Skip to main content

Dna Repair In Cancer Therapy

In Order to Read Online or Download Dna Repair In Cancer Therapy Full eBooks in PDF, EPUB, Tuebl and Mobi you need to create a Free account. Get any books you like and read everywhere you want. Fast Download Speed ~ Commercial & Ad Free. We cannot guarantee that every book is in the library!

DNA Repair in Cancer Therapy

DNA Repair in Cancer Therapy Book
Author : Mark R. Kelley,Melissa L. Fishel
Publisher : Academic Press
Release : 2016-06-07
ISBN : 0128035994
Language : En, Es, Fr & De

GET BOOK

Book Description :

DNA Repair and Cancer Therapy: Molecular Targets and Clinical Applications, Second Edition provides a comprehensive and timely reference that focuses on the translational and clinical use of DNA repair as a target area for the development of diagnostic biomarkers and the enhancement of cancer treatment. Experts on DNA repair proteins from all areas of cancer biology research take readers from bench research to new therapeutic approaches. This book provides a detailed discussion of combination therapies, in other words, how the inhibition of repair pathways can be coupled with chemotherapy, radiation, or DNA damaging drugs. Newer areas in this edition include the role of DNA repair in chemotherapy induced peripheral neuropathy, radiation DNA damage, Fanconi anemia cross-link repair, translesion DNA polymerases, BRCA1-BRCA2 pathway for HR and synthetic lethality, and mechanisms of resistance to clinical PARP inhibitors. Provides a comprehensive overview of the basic and translational research in DNA repair as a cancer therapeutic target Includes timely updates from the earlier edition, including Fanconi Anemia cross-link repair, translesion DNA polymerases, chemotherapy induced peripheral neuropathy, and many other new areas within DNA repair and cancer therapy Saves academic, medical, and pharma researchers time by allowing them to quickly access the very latest details on DNA repair and cancer therapy Assists researchers and research clinicians in understanding the importance of the breakthroughs that are contributing to advances in disease-specific research

Advances in DNA Repair in Cancer Therapy

Advances in DNA Repair in Cancer Therapy Book
Author : Lawrence Panasci,Raquel Aloyz,Moulay Alaoui-Jamali
Publisher : Springer Science & Business Media
Release : 2012-12-09
ISBN : 1461447410
Language : En, Es, Fr & De

GET BOOK

Book Description :

​A comprehensive review of the recent developments in DNA repair research that have potential for translational applications. The book explains in detail the various biological mechanisms by which cancer cells can circumvent anticancer therapy and limits its usefulness in patients. They also review the impact of such novel inhibitors of DNA repair mechanisms as methylguanine-DNA-methyltransferase. Also examined are inhibitors of other DNA repair enzymes such as PARP and DNA-PK. The book captures-for both cancer researchers and oncologists dealing with hallmark "relapse" or "drug resistance" phenomena on a daily basis-the many exciting new uses of DNA repair inhibitors, either alone or in combination with anticancer therapies.​

DNA Repair in Cancer Therapy

DNA Repair in Cancer Therapy Book
Author : Lawrence C. Panasci,Moulay A. Alaoui-Jamali
Publisher : Springer Science & Business Media
Release : 2004-03-19
ISBN : 1592597351
Language : En, Es, Fr & De

GET BOOK

Book Description :

A comprehensive review of the recent developments in DNA repair that have potential for translational and clinical applications. The authors explain in detail the various mechanisms by which cancer cells can circumvent anticancer therapy and limits its usefulness in patients. They also review the clinical impact of such novel inhibitors of DNA repair mechanisms as methylguanine-DNA-methyltransferase. Also examined are inhibitors of other DNA repair enzymes such as PARP and DNA-PK, now under development and close to clinical trials. The book captures-for both cancer researchers and practicing oncologists dealing with hallmark "relapse" or "drug resistance" phenomena on a daily basis-the many exciting new uses of DNA repair inhibitors, either alone or in combination with anticancer therapies.

