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Provides information on the exciting and fast-moving field of cancer research.
This book reviews the latest developments in the design, synthesis, and molecular mechanism of action of Histone Deacetylase (HDAC) inhibitors in the context of potential cancer therapy. HDAC inhibitors are emerging as promising anticancer drug molecules that promote growth arrest, differentiation and apoptosis of cancer cells with tumor selective toxicity. The book begins with an overview of various epigenetic modifying enzymes that are involved in cancer transition and progression; before exploring the potential of HDACs in cancer treatment. It provides a classification of HDAC inhibitors based on their structural attributes, and addresses HDAC-induced cytotoxicity.. Lastly, it discusses and assesses the rationale behind therapies that combine HDAC inhibitors with other anticancer agents to treat solid tumors. Given its scope, it offers a valuable resource for all researchers, clinicians, and students working in formulation, drug discovery, oncology, and personalized medicine.
Activating mutations of ras genes are frequently found in human cancers. Since Ras proteins and their functions play an important role in tumorigenesis, it is important to develop targeted anticancer therapeutics against Ras-related human cancers. We observed that in addition to tumorigenic ability, oncogenic H-Ras possesses a novel proapoptotic ability to facilitate the induction of apoptosis by histone deacetylase inhibitors (HDACIs), such as FR901228 and trichostatin A (TSA). HDACIs make up a new class of structurally diverse anticancer agents and have been shown to exhibit antimetastatic and antiangiogenic activities toward malignantly transformed cells. We detected that expression of oncogenic H-Ras potentiated intracellular reactive oxygen species (ROS) in human and mouse cells to enhance HDACI-induced ROS, thereby contributing to the induction of selective apoptosis and caspase activation. The first part (Part I) of this dissertation focuses on the understanding of Ras proteins, their role in normal and transformed cell physiology, and current treatment options against Ras-related human cancers, as well as the role of HDACIs and ROS in anticancer therapeutics. The next three parts (Part II-IV) focus on revealing the mechanisms for the novel pro-apoptotic ability of oncogenic H-Ras that allow HDACIs to induce selective apoptosis of the oncogenic H-Ras expressing cells. Results in Part II & III verify the pro-apoptotic activity of oncogenic H-Ras in the increased susceptibility of human cancer cells to HDACIs. The caspase pathways, the B-Raf and extracellular signal regulated kinase pathway, p21[superscript Cip]1 and p27[superscript Kip]1, and core histone contents are regulated differently by FR901228 in oncogenic H-Ras-expressed cells than their counterparts in parental cells, contributing to the increased susceptibility to the induction of selective apoptosis. Results in Part IV describe the role of reactive oxygen species in the pro-apoptotic ability of oncogenic H-Ras to enhance the cell susceptibility to HDACIs. Intracellular ROS was cooperatively up-regulated by oncogenc H-Ras and HDACI treatment to induce selective apoptosis of oncogenic H-Ras-expressing cells. The last section (Part V) summarizes the findings with their importance and discusses future directions.
