Long duration exposure to cadmium leads to increased cell survival, decreased DNA repair capacity, and genomic instability in mouse testicular Leydig cells

2009 ◽  
Vol 279 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Kamaleshwar P Singh ◽  
Ragini Kumari ◽  
Christina Pevey ◽  
Desiree Jackson ◽  
James W. DuMond
Keyword(s):  
Dna Repair ◽  
Cell Survival ◽  
Genomic Instability ◽  
Leydig Cells ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Long Duration

scholarly journals Bad neighbours: hypoxia and genomic instability in prostate cancer

2020 ◽  
Vol 93 (1115) ◽  
pp. 20200087 ◽  
Author(s):  
Jack Ashton ◽  
Robert Bristow
Keyword(s):  
Prostate Cancer ◽  
Dna Repair ◽  
Genomic Instability ◽  
Tumour Progression ◽  
Clonal Evolution ◽  
Treatment Strategies ◽  
Repair Capacity ◽  
Functional Studies ◽  
Dna Repair Capacity ◽  
Mechanistic Basis

Prostate cancer (PCa) is a clinically heterogeneous disease and has poor patient outcome when tumours progress to castration-resistant and metastatic states. Understanding the mechanistic basis for transition to late stage aggressive disease is vital for both assigning patient risk status in the localised setting and also identifying novel treatment strategies to prevent progression. Subregions of intratumoral hypoxia are found in all solid tumours and are associated with many biologic drivers of tumour progression. Crucially, more recent findings show the co-presence of hypoxia and genomic instability can confer a uniquely adverse prognosis in localised PCa patients. In-depth informatic and functional studies suggests a role for hypoxia in co-operating with oncogenic drivers (e.g. loss of PTEN) and suppressing DNA repair capacity to alter clonal evolution due to an aggressive mutator phenotype. More specifically, hypoxic suppression of homologous recombination represents a “contextual lethal“ vulnerability in hypoxic prostate tumours which could extend the application of existing DNA repair targeting agents such as poly-ADP ribose polymerase inhibitors. Further investigation is now required to assess this relationship on the background of existing genomic alterations relevant to PCa, and also characterise the role of hypoxia in driving early metastatic spread. On this basis, PCa patients with hypoxic tumours can be better stratified into risk categories and treated with appropriate therapies to prevent progression.

Decreased cell survival and DNA repair capacity after UVC irradiation in association with down-regulation of GRP78/BiP in human RSa cells

2005 ◽  
Vol 305 (2) ◽  
pp. 244-252 ◽  
Author(s):  
Ling Zhai ◽  
Kazuko Kita ◽  
Chieko Wano ◽  
Yuping Wu ◽  
Shigeru Sugaya ◽  
...  
Keyword(s):  
Dna Repair ◽  
Cell Survival ◽  
Down Regulation ◽  
Repair Capacity ◽  
Dna Repair Capacity

High-Throughput Screening Platform for Nanoparticle-Mediated Alterations of DNA Repair Capacity

ACS Nano ◽  
2021 ◽  
Author(s):  
Sneh M. Toprani ◽  
Dimitrios Bitounis ◽  
Qiansheng Huang ◽  
Nathalia Oliveira ◽  
Kee Woei Ng ◽  
...  
Keyword(s):  
Dna Repair ◽  
High Throughput ◽  
High Throughput Screening ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Screening Platform

scholarly journals DNA Repair Gene Polymorphism and the Risk of Mitral Chordae Tendineae Rupture

2015 ◽  
Vol 2015 ◽  
pp. 1-6
Author(s):  
Aysel Kalayci Yigin ◽  
Mehmet Bulent Vatan ◽  
Ramazan Akdemir ◽  
Muhammed Necati Murat Aksoy ◽  
Mehmet Akif Cakar ◽  
...  
Keyword(s):  
Dna Repair ◽  
Fragment Length Polymorphism ◽  
Control Group ◽  
Chordae Tendineae ◽  
Repair Gene ◽  
Repair Capacity ◽  
Dna Repair Capacity ◽  
Dna Repair Gene ◽  
Increased Risk ◽  
Polymerase Chain

Polymorphisms in Lys939Gln XPC gene may diminish DNA repair capacity, eventually increasing the risk of carcinogenesis. The aim of the present study was to evaluate the significance of polymorphism Lys939Gln in XPC gene in patients with mitral chordae tendinea rupture (MCTR). Twenty-one patients with MCTR and thirty-seven age and sex matched controls were enrolled in the study. Genotyping of XPC gene Lys939Gln polymorphism was carried out using polymerase chain reaction- (PCR-) restriction fragment length polymorphism (RFLP). The frequencies of the heterozygote genotype (Lys/Gln-AC) and homozygote genotype (Gln/Gln-CC) were significantly different in MCTR as compared to control group, respectively (52.4% versus 43.2%,p=0.049; 38.15% versus 16.2%,p=0.018). Homozygote variant (Gln/Gln) genotype was significantly associated with increased risk of MCTR (OR = 2.059; 95% CI: 1.097–3.863;p=0.018). Heterozygote variant (Lys/Gln) genotype was also highly significantly associated with increased risk of MCTR (OR = 1.489; 95% CI: 1.041–2.129;p=0.049). The variant allele C was found to be significantly associated with MCTR (OR = 1.481; 95% CI: 1.101–1.992;p=0.011). This study has demonstrated the association of XPC gene Lys939Gln polymorphism with MCTR, which is significantly associated with increased risk of MCTR.

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