DNA Repair and Cancer

DNA Repair and Cancer Book
Author : Srinivasan Madhusudan,David M. Wilson III
Publisher : CRC Press
Release : 2013-01-22
ISBN : 1466577444
Language : En, Es, Fr & De

GET BOOK

Book Description :

DNA repair is a rapidly advancing field in biology and these systems represent a major defense mechanism against environmental and intracellular damaging agents such as sunlight, ionizing radiation, and reactive oxygen species. With contributions from eminent researchers, this book explores the basics and current trends in this critical field. Topics include carcinogenesis as a predictive and/or prognostic biomarker for cancer therapy, nucleotide excision repair, and tumor genetics and personalized medicine. The contributions provide essential information to scientists, pharmaceutical investigators, and clinicians interested in cancer therapy.

Targeting the DNA Damage Response for Anti Cancer Therapy

Targeting the DNA Damage Response for Anti Cancer Therapy Book
Author : John Pollard,Nicola Curtin
Publisher : Springer
Release : 2018-05-26
ISBN : 3319758365
Language : En, Es, Fr & De

GET BOOK

Book Description :

Over the past decade a complex role for DNA damage response (DDR) in tumorigenesis has emerged. A proficient DDR has been shown to be a primary cause for cellular resistance to the very many DNA damaging drugs, and IR, that are widely used as standard-of-care across multiple cancer types. It has also been shown that defects in this network, predominantly within the ATM mediated signaling pathway, are commonly observed in cancers and may be a primary event during tumorigenesis. Such defects may promote a genomically unstable environment, facilitating the persistence of mutations, any of which may provide a growth or survival advantage to the developing tumor. In addition, these somatic defects provide opportunities to exploit a reliance on remaining repair pathways for survival, a process which has been termed synthetic lethality. As a result of all these observations there has been a great interest in targeting the DDR to provide anti-cancer agents that may have benefit as monotherapy in cancers with high background DNA damage levels or as a means to increase the efficacy of DNA damaging drugs and IR. In this book we will review a series of important topics that are of great interest to a broad range of academic, industrial and clinical researchers, including the basic science of the DDR, its role in tumorigenesis and in dictating response to DNA damaging drugs and IR. Additionally, we will focus on the several proteins that have been targeted in attempts to provide drug candidates, each of which appear to have quite distinct profiles and could represent very different opportunities to provide patient benefit.

PARP Inhibitors for Cancer Therapy

PARP Inhibitors for Cancer Therapy Book
Author : Nicola J. Curtin,Ricky A. Sharma
Publisher : Humana Press
Release : 2015-06-13
ISBN : 3319141511
Language : En, Es, Fr & De

GET BOOK

Book Description :

PARP Inhibitors for Cancer Therapy provides a comprehensive overview of the role of PARP in cancer therapy. The volume covers the history of the discovery of PARP (poly ADP ribose polymerase) and its role in DNA repair. In addition, a description of discovery of the PARP family, and other DNA maintenance-associated PARPs will also be discussed. The volume also features a section on accessible chemistry behind the development of inhibitors. PARP inhibitors are a group of pharmacological inhibitors that are a particularly good target for cancer therapy. PARP plays a pivotal role in DNA repair and may contribute to the therapeutic resistance to DNA damaging agents used to treat cancer. Researchers have learned a tremendous amount about the biology of PARP and how tumour-specific defects in DNA repair can be exploited by PARPi. The “synthetic lethality” of PARPi is an exciting concept for cancer therapy and has led to a heightened activity in this area.

Inhibition of RAD52 based DNA Repair for Cancer Therapy

Inhibition of RAD52 based DNA Repair for Cancer Therapy Book
Author : Mona Hadi Al-Mugotir
Publisher : Unknown
Release : 2018
ISBN : 0987650XXX
Language : En, Es, Fr & De

GET BOOK

Book Description :

