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المؤلفAlhmoud, Jehad F.
المؤلفWoolley, John F.
المؤلفAl Moustafa, Ala-Eddin
المؤلفMalki, Mohammed Imad
تاريخ الإتاحة2021-11-24T09:40:06Z
تاريخ النشر2021-12-23
اسم المنشورAdvances in Medical Biochemistry, Genomics, Physiology, and Pathology
الاقتباسAlhmoud, Jehad F. , Woolley, John F. , Al Moustafa, Ala-Eddin & Malki, Mohammed Imad (2021). DNA Damage/Repair Management in Cancers. Advances in Medical Biochemistry, Genomics, Physiology, and Pathology. 309 - 339. UK: Routledge.
الترقيم الدولي الموحد للكتاب 9789814877442
معرّف المصادر الموحدhttps://www.routledge.com/Advances-in-Medical-Biochemistry-Genomics-Physiology-and-Pathology/Bawa-Chang-Audette-Diwan-Faiz/p/book/9789814877442#
معرّف المصادر الموحدhttp://hdl.handle.net/10576/25103
الملخصDNA damage can alter nucleotide sequences and lead to expression of dysfunctional proteins that impact normal cellular physiology. Sources of DNA damage can be endogenous or exogenous and include reactive oxygen species (ROS) or ionizing radiation. DNA damaging agents can broadly be classified into two different categories: clastogens and aneugens. Clastogens cause chromosomal breaks and induce micronuclei (MN) due to generation of acentric chromosomal fragments. In contrast, aneugens lead to the incorporation of whole chromosomes in MN by generation of aneuploidy that affects cell proliferation and the mitotic spindle apparatus
راعي المشروعFunding: Research of Dr. Malki’s Lab has been supported by grants from Qatar University: QUCG-CMED-20/21-3, QUST-1-CMED-2019-23 and QUST-1-CMED-2020-13 Acknowledgments: We are thankful to Nagesh Kalakonda and Shifa Rostom for their critical reading of the chapter. The publication of this chapter was funded by the Qatar National Library.
اللغةen
الناشرRoutledge
العلاقةhttp://hdl.handle.net/10576/14494
الموضوعDNA damage
DNA repair pathway
DNA lesion
reactive oxygen species
clastogens
aneugens
genomic instability
DNA damaging agents
micronuclei
nucleoplasmic bridges
nuclear buds
misrepaired DNA
single strand breaks
double strand breaks
ionizing irradiation
apoptosis
programmed cell death
ataxia telangiectasia
RAD3-related
base excision repair
nucleotide excision repair
non-homologous end joining
homologous recombination
DNA mismatch repair
cyclin-dependent kinase
Xeroderma pigmentosum
trichothiodystrophy
microsatellite instability
cell cycle
biomarkers
العنوانDNA Damage/Repair Management in Cancers
النوعBook chapter
الصفحات309 - 339
رقم المجلد1


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