based Toxicity as a Major Influence
Inhibition of the Peptidyl-Prolyl-Isomerase Pin1 Enhances the Responses of Acute Myeloid Leukemia Cells to Retinoic Acid via Stabilization of RARα and PML-RARα
Immunology
A Long, Naturally Presented Immunodominant Epitope from NY-ESO-1 Tumor Antigen: Implications for Cancer Vaccine Design
Molecular Biology, Pathobiology, and Genetics
Prediction of Clinical Outcome in Multiple Lung Cancer Cohorts by Integrative Genomics: Implications for Chemotherapy Selection
IFN Regulatory Factor 8 Sensitizes Soft Tissue Sarcoma Cells to Death Receptor–Initiated Apoptosis via Repression of FLICE-like Protein Expression
Akt Activation Synergizes with Trp53 Loss in Oral Epithelium to Produce a Novel Mouse Model for Head and Neck Squamous Cell Carcinoma
Consistent Deregulation of Gene Expression between Human and Murine MLL Rearrangement Leukemias
Distinct Roles of BARD1 Isoforms in Mitosis: Full-Length BARD1 Mediates Aurora B Degradation, Cancer-Associated BARD1β Scaffolds Aurora B and BRCA2
Prevention
Systems Biology and Emerging Technologies
Tumor Microenvironment
Vasculostatin Inhibits Intracranial Glioma Growth and Negatively Regulates In vivo Angiogenesis through a CD36-Dependent Mechanism
Letters to the Editor
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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