Germline BRCA mutations underlay a significant risk for breast and ovarian cancer that increases in age. BRCA mutations are usually associated with the most aggressive subtypes of these cancers such as triple negative breast cancer and high-grade serous ovarian cancer. Conventional chemotherapeutic or hormonal therapies do not address the molecular deficiencies responsible for their resistance and there is a high rate of recurrence. Targeted therapy that can address the unique molecular features in these subtypes of cancer is the only way to cure the disease or, at the very least, improve patients’ quality of life. Homologous recombination repair is an accurate repair pathway that utilizes a copy of a homologous sequence to relay information to the break site. Cancer cells copy their DNA extensively meeting the principle demand for this high-fidelity repair pathway. Homologous recombination repair is utilized by cancer cells to cope with the most challenging forms of DNA damage such as DNA double strand breaks, stalled replication forks, adducts, and interstrand crosslinks. Among the key proteins in homologous recombination repair, RAD52 activity promotes cancer cells’ tolerance and survival. Therefore, there is a therapeutic opportunity in inhibiting RAD52 activity to push DNA damage levels in homologous recombination repair-deficient tumors beyond the limits of viability. One of the early events in this repair is resection of the broken strand and generation of single strand DNA. Replication protein A cover and protect those strands and interact with key DNA repair proteins. RAD52 activity in DNA repair is dependent on its interaction with replication protein A. The hypothesis of this thesis is that it is possible to inhibit RAD52 activity by inhibiting its interaction with RPA and this inhibition will have therapeutic benefits for cancer patients. We explored the binding activity and affinity of the RAD52 interaction with RPA. Kinetic, and thermodynamic parameters dictating this protein:protein interaction were measured. The characterization of RAD52:RPA interaction data guided remapping of the RPA interaction domains on RAD52. To target RAD52 activity by inhibiting its interaction with RPA, we designed an in vitro fluorescent-based protein-protein interaction assay. This assay was further optimized for high throughput settings with a robust signal, minimal steps, statistical accuracy, and low cost. We screened over 100,000 compounds to look for small molecule inhibitors. Eleven hits were found and five were selected for their high EC50 values. Three of the five hits are FDA approved drugs and were selected for cytotoxicity tests in BRCA-deficient cell lines. The outcome of our characterization for these three candidate small molecule inhibitors may shed light on the variation of their efficacy and sensitivity among breast or ovarian cancer patients with BRCA-defective pathway versus those with none. Additionally, we present fluorescent-based protein-protein interaction assay as an affordable method to detect many protein:protein interactions in low-scale or high throughput settings applicable to finding small molecule inhibitors or aptamer modulators for protein:protein interactions.

DNA Repair Cancer and Cancer Therapy

DNA Repair  Cancer and Cancer Therapy Book
Author : Mu Wang
Publisher : Unknown
Release : 2011
ISBN : 9789533076126
Language : En, Es, Fr & De

GET BOOK

Book Description :

Download DNA Repair Cancer and Cancer Therapy book written by Mu Wang, available in PDF, EPUB, and Kindle, or read full book online anywhere and anytime. Compatible with any devices.

The DNA Damage Response Implications on Cancer Formation and Treatment

The DNA Damage Response  Implications on Cancer Formation and Treatment Book
Author : Kum Kum Khanna,Yosef Shiloh
Publisher : Springer Science & Business Media
Release : 2009-09-18
ISBN : 9789048125616
Language : En, Es, Fr & De

GET BOOK

Book Description :

The ?eld of cellular responses to DNA damage has attained widespread recognition and interest in recent years commensurate with its fundamental role in the ma- tenance of genomic stability. These responses, which are essential to preventing cellular death or malignant transformation, are organized into a sophisticated s- tem designated the “DNA damage response”. This system operates in all living organisms to maintain genomic stability in the face of constant attacks on the DNA from a variety of endogenous by-products of normal metabolism, as well as exogenous agents such as radiation and toxic chemicals in the environment. The response repairs DNA damage via an intricate cellular signal transduction network that coordinates with various processes such as regulation of DNA replication, tr- scriptional responses, and temporary cell cycle arrest to allow the repair to take place. Defects in this system result in severe genetic disorders involving tissue degeneration, sensitivity to speci?c damaging agents, immunode?ciency, genomic instability, cancer predisposition and premature aging. The ?nding that many of the crucial players involved in DNA damage response are structurally and functionally conserved in different species spurred discoveries of new players through similar analyses in yeast and mammals. We now understand the chain of events that leads to instantaneous activation of the massive cellular responses to DNA lesions. This book summarizes several new concepts in this rapidly evolving ?eld, and the advances in our understanding of the complex network of processes that respond to DNA damage.

