Hyaluronan signaling and turnover /

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Bibliographic Details
Edition:First edition.
Imprint:San Diego, California : Elsevier, 2014.
©2014
Description:1 online resource (418 pages, 26 unnumbered pages of plates) : color illustrations
Language:English
Series:Advances in cancer research ; v. 123.
Subject:
Format: E-Resource Book
URL for this record:http://pi.lib.uchicago.edu/1001/cat/bib/12378568
Hidden Bibliographic Details
Other authors / contributors:Simpson, Melanie A., editor.
Heldin, Paraskevi, editor.
ISBN:9780128003930
0128003936
9780128000922
0128000929
Digital file characteristics:text file
Notes:Includes bibliographical references and index.
Text in English.
Online resource; title from PDF title page (ebrary, viewed August 5, 2014).
Summary:Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. Here, once again, outstanding and original reviews are presented on a variety of topics. This volume covers hyaluronan signaling and turnover. Provides information on cancer research Outstanding and original reviews Suitable for researchers and students.
Other form:Print version: Hyaluronan signaling and turnover. First edition. San Diego, California : Elsevier, ©2014 xvi, 385 pages Advances In Cancer Research ; Volume 123 0065-230X 9780128000922
Table of Contents:
  • Front Cover; Hyaluronan Signaling and Turnover; Copyright; Contents; Contributors; Preface; Chapter One: Emerging Roles for Hyaluronidase in Cancer Metastasis and Therapy; 1. Introduction; 2. Of Mole Rats and Men: Insights About HA and Cancer; 2.1. HA and hyaluronidase accelerate human cancers; 2.2. Naked mole rats resist cancer; 3. Hyaluronidase Expression in Cancer; 3.1. Hyal1; 3.2. Hyal2; 3.3. Hyal3, Hyal4, and PH-20; 4. Hyaluronidase Function and the Metastatic Process; 4.1. Vesicle trafficking and cell motility; 4.2. Vesicle shedding.
  • 4.3. Products of hyaluronidase: Fragments versus oligos4.4. Products of hyaluronidase: Beyond HA; 5. Hyaluronidase Targeting in Cancer Therapy and Imaging; 5.1. Structural and functional features of human Hyals; 5.2. Targeting of hyaluronidase for cancer therapy; 5.3. Hyaluronidase-targeting agents for tumor imaging; 6. Conclusions and Future Perspective; Acknowledgments; References; Chapter Two: Targeting Hyaluronic Acid Family for Cancer Chemoprevention and Therapy; 1. Introduction; 2. Targeting HA Production; 2.1. Targeting HA synthases; 2.2. Chemical inhibitors of HA synthesis.
  • 2.2.1. 4-Methylumbelliferone2.2.2. Other HA synthesis inhibitors; 3. Targeting HA Signaling; 3.1. HA oligosaccharides; 4. HA as a Carrier for Drug Delivery; 5. Targeting HA Receptors; 5.1. CD44; 5.1.1. CD44 vaccines; 5.1.2. CD44 siRNA delivery; 5.1.3. Targeting CD44 for delivering antitumor therapies; 5.1.4. Targeting of CD44 protein; 5.2. RHAMM; 6. Targeting HAase; 7. Conclusion; Acknowledgments; References; Chapter Three: Aberrant Posttranscriptional Processing of Hyaluronan Synthase 1 in Malignant Transformation and Tumor Prog ... ; 1. Splicing and Cancer; 1.1. Splicing in the human genome.
  • 2. Control of Pre-mRNA Splicing2.1. Splicing mutations; 3. Impact on Cancer of Alterations in Splicing Machinery; 4. Aberrant Splicing of Hyaluronan Synthase 1; 4.1. B lineage malignancies; 4.1.1. Multiple myeloma; 4.1.2. Waldenstrom macroglobulinemia; 4.2. Aberrant splice variants in hyaluronan synthase 1; 5. Clinical Impact of Aberrant HAS1 Splicing; 6. Genetic Variations in HAS1; 7. Functional Impact of HAS1Vs; 7.1. Synthesis of HA; 7.2. Functional outcomes of HA synthesis in patients; 7.2.1. Motility and malignant spread; 7.2.2. HAS1Vs and oncogenic events.
  • 7.2.3. Intermolecular interactions of HAS1Vs7.2.4. HAS1Vs and genetic instability; 8. Functional Outcomes of HAS1Vs in Transfectants; 8.1. HAS1Vs synthesize intracellular HA; 8.2. HAS1FL and HAS1Vs form heteromultimers with HAS1Vs as the dominant partners; 8.3. Multimers with HAS1Vs stabilize HAS1FL and maintain intracellular HA; 9. HAS1Vs and Mitotic Catastrophe; 9.1. A potential mechanism underlying the oncogenic properties of aberrant HAS1 splice variants: HAS1V-mediated rescue fro ... ; 9.1.1. Receptor for hyaluronan-mediated motility (RHAMM).