عنوان

Targeting the DNA damage response for anti-cancer therapy /

شابک

3319758365

شابک

9783319758367

شابک اشتباه

9783319758343

عنوان اصلي

Targeting the DNA damage response for anti-cancer therapy /

نام عام مواد

[Book]

نام نخستين پديدآور

John Pollard, Nicola Curtin, editors.

محل نشرو پخش و غیره

Cham, Switzerland :

نام ناشر، پخش کننده و غيره

Humana Press,

تاریخ نشرو بخش و غیره

2018.

نام خاص و کميت اثر

1 online resource (ix, 401 pages) :

ساير جزييات

illustrations (some color)

عنوان فروست

Cancer drug discovery and development,

شاپا ي ISSN فروست

2196-9906

متن يادداشت

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

متن يادداشت

2.2 The Promise of Targeted Cancer Treatment2.3 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

متن يادداشت

3.3.1 First Step: ssDNA Recruits the ATR-ATRIP Complex3.3.2 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

متن يادداشت

3.5.2 Malignant Transformation Generates Replication Stress3.5.3 The Replication Stress Response Favours Malignant Transformation; 3.5.4 Targeting the Replication Stress Response in Cancer; 3.6 Concluding Remarks; References; Chapter 4: Targeting ATR for Cancer Therapy: Profile and Expectations for ATR Inhibitors; 4.1 Role of ATR in the DNA Damage Response; 4.1.1 ATR Signaling to Regulate DNA Replication and Cell Cycle Progression; 4.1.2 ATR Signaling to DNA Repair; 4.2 Validation of ATR as a Therapeutic Target; 4.3 Development of ATR Inhibitors

متن يادداشت

4.4 ATR Inhibition as Combination Therapy with DNA Damaging Chemotherapy4.5 ATR Inhibition as Combination Therapy with Ionising Radiation (IR); 4.6 ATR Inhibition as Monotherapy; 4.7 ATR Inhibition in Combination with Targeted Drugs; 4.8 Conclusion; References; Chapter 5: Targeting ATR for Cancer Therapy: ATR-Targeted Drug Candidates; 5.1 Background; 5.2 Current Clinical Candidates; 5.2.1 VX-970 (M6620); 5.2.1.1 NCT02157792: First-in-Human Study of VX-970 (M6620) in Combination with Cytotoxic Chemotherapy; 5.2.2 AZD6738

بدون عنوان

0

بدون عنوان

8

بدون عنوان

8

بدون عنوان

8

بدون عنوان

8

متن يادداشت

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.

منبع سفارش / آدرس اشتراک

Springer Nature

شماره انبار

com.springer.onix.9783319758367

موضوع مستند نشده

Cancer-- Treatment-- Genetic aspects.

موضوع مستند نشده

DNA damage.

موضوع مستند نشده

DNA damage.

موضوع مستند نشده

HEALTH & FITNESS-- Diseases-- General.

موضوع مستند نشده

MEDICAL-- Clinical Medicine.

موضوع مستند نشده

MEDICAL-- Diseases.

موضوع مستند نشده

MEDICAL-- Evidence-Based Medicine.

موضوع مستند نشده

Medical genetics.

موضوع مستند نشده

MEDICAL-- Internal Medicine.

موضوع مستند نشده

Oncology.

موضوع مستند نشده

HEA-- 039000

موضوع مستند نشده

MED-- 014000

موضوع مستند نشده

MED-- 022000

موضوع مستند نشده

MED-- 045000

موضوع مستند نشده

MED-- 112000

موضوع مستند نشده

MJCL

شماره

ويراست

شماره رده

مستند نام اشخاص تاييد نشده

Curtin, Nicola J.

مستند نام اشخاص تاييد نشده

Pollard, John

تاريخ عمليات

20200823110342.0

قواعد فهرست نويسي ( بخش توصيفي )

pn

نام الکترونيکي

نوع ماده

[Book]

تكميل شده

Y