DNA Repair Genetic Instability and Cancer

DNA Repair  Genetic Instability  and Cancer Book
Author : Qingyi Wei,Dr. Lei Li,Dr. David Chen
Publisher : World Scientific
Release : 2007
ISBN : 9812700145
Language : En, Es, Fr & De

GET BOOK

Book Description :

This volume describes the elaborate surveillance systems and various DNA repair mechanisms that ensure accurate passage of genetic information onto daughter cells. In particular, it narrates how the cell cycle checkpoint and DNA repair machineries detect and restore DNA damages that are embedded in millions to billions of normal base pairs. The scope of the book ranges from biochemical analyses and structural details of DNA repair proteins, to integrative genomics and population-based studies. It provides a snapshot of current understanding about some of the major DNA repair pathways, including base-excision repair, nucleotide excision repair, mismatch repair, homologous recombination, and non-homologous end-joining as well as cell cycle checkpoints and translesion DNA synthesis. One of the particular emphases of the book is the link between inherited DNA repair deficiencies and susceptibility to cancer in the general population. For the first time, the book brings together a collection of review articles written by a group of active and laboratory-based investigators who have a clear understanding of the recent advances in the fields of DNA damage repair and genomic stability and their implications in carcinogenesis, new approaches in cancer therapy, and cancer prevention.

A Novel DNA Damage Quantification Platform Enables High Throughput Screening for Genes that Impact DNA Double Strand Breaks

A Novel DNA Damage Quantification Platform Enables High Throughput Screening for Genes that Impact DNA Double Strand Breaks Book
Author : Ian Jun Jie Tay
Publisher : Unknown
Release : 2018
ISBN : 0987650XXX
Language : En, Es, Fr & De

GET BOOK

Book Description :

DNA is the blueprint of life, and the high fidelity transmission of genetic information from parent cells to progeny is essential for an organism's viability. However, our genomes are constantly being damaged by reactive molecules generated from cellular metabolic processes or introduced from the environment. The resulting DNA damage can alter the information encoded in DNA, and can interfere with the accurate transmission of genetic information when cells divide. The accumulation of cells with highly damaged or altered DNA within an organism can cause diseases, such as growth defects, aging and cancer. Fortunately, cells possess the capability to repair damaged DNA. Since DNA repair mechanisms can reverse the deleterious effects of DNA damage, they are important in disease prevention, and in particular play an important role in preventing cancer. DNA repair factors are also important targets for cancer therapies. Tumor cells frequently harbor defects in DNA repair, rendering them vulnerable to DNA damage. Many cancer therapies exploit this vulnerability by treatment with DNA damaging agents. However, tumor cells can have differential DNA repair capacities based on the expression levels of various DNA repair genes. Thus, some cancer cells are variable in their response to chemotherapy and radiation. It is well established that inhibiting DNA repair can increase the efficacy of treatment. Therefore, it is critical to develop a better understanding of the network of genes that regulate DNA repair mechanisms both to understand susceptibility to cancer, and also in order to improve the outcomes of cancer therapy. DNA repair is a complex process that requires the coordination of many proteins to respond to specific classes of DNA damage. Many of the major proteins that directly participate in DNA repair pathways are well characterized. However, recent research has indicated that the core DNA repair factors make up only a small fraction of the proteins that respond to DNA damage, suggesting that a large number of novel DNA repair factors have yet to be discovered and characterized. In this work, we leveraged the CometChip, a high-throughput DNA damage quantification assay, to screen thousands of genes for their ability to modulate DNA repair, by knocking them down with shRNAs. We first designed hardware for the CometChip to make it compatible with high-throughput robotics so as to reduce the amount of manual labor needed to execute our screen. We then exploited the ability of our assay to measure DNA damage at an unparalleled rate to screen an shRNA library targeting 2564 oncology-associated genes. We performed gene network analysis on the top candidate genes and found LATS2 to be a novel DNA repair factor. Further investigation revealed that LATS2 is a modulator of the homologous recombination repair pathway. In addition, we merged our screen data with that from an assay that queries proteins for their ability to bind to DNA double strand breaks. Our results showed that we were able to identify known DNA repair factors via the intersection of the two datasets, and we pinpointed at least one other novel DNA repair gene for further investigation. Taken together, this work represents an advancement in the ability to discover novel DNA repair factors by large-scale parallel measurement of physical DNA damage in cells. Our technology enables high-throughput screening for DNA damage and repair factors faster than ever before, allowing for extensive studies of DNA damage and opening doors to the discovery of new genes and molecules that affect DNA repair.