Histone Modifications in Therapy provides an in-depth analysis of the role of histone mechanisms in major diseases and the promise of targeting histone modifications for disease prevention and treatment. Here, researchers, clinicians and students will discover a thorough, evidence-based discussion of the biology of histones, the diseases engaged by aberrant histone modifications, and pathways with therapeutic potential. Expert chapter addresses the role of histone modifications across a variety of disorders, including cancer, neuropsychiatric, neurodegenerative, cardiac, metabolic, infectious, bacterial, autoimmune and inflammatory disorders, among others. In relation to these disease types, histone modifications are discussed, both as mechanisms of prevention and possible treatment. A concluding chapter brings together future perspectives for targeting histone modifications in therapy and next steps in research. Examines the use of histone modifications in disease prevention and therapy Explores the role of histone modifications in cancer, neuropsychiatric, neurodegenerative, cardiac, metabolic, infectious, bacterial, and inflammatory disease, among others Features chapters from a broad range of international authors and disease specialists
Natural HDAC Inhibitors for Epigenetic Combating of Cancer Progression deals only with HDAC inhibitors from natural origins including bacteria, fungi, marine organisms and, notably, from diverse plant sources. This book is unique in the sense that it is the only book that discusses wholly and solely HDAC inhibitors of natural origin in the context of cancer chemotherapy. Another peculiar feature of this book is that it debates futuristic nanotechnology approaches for escalating the aqueous solubility, cancer cell uptake, bioavailability and other favourable pharmacological parameters, including the cytotoxicity of natural HDAC inhibitors against cancer cells. The major features of this book encompass General compendium of HDAC inhibitors with deep emphasis on the toxicity issues of synthetic HDAC inhibitors Various groups of natural HDAC inhibitors, their representatives and premier sources Cyclic tetrapeptides of natural origin and their importance as cancer chemotherapeutic agents Hydroxamates and depsipeptides from natural sources and their promising role in cancer therapy Natural flavonoids, their HDAC inhibitory tendency and marvellous anticancer activity Non-flavonoid natural HDAC inhibitors and their pleasing cytotoxic effects towards cancer models Combined therapy involving natural flavonoids with other anticancer molecules for synergistic and additive benefits against cancer models Non-flavonoid HDAC inhibitors and conventional drugs in collaborative mode against aggressive malignancies Nanotechnology-based delivery of natural HDAC inhibitors for greater therapeutic efficacy over traditional combinatorial therapy This book is highly beneficial to university professors and research scholars working on epigenetic therapeutics in general, and natural HDAC inhibitors in particular. This book is equally important to medical oncologists, biochemistry as well as pharmacy candidates and students of master's and undergraduate level with a desire to do a doctorate on HDACs, natural HDAC inhibitors, HDAC inhibitor (natural)-based combinatorial chemotherapy and delivery of these inhibitors selectively to tumour sites through revolutionary nanotechnological tactics.
Epigenetics of Cancer Prevention, Volume Ten is the first to look at epigenetics and chemoprevention together. Although there is numerous scientific data available on how epigenetics can lead to cancer and how chemoprevention can be beneficial in the treatment of, or improvement of quality of life, together they will set an advanced understanding for the reader in this upcoming field of chemoprevention influencing epigenetics. This book discusses molecular epigenetic targets of natural products, such as green tea polyphenols, curcumin and resveratrol, and organ specific epigenetic targets related to diverse types of cancer, for example prostate, colorectal, breast, lung and skin cancers. Additionally, it encompasses a discussion on research methods and limitations to study epigenetics and epigenomics of chemopreventive drugs and personalized cancer treatment with phytochemicals. The book is ideal for cancer researchers, health care professionals and all individuals who are interested in cancer prevention research and its clinical applications, especially in natural remedies.
The present invention relates generally to methods for treating cancer. In one respect, the present invention relates to a method of treating a hematological cancer (e.g., multiple myeloma, leukemia, lymphoma) comprising administering to a patient in need thereof a therapeutically effective amount of a histone deacetylase inhibitor, for example, a histone deacetylase (HDAC) inhibitor as described herein, for example, PXD-101. In another respect, the present invention relates to a method of treating cancer (e.g., solid tumor cancer, e.g., rectal cancer, colon cancer, ovarian cancer, hematological cancer, e.g., multiple myeloma, leukemia, lymphoma) comprising administering to a patient in need thereof, a first amount of a histone deacetylase (HDAC) inhibitor, for example, a histone deacetylase inhibitor as described herein, for example, PXD-101, and a second amount of another chemotherapeutic agent, for example, another chemotherapeutic agent selected from: an antibody against VEGF, AVASTIN.RTM. (bevacizumab), an antibody against CD20, rituximab, bortezomib, thalidomide, dexamethasone, vincristine, doxorubicin, and melphalan, wherein the first and second amounts together comprise a therapeutically effective amount.