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Clinical Cancer Research
Clinical Cancer Research
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About the Cover

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Epithelial junctions between tumor cells inhibit the penetration of anticancer drugs into tumors and represent one of the mechanisms that cancers use to protect themselves from attacks by the host-immune system as well as elimination by cancer therapeutics. Beyer and colleagues have developed a recombinant protein (JO-1), which triggers transient opening of intercellular junctions in epithelial tumors through binding to desmoglein 2 (DSG2) and thus increases the safety and therapeutic efficacy of monoclonal antibodies and chemotherapy drugs. Whereas DSG2 is readily accessible in tumors, in intestinal epithelial cells it is trapped in intercellular junctions as shown in the figure by overlapping signals for the DSG2 (green) and the junction marker claudin 7 (red). Therefore, JO-1 preferentially acts on epithelial junctions in tumors, thereby creating a “sink” for therapeutics. For details, see the article by Beyer and colleagues on page 3340 of this issue.

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Clinical Cancer Research: 18 (12)
June 2012
Volume 18, Issue 12
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Issue Highlights

  • Coadministration of Epithelial Junction Opener JO-1 Improves the Efficacy and Safety of Chemotherapeutic Drugs
  • Detection of Tumor PIK3CA Status in Metastatic Breast Cancer Using Peripheral Blood
  • Changes in Gene Transcription Underlying the Aberrant Citrate and Choline Metabolism in Human Prostate Cancer Samples
  • Profiling Three-Dimensional Nuclear Telomeric Architecture of Myelodysplastic Syndromes and Acute Myeloid Leukemia Defines Patient Subgroups
  • Phase I Trial of Combretastatin A4 Phosphate (CA4P) in Combination with Bevacizumab in Patients with Advanced Cancer
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Clinical Cancer Research
eISSN: 1557-3265
ISSN: 1078-0432

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