System Biology Analysis of the Role of DNA Repair in Cancer Treatment Outcome

System Biology Analysis of the Role of DNA Repair in Cancer Treatment Outcome Book
Author : Mengdi Qian
Publisher : Unknown
Release : 2019
ISBN : 0987650XXX
Language : En, Es, Fr & De

GET BOOK

Book Description :

Cancer is one of the most lethal and hard to cure diseases. The common treatments for cancer include surgery, radiation therapy, chemotherapy, immunotherapy and hormone therapy. Ionizing radiation (IR) is one of the main clinical treatments for cancer and it works by inducing DNA double strand breaks (DSBs), which are the most toxic DNA lesions that lead to cell death. The effectiveness of IR treatment depends on the amount of induced damage and the DNA damage repair status of the cancer cells. DSBs are repaired by multiple DNA repair pathways and this repair reduces the effectiveness of the treatment leading to resistance to IR. It has been shown in the literature that by targeting the DNA repair pathways the treatment efficacy can be modulated.In this work, a systems biology approach is used to quantitatively study the role of DNA repair pathways in determining and improving the radiation treatment outcome. Specifically, the mathematical models of DNA repair pathways, non-homologous end joining (NHEJ) and homologous recombination (HR), are developed for analyzing the role of DNA repair in enhancing the treatment sensitivity for prostate cancer (PCa) when a combination of radiation and hormone deprivation therapies is used. DSBs are repaired by one of the two DNA repair pathways: NHEJ and homologous recombination (HR). NHEJ is the major pathway, whereas HR is restricted to S- or G2-phases of the cell cycle after DNA replication has been completed. The cell cycle specific contribution of the repair pathways are incorporated into the computational models. A comprehensive identifiability analysis is carried out to determine the factors affecting parameter identifiability and strategies to increase identifiability are developed. In parallel to the NHEJ and HR models, a computational model of the base excision repair (BER) pathway is developed to analyze its role in response to chemotherapy under different treatment scenarios.Combination treatment strategies that aim to inhibit the functional DNA repair pathways for the cancer cells that are defective in other repair pathways achieve synthetic lethality. One such strategy is the use of PARP inhibitors (PARPi) in addition to the combination treatment with IR and ADT. The experimental data in the literature show that AR promotes both NHEJ and HR following IR, and inhibition of AR by ADT impairs both of these pathways in PCa cells leading to either increased radiosensitivity or sensitization to PARP inhibitors. The effect of using PARPi in this scenario has been computationally analyzed in this work by extending the modeling efforts to include the effect of PARP inhibitors on the treatment outcome. The inhibition of BER by PARPi is also quantitatively studied. The models and findings in this work can then be extended to other cancers, such as lung cancer and ovarian cancer that benefit from similar synthetic lethality.

Checkpoint Controls and Targets in Cancer Therapy

Checkpoint Controls and Targets in Cancer Therapy Book
Author : Zahid H. Siddik
Publisher : Springer Science & Business Media
Release : 2010-03-12
ISBN : 9781607611783
Language : En, Es, Fr & De

GET BOOK

Book Description :

Much work over the last two decades has firmly established that loss of cell cycle checkpoint regulation, and resultant unabated cellular proliferation, is an inherent characteristic of cancer. This loss may occur through aberration in any single component involved in signal transduction pathways that orchestrate checkpoint regulation, which may manifest through either a failure to activate the checkpoint or a failure to respond to the activated checkpoint. In normal cells, checkpoint pathways are activated when genetic or cellular homeostasis is compromised, and signals are then transduced to re-stabilize homeostasis, and, failing this, to activate the apoptotic machinery to induce a cellular suicidal response. This implies that both survival and cell death pathways are induced following checkpoint activation, and that the final decision is dependant on the net result of integrating the two sets of signals. It is intriguing that checkpoint pathways are also critical in cancer therapy to provide an apoptotic stimulus when cellular damage induced by the therapeutic agent is detected by the sensor system. Therefore, it is not surprising that failure in pro-survival checkpoint response will render tumor cells hypersensitive to cytotoxics and, conversely, failure in pro-apoptotic checkpoint response will induce genetic instability and/or therapeutic resistance. Understanding the intricacies of checkpoint response is, therefore, central to the design of therapeutic regimen that will enhance antitumor effects. Although early versions of this design entail combination of cytotoxic agents with cell cycle or checkpoint inhibitors, a greater understanding of the concepts could make such combinations clinically more effective. The contributions in this book will consolidate the current state of knowledge on checkpoint responses that may lay the foundation for hypothesis-driven rational approaches in advancing the management of cancer. The immediate attraction of the book to the scientific community is that it represents a timely opportunity to build upon existing concepts of checkpoints to expand our understanding of the inner workings of the critical checkpoint machinery. The present understanding has provided ample appreciation that response to checkpoint activation is manifested through coordinated inhibition of cyclin-dependent kinase (CDK) complexes in G1, S and/or the G2 phase in order to arrest the cell cycle. Kinase inhibition can occur through several mechanisms, including inhibitory phosphorylation of CDK, destruction of the cognate cyclins, and recruitment of CDK inhibitors from the INK and WAF1/CIP1 families. However, the wealth of information from recent discoveries needs to be examined critically to consolidate our conceptual knowledge of checkpoints. At the same time, there is acute awareness in the diversity of checkpoint response between cytotoxic agents, and this serves as a reminder of the magnitude of complexity that is inherent in checkpoint regulation. This volume is intended to bring the cancer research community closer toward an improved understanding of this regulation, how checkpoint abnormalities can impact negatively on cancer therapy, and emerging strategies to target checkpoint response as a therapeutic end-point.

