scholarly journals Nibrin Double Strand Breakage and its Role in Development of Cancers

2020 ◽  
Vol 29 (02) ◽  
pp. 94-99
Author(s):  
Fizza Abidi ◽  
◽  
Mervyn Hossein ◽  
Saima Akram ◽  
Angabeen Anjum
Keyword(s):  
Strand Breakage

scholarly journals Synthesis and DNA Strand Breakage Activity of Some 1,4-Diazepines

2003 ◽  
Vol 51 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Nobuko Mibu ◽  
Miho Yukawa ◽  
Nobuhiro Kashige ◽  
Yukiko Iwase ◽  
Yoshinobu Goto ◽  
...  
Keyword(s):  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

Factors which affect DNA strand breakage in human leukocytes exposed to a tumor promoter, phorbol myristate acetate

1982 ◽  
Vol 60 (11) ◽  
pp. 1359-1366 ◽  
Author(s):  
H. C. Birnboim
Keyword(s):  
Hydrogen Peroxide ◽  
Dna Damage ◽  
Phorbol Myristate Acetate ◽  
Respiratory Burst ◽  
Superoxide Anion ◽  
Tumor Promoter ◽  
Myristate Acetate ◽  
Strand Breakage ◽  
Dna Strand ◽  
Dna Strand Breakage

We have recently reported that phorbol myristate acetate (PMA) induces extensive DNA strand break damage in human peripheral blood leukocytes. The mechanism of action involves superoxide anion and hydrogen peroxide which are generated by phagocytes during the "respiratory burst." In this report, we describe the effect of various inhibitors and scavengers on PMA-induced DNA damage. Azide and cyanide greatly increased the level of damage; sulfhydryl compounds (glutathione, cysteine, and cysteamine) and ascorbate markedly decreased the level of damage. Hydroxyl radical scavengers such as dimethyl sulfoxide (DMSO) and glycerol also decreased the level of damage but apparently did so by inhibiting the respiratory burst. Diethyldithiocarbamate (DDC) increased the level of DNA damage at low concentrations (<1 mM), but decreased DNA damage at ≥1 mM. The results are consistent with a mechanism involving superoxide anion and hydrogen peroxide, but the precise reaction (free radical or enzymatic) responsible for DNA strand breakage has not been determined. The PMA-stimulated phagocyte is an interesting model system for looking at "active oxygen" mediated DNA damage and factors which influence it.

scholarly journals Strand breakage in solutions of DNA and ethidium bromide exposed to visible light

1977 ◽  
Vol 4 (5) ◽  
pp. 1393-1408 ◽  
Author(s):  
Phillip A. Martens ◽  
David A. Clayton
Keyword(s):  
Visible Light ◽  
Ethidium Bromide ◽  
Strand Breakage

scholarly journals DNA deaminases induce break-associated mutation showers with implication of APOBEC3B and 3A in breast cancer kataegis

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Benjamin JM Taylor ◽  
Serena Nik-Zainal ◽  
Yee Ling Wu ◽  
Lucy A Stebbings ◽  
Keiran Raine ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Abasic Site ◽  
Dna Breaks ◽  
Mutational Signatures ◽  
Genome Wide ◽  
Cancer Genomes ◽  
Strand Breakage ◽  
Cytidine Deamination ◽  
Apobec Family ◽  
Insight Into

Breast cancer genomes have revealed a novel form of mutation showers (kataegis) in which multiple same-strand substitutions at C:G pairs spaced one to several hundred nucleotides apart are clustered over kilobase-sized regions, often associated with sites of DNA rearrangement. We show kataegis can result from AID/APOBEC-catalysed cytidine deamination in the vicinity of DNA breaks, likely through action on single-stranded DNA exposed during resection. Cancer-like kataegis can be recapitulated by expression of AID/APOBEC family deaminases in yeast where it largely depends on uracil excision, which generates an abasic site for strand breakage. Localized kataegis can also be nucleated by an I-SceI-induced break. Genome-wide patterns of APOBEC3-catalyzed deamination in yeast reveal APOBEC3B and 3A as the deaminases whose mutational signatures are most similar to those of breast cancer kataegic mutations. Together with expression and functional assays, the results implicate APOBEC3B/A in breast cancer hypermutation and give insight into the mechanism of kataegis.

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