scholarly journals Genetic variation in DNA repair pathway genes and melanoma risk☆

DNA Repair ◽  
2011 ◽  
Vol 10 (1) ◽  
pp. 111-116 ◽  
Author(s):  
Mingfeng Zhang ◽  
Abrar A. Qureshi ◽  
Qun Guo ◽  
Jiali Han
2017 ◽  
Vol 233 (4) ◽  
pp. 2752-2758 ◽  
Author(s):  
Farimah Beheshti ◽  
Seyed Mahdi Hassanian ◽  
Majid Khazaei ◽  
Mahmoud Hosseini ◽  
Soodabeh ShahidSales ◽  
...  

2008 ◽  
Vol 115 (3) ◽  
pp. 613-622 ◽  
Author(s):  
Jiali Han ◽  
Christopher Haiman ◽  
Tianhua Niu ◽  
Qun Guo ◽  
David G. Cox ◽  
...  

2017 ◽  
Vol 141 (5) ◽  
pp. 952-957 ◽  
Author(s):  
Yuan Lin ◽  
Harvind S. Chahal ◽  
Wenting Wu ◽  
Hyunje G. Cho ◽  
Katherine J. Ransohoff ◽  
...  

2020 ◽  
Vol 20 (9) ◽  
pp. 779-787
Author(s):  
Kajal Ghosal ◽  
Christian Agatemor ◽  
Richard I. Han ◽  
Amy T. Ku ◽  
Sabu Thomas ◽  
...  

Chemotherapy employs anti-cancer drugs to stop the growth of cancerous cells, but one common obstacle to the success is the development of chemoresistance, which leads to failure of the previously effective anti-cancer drugs. Resistance arises from different mechanistic pathways, and in this critical review, we focus on the Fanconi Anemia (FA) pathway in chemoresistance. This pathway has yet to be intensively researched by mainstream cancer researchers. This review aims to inspire a new thrust toward the contribution of the FA pathway to drug resistance in cancer. We believe an indepth understanding of this pathway will open new frontiers to effectively treat drug-resistant cancer.


Genetics ◽  
1990 ◽  
Vol 124 (4) ◽  
pp. 817-831 ◽  
Author(s):  
R H Schiestl ◽  
S Prakash ◽  
L Prakash

Abstract rad6 mutants of Saccharomyces cerevisiae are defective in the repair of damaged DNA, DNA damage induced mutagenesis, and sporulation. In order to identify genes that can substitute for RAD6 function, we have isolated genomic suppressors of the UV sensitivity of rad6 deletion (rad6 delta) mutations and show that they also suppress the gamma-ray sensitivity but not the UV mutagenesis or sporulation defects of rad6. The suppressors show semidominance for suppression of UV sensitivity and dominance for suppression of gamma-ray sensitivity. The six suppressor mutations we isolated are all alleles of the same locus and are also allelic to a previously described suppressor of the rad6-1 nonsense mutation, SRS2. We show that suppression of rad6 delta is dependent on the RAD52 recombinational repair pathway since suppression is not observed in the rad6 delta SRS2 strain containing an additional mutation in either the RAD51, RAD52, RAD54, RAD55 or RAD57 genes. Possible mechanisms by which SRS2 may channel unrepaired DNA lesions into the RAD52 DNA repair pathway are discussed.


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