Cancer Associated Defects in the DNA Damage Response Drivers for Malignant Transformation and Potential Therapeutic Targets

Cancer Associated Defects in the DNA Damage Response  Drivers for Malignant Transformation and Potential Therapeutic Targets Book
Author : Marcel van Vugt,H. Christian Reinhardt
Publisher : Frontiers Media SA
Release : 2016-10-17
ISBN : 2889199495
Language : En, Es, Fr & De

GET BOOK

Book Description :

For this eBook, and the associated Research Topic in Frontiers in Genetics, entitled: ‘Cancer-associated defects in the DNA damage response: drivers for malignant transformation and potential therapeutic targets’ we have selected 10 papers that each discusses important, yet distinct aspects of the response to DNA damage in normal cells and cancer cells. Using an evolutionary conserved signaling network called the ‘DNA damage response (DDR)’ cells maintain the integrity of their genome, and thus safeguard cellular functioning and the ability to create viably progeny. Initially, the DDR appeared to consist of few linear kinase-driven pathways. However, research over the past decades in model organisms, as well as in the human system has revealed that the DDR is a complex signaling network, wired by multiple parallel pathways and displaying extensive crosstalk. Besides phosphorylation, multiple other post-translational modifications, including ubiquitination and sumoylation, are involved to achieve chromatin remodeling and initiation of DNA repair. Also, rather than being a cell-intrinsic phenomenon, we increasingly appreciate that cell-cell communication is involved. The recognition and repair of DNA damage is essential to maintain normal physiology. Multiple pathological conditions have been attributed to defective DNA repair, most notably accelerated aging, neurodegeneration and cancer. In the context of cancer, through repair of DNA damage or elimination of irreparably damaged cells, the DDR clearly has a tumor-suppressive role. Indeed, many tumor cells show partially inactivated DDR signaling, which allows proliferation in the context of DNA damage-inducing oncogenes. Simultaneously, loss of specific DDR signaling nodes creates a specific dependence of tumor cells on their remaining DDR components, and thus creates therapeutic opportunities. Especially in the context of cancer treatment, numerous targeted agents are under investigation, either to potentiate the cytotoxic effects of chemo-radiotherapy, or to induce synthetic lethality with cancer-specific alterations, with the treatment of BRCA1/2 mutant cancers with PARP1 inhibitors as a prototype example. We have selected four review articles that provide insight into the key components and the wiring of the DDR and DNA repair. Torgovnick and Schumacher review the involvement of DNA repair in the initiation and treatment of cancer, Brinkmann et al., describe the involvement of ubiquitination in DNA damage signaling and Jaiswal and Lindqvist discuss how cell-extrinsic signaling participates in communication of DNA damage to neighboring cells. In addition, Shatneyeva and colleagues review the connection between the cellular response to DNA damage and escape from immune surveillance. Concerning the therapeutic application of targeting the DDR and DNA repair, three articles were included. Krajewska and van Vugt review the wiring of homologous recombination and how this offers therapeutic opportunities. Additionally, Knittel and colleagues describe how genetic loss of the central DDR component ATM in chronic lymphocytic leukemia can be exploited therapeutically by targeting certain parallel DNA repair pathways. Syljuasen and colleagues report on how targeting of the DDR can be used as a therapeutic strategy in lung cancer. Finally, three chapters describe newly identified regulators of the cellular response to DNA damage. Von Morgen et al. describe the R2TP complex, Lezzi and Fanciluuli review the involvement of Che-1/AATF in the DDR, and Ohms and co-authors describe how retrotransposons are at the basis of increased genomic instability. Altogether, these articles describe how defective responses to DNA damage underlie disease - and especially in the context of cancer -can be exploited to better treat disease.

