Advances in cancer research

Advances in cancer research

by Grant, Steven

Type Book
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Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. This thematic volume looks at ""Histone Deacetylase Inhibitors as Cancer Therapeutics."" Provides invaluable information on the exciting and fast-moving field of cancer researchThis thematic volume looks at ""Histone Deacetylase Inhibitors as Cancer Therapeutics""Outstanding and original reviews.

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Title Statements

  • Full title :Advances in cancer research / edited by Steven Grant.

Summary

Advances in Cancer Research provides invaluable information on the exciting and fast-moving field of cancer research. This thematic volume looks at ""Histone Deacetylase Inhibitors as Cancer Therapeutics."" Provides invaluable information on the exciting and fast-moving field of cancer researchThis thematic volume looks at ""Histone Deacetylase Inhibitors as Cancer Therapeutics""Outstanding and original reviews.

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Edition Statements

  • Publication Date:2012.
  • Edition:1st ed

Publication Statements

  • Publisher(s):Elsevier
  • Place of Publication:Amsterdam
  • Language:eng
  • Publication Date:2012.

Notes

4.1. Studies in knockout mice

The Physical Object

  • Description:1 online resource (289 pages)

Edition Identifiers

  • ISBN:1283706547, 9781283706544, 0123946085, 9780123946089, 9780123943873, 0123943876
  • oclc:on1113010615
  • LC Classification:RC267
  • Dewey Decimal:571.9/36

Table of Contents

Front Cover; Histone Deacetylase Inhibitors asCancer Therapeutics; Copyright; Contents; Contributors; Preface; Chapter 1: Histone Deacetylase Inhibitors Disrupt the Mitotic Spindle Assembly Checkpoint By Targeting Histone and Nonhistone Proteins; 1. Introduction; 2. HDACi Dysregulate Cell Cycle Progression; 2.1. HDACi-induced G1 phase arrest; 2.2. HDACi-induced G2/M phase responses; 2.3. Mechanisms governing normal G2/M phase progression; 2.4. HDACi-sensitive G2 phase arrest; 3. HDACi Disrupt Normal Mitosis; 3.1. Mitotic effects of HDACi treatment; 3.2. The SAC

3.3. The centromere: the constitutive heterochromatin underlying the kinetochore3.4. Cohesins: maintaining sister chromatid cohesion until anaphase; 3.5. SAC activation is required for signaling apoptosis after mitotic failure; 4. Mechanism of HDACi-Induced Aberrant Mitosis; 4.1. HDACi treatment overcomes the SAC by disrupting CPC localization to the centromere in mitosis; 4.2. HDACi disrupts Aurora B localization to the centromere; 4.3. Nonhistone targets HDACi can contribute to aberrant mitosis; 4.4. HDACi kill tumor cells by driving premature exit from aberrant mitosis; 5. Conclusions

2.4.4. Retinoic acid signaling2.5.…

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Subjects

Cancer -- Recherche Cancer -- Traitement Cancer -- Treatment Cancer Research

Writers

Grant, Steven Grant, Steven

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