Targeting the DNA Damage Response for Anti-Cancer Therapy.
Intro -- Contents -- Contributors -- Chapter 1: Targeting DNA Repair in Anti-Cancer Treatments -- 1.1 PARP Inhibitors to Targeted DNA Repair -- 1.2 Limits to the Synthetic Lethal Approach of Targeting Cancer -- 1.3 Combining Chemotherapy Treatment with DNA Repair Inhibitors -- 1.4 Exploiting the Inherent High Level of DNA Damage in Cancers -- Replication Stress -- 1.5 Future Challenges in Targeting DNA Repair for Cancer Treatments -- References -- Chapter 2: The DNA Damage Response: Roles in Cancer Etiology and Treatment -- 2.1 Problems Associated with Current Chemo- and Radiotherapies -- 2.2 The Promise of Targeted Cancer Treatment -- 2.3 The DNA Damage Response (DDR) -- 2.4 Oncogenes Cause Genomic Instability and DDR Activation -- 2.5 Tumor Suppression Through Checkpoint Activation and DNA Repair -- 2.6 Targeting HR and ATM Deficiencies with PARP and DNA-PK Inhibition -- 2.7 Targeting Oncogenic Stress, ATM-p53 Loss, and HR Deficiency with ATR, CHK1 and WEE1 Inhibitors -- 2.8 Future Areas of Research -- References -- Chapter 3: Control of DNA Replication by ATR -- 3.1 Introduction -- 3.2 ATR Is a PI3K-Related Kinase (PIKK) -- 3.3 ATR Activation -- 3.3.1 First Step: ssDNA Recruits the ATR-ATRIP Complex -- 3.3.2 Second Step: TOPBP1 Is Necessary for Full Activation of ATR-ATRIP -- 3.3.3 Third Step: CLASPIN Is an Adaptor for CHK1 Phosphorylation -- 3.3.4 Fine Tuning: Post-Translational Modifications Regulate the Activation of ATR-ATRIP -- 3.4 Local, Regional and Global Checkpoint Functions of ATR-ATRIP -- 3.4.1 Local Action of ATR-ATRIP on Replication Forks -- 3.4.2 Regional Modulation of Replication Factories -- 3.4.3 Global Regulation of DNA Replication and the Cell Cycle -- 3.5 Functions of ATR and CHK1 in Cancer -- 3.5.1 ATR and CHK1 Are Essential -- 3.5.2 Malignant Transformation Generates Replication Stress..
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E-Book |
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Erscheinungsjahr: |
2018 ©2018 |
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Erschienen: |
Cham: Humana Press ; 2018 ©2018 |
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Sprache: |
Englisch |
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Beteiligte Personen: |
Pollard, John [VerfasserIn] |
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Links: |
ebookcentral.proquest.com [lizenzpflichtig] |
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Description based on publisher supplied metadata and other sources |
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Umfang: |
1 online resource (402 pages) |
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PPN (Katalog-ID): |
167322346X |
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520 | |a Intro -- Contents -- Contributors -- Chapter 1: Targeting DNA Repair in Anti-Cancer Treatments -- 1.1 PARP Inhibitors to Targeted DNA Repair -- 1.2 Limits to the Synthetic Lethal Approach of Targeting Cancer -- 1.3 Combining Chemotherapy Treatment with DNA Repair Inhibitors -- 1.4 Exploiting the Inherent High Level of DNA Damage in Cancers -- Replication Stress -- 1.5 Future Challenges in Targeting DNA Repair for Cancer Treatments -- References -- Chapter 2: The DNA Damage Response: Roles in Cancer Etiology and Treatment -- 2.1 Problems Associated with Current Chemo- and Radiotherapies -- 2.2 The Promise of Targeted Cancer Treatment -- 2.3 The DNA Damage Response (DDR) -- 2.4 Oncogenes Cause Genomic Instability and DDR Activation -- 2.5 Tumor Suppression Through Checkpoint Activation and DNA Repair -- 2.6 Targeting HR and ATM Deficiencies with PARP and DNA-PK Inhibition -- 2.7 Targeting Oncogenic Stress, ATM-p53 Loss, and HR Deficiency with ATR, CHK1 and WEE1 Inhibitors -- 2.8 Future Areas of Research -- References -- Chapter 3: Control of DNA Replication by ATR -- 3.1 Introduction -- 3.2 ATR Is a PI3K-Related Kinase (PIKK) -- 3.3 ATR Activation -- 3.3.1 First Step: ssDNA Recruits the ATR-ATRIP Complex -- 3.3.2 Second Step: TOPBP1 Is Necessary for Full Activation of ATR-ATRIP -- 3.3.3 Third Step: CLASPIN Is an Adaptor for CHK1 Phosphorylation -- 3.3.4 Fine Tuning: Post-Translational Modifications Regulate the Activation of ATR-ATRIP -- 3.4 Local, Regional and Global Checkpoint Functions of ATR-ATRIP -- 3.4.1 Local Action of ATR-ATRIP on Replication Forks -- 3.4.2 Regional Modulation of Replication Factories -- 3.4.3 Global Regulation of DNA Replication and the Cell Cycle -- 3.5 Functions of ATR and CHK1 in Cancer -- 3.5.1 ATR and CHK1 Are Essential -- 3.5.2 Malignant Transformation Generates Replication Stress. | ||
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