Checkpoint Responses in Cancer Therapy

Checkpoint Responses in Cancer Therapy Book
Author : Wei Dai
Publisher : Springer Science & Business Media
Release : 2008-05-01
ISBN : 9781597452748
Language : En, Es, Fr & De

GET BOOK

Book Description :

Extensive research has uncovered a set of molecular surveillance mechanisms – commonly called “checkpoints” – which tightly monitor cell-cycle processes. Today’s anticancer drug development has identified many of these cell-cycle checkpoint molecules as effective targets. Research now promises to uncover a new generation of anticancer drugs with improved therapeutic indices based on their ability to target emerging checkpoint components. Checkpoint Responses in Cancer Therapy summarizes the advances made over the past 20 years, identifying components of cell-cycle checkpoints and their molecular regulation during checkpoint activation and validating the use of checkpoint proteins as targets for the development of anticancer drugs. This book’s distinguished panel of authors takes a close look at topics ranging from the major molecular players affecting DNA synthesis and the response to DNA damage to advances made in the identification of chemical compounds capable of inhibiting individual mitotic kinases. Illuminating and authoritative, Checkpoint Responses in Cancer Therapy offers a critical summary of findings for researchers in the pharmaceutical and biotechnology industries and a valuable resource for academic scientists in cancer research and the study of cell-cycle regulation, signal transduction and apoptosis.

DNA Damage and Repair

DNA Damage and Repair Book
Author : Jac A. Nickoloff,Merl F. Hoekstra
Publisher : Springer Science & Business Media
Release : 2001-03-13
ISBN : 1592590950
Language : En, Es, Fr & De

GET BOOK

Book Description :

Jac A. Nickoloff and Merl F. Hoekstra update and expand their two earlier acclaimed volumes (Vol. I: DNA Repair in Prokaryotes and Lower Eukaryotes and Vol. II: DNA Repair in Higher Eurkaryotes) with cutting-edge reviews by leading authorities of primary experimental findings about DNA repair processes in cancer biology. The reviews cover a wide range of topics from viruses and prokaryotes to higher eukaryotes, and include several new topics, among them the role of recombination in replication of damaged DNA, X-ray crystallographic analysis of DNA repair protein structures, DNA repair proteins and teleomere function, and the roles of BRCA1 and BRCA2 in DNA repair. Authoritative and up-to-date, DNA Damage and Repair, Vol. III: Advances from Phage to Humans surveys the rapidly moving research in DNA damage and repair, and explains the important functional relationships among different DNA repair pathways and the relationship between DNA repair pathways, cancer etiology, and cancer therapies.

DNA Damage Repair and Misrepair in Cancer and in Cancer Therapy

DNA Damage  Repair and Misrepair in Cancer and in Cancer Therapy Book
Author : Ana M. Urbano,Carlos F. Rodrigues,Joana F. Cerveira,Leonardo M. R. Ferreira,Maria C. Alpoim
Publisher : Unknown
Release : 2011
ISBN : 9789533076126
Language : En, Es, Fr & De

GET BOOK

Book Description :

Download DNA Damage Repair and Misrepair in Cancer and in Cancer Therapy book written by Ana M. Urbano,Carlos F. Rodrigues,Joana F. Cerveira,Leonardo M. R. Ferreira,Maria C. Alpoim, available in PDF, EPUB, and Kindle, or read full book online anywhere and anytime. Compatible with any devices.

Modulation of Protein Stability in Cancer Therapy

Modulation of Protein Stability in Cancer Therapy Book
Author : Kathleen Sakamoto,Eric Rubin
Publisher : Springer Science & Business Media
Release : 2009-04-20
ISBN : 9780387691473
Language : En, Es, Fr & De

GET BOOK

Book Description :

This comprehensive monograph on the role of protein modulation in cancer therapeutics focuses on targeting molecules that regulate protein stability in a variety of tumors. Topics covered include ubiquitin ligases, deubiquitinating enzymes, and the proteasome.