Molecular Epidemiology of DNA Repair and Cancer Susceptibility — A Review of Population-based Studies

Author(s):  
Zhibin Hu ◽  
Li-E Wang ◽  
Qingyi Wei
2003 ◽  
Vol 1 (3) ◽  
pp. 175-186
Author(s):  
Jang-Ming Lee ◽  
Yung-Chie Lee ◽  
Chien-Jen Chen ◽  
Ming-Tsang Wu

2015 ◽  
Vol 148 (4) ◽  
pp. S-63 ◽  
Author(s):  
Maria Asuncion García-González ◽  
Luis Bujanda ◽  
Enrique Quintero ◽  
Santos Santolaria ◽  
Rafael Benito ◽  
...  

2011 ◽  
pp. 453-465 ◽  
Author(s):  
T. HUCL ◽  
E. GALLMEIER

DNA repair is an active cellular process to respond to constant DNA damage caused by metabolic processes and environmental factors. Since the outcome of DNA damage is generally adverse and long term effects may contribute to oncogenesis, cells have developed a variety of DNA repair mechanisms, which operate depending on the type of DNA damage inflicted. At least 15 Fanconi anemia (FA) proteins interact in a common pathway involved in homologous recombination. Inherited homozygous mutations in any of these FA genes cause a rare disease, Fanconi anemia, characterized by congenital abnormalities, progressive bone-marrow failure and cancer susceptibility. Heterozygous germline FA mutations predispose to various types of cancer. In addition, somatic FA mutations have been identified in diverse cancer types. Evidence exists that cells deficient in the FA pathway become dependent on alternative pathways for survival. Additional inhibition of such alternative pathways is thus expected to result in cell death, creating a relationship of synthetic lethality. Identifying these relationships can reveal yet unknown mechanisms of DNA repair and new targets for therapy.


2008 ◽  
Vol 1 ◽  
pp. 117822340800100
Author(s):  
Goberdhan P. Dimri

I would like to welcome breast cancer research community to the first editorial of our newest journal “Breast Cancer: Basic and Clinical Research”. In pursuit of breast cancer culprits, we have come a long way since the early 90's when the first breast cancer susceptibility gene BRCA1 was mapped and cloned. In the past few years, several new loci associated with the various degree of breast cancer risk have been identified using “Candidate Gene Association Study (CGAS) and Genome-Wide Association Study (GWAS)” approaches. This editorial is meant to quickly glance over recent findings of these population-based association studies.


2008 ◽  
Vol 17 (8) ◽  
pp. 2123-2127 ◽  
Author(s):  
Mingdong Zhang ◽  
Wen-Yi Huang ◽  
Gabriella Andreotti ◽  
Yu-Tang Gao ◽  
Asif Rashid ◽  
...  

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Jing Wen ◽  
Zhi Lv ◽  
Hanxi Ding ◽  
Xinxin Fang ◽  
Mingjun Sun

Single nucleotide polymorphisms (SNPs) in miRNA biosynthesis genes DROSHA and DGCR8 were indicated to be correlated with cancer risk. We comprehensively reviewed and analyzed the effect of DROSHA and DGCR8 polymorphisms on cancer risk. Eligible articles were selected according to a series of inclusion and exclusion criteria. Consequently, ten case–control studies (from nine citations) with 4265 cancer cases and 4349 controls were involved in a meta-analysis of seven most prevalent SNPs (rs10719 T/C, rs6877842 G/C, rs2291109 A/T, rs642321 C/T, rs3757 G/A, rs417309 G/A, rs1640299 T/G). Our findings demonstrated that the rs417309 SNP in DGCR8 was significantly associated with an elevated risk of overall cancer in every genetic model. In stratified analysis, correlations of DROSHA rs10719 and rs6877842 SNPs were observed in Asian and laryngeal cancer subgroups, respectively. Moreover, associations of the rs417309 SNP could also be found in numerous subgroups including: Asian and Caucasian population subgroups; laryngeal and breast cancer subgroups; population-based (PB) and hospital-based (HB) subgroups. In conclusion, the DROSHA rs10719, rs6877842 SNPs, and DGCR8 rs417309 SNP play pivotal roles in cancerogenesis and may be potential biomarkers for cancer-forewarning.


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