Common Chromosomal Fragile Sites and Cancer

Author(s):  
Yanwen Jiang ◽  
Isabelle Lucas ◽  
Michelle M. Le Beau
Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1743
Author(s):  
Marta Kuchta-Gładysz ◽  
Ewa Wójcik ◽  
Anna Grzesiakowska ◽  
Katarzyna Rymuza ◽  
Olga Szeleszczuk

A cytogenetic assay based on fragile sites (FS) enables the identification of breaks, chromatid gaps, and deletions. In healthy individuals, the number of these instabilities remains low. Genome stability in these species is affected by Robertsonian translocations in the karyotype of the blue fox and by B chromosomes in the silver fox. The aims of the study were to characterise the karyotype of blue foxes, silver foxes, and their hybrids and to identify chromosomal fragile sites used to evaluate genome stability. The diploid number of A chromosomes in blue foxes ranged from 48 to 50, while the number of B chromosomes in silver foxes varied from one to four, with a constant number of A chromosomes (2n = 34). In interspecific hybrids, both types of karyotypic variation were identified, with the diploid number of A chromosomes ranging from 40 to 44 and the number of B chromosomes varying from 0 to 3. The mean frequency of FS in foxes was 4.06 ± 0.19: 4.61 ± 0.37 in blue foxes, 3.46 ± 0.28 in silver foxes, and 4.12 ± 0.22 in hybrids. A relationship was identified between an increased number of A chromosomes in the karyotype of the hybrids and the frequency of chromosomal breaks. The FS assay was used as a biomarker for the evaluation of genomic stability in the animals in the study.


1991 ◽  
Vol 38 (2-3) ◽  
pp. 249-250 ◽  
Author(s):  
S. A. Musumeci ◽  
R. Ferri ◽  
M. Viglianesi ◽  
M. Elia ◽  
R. M. Ragusa ◽  
...  

2018 ◽  
Vol 19 (10) ◽  
pp. 3255 ◽  
Author(s):  
Wei-Chung Tsao ◽  
Kristin Eckert

Incomplete and low-fidelity genome duplication contribute to genomic instability and cancer development. Difficult-to-Replicate Sequences, or DiToRS, are natural impediments in the genome that require specialized DNA polymerases and repair pathways to complete and maintain faithful DNA synthesis. DiToRS include non B-DNA secondary structures formed by repetitive sequences, for example within chromosomal fragile sites and telomeres, which inhibit DNA replication under endogenous stress conditions. Oncogene activation alters DNA replication dynamics and creates oncogenic replication stress, resulting in persistent activation of the DNA damage and replication stress responses, cell cycle arrest, and cell death. The response to oncogenic replication stress is highly complex and must be tightly regulated to prevent mutations and tumorigenesis. In this review, we summarize types of known DiToRS and the experimental evidence supporting replication inhibition, with a focus on the specialized DNA polymerases utilized to cope with these obstacles. In addition, we discuss different causes of oncogenic replication stress and its impact on DiToRS stability. We highlight recent findings regarding the regulation of DNA polymerases during oncogenic replication stress and the implications for cancer development.


2001 ◽  
Vol 1 (4) ◽  
pp. 293-299 ◽  
Author(s):  
K.R. Manjunatha ◽  
G.K. Chetan ◽  
R. Arathi ◽  
S. Padma ◽  
H.N. Venkatesh ◽  
...  

1993 ◽  
Vol 58 (0) ◽  
pp. 633-635 ◽  
Author(s):  
C.D. Laird ◽  
R.S. Hansen ◽  
T.K. Canfield ◽  
M.M. Lamb ◽  
S.M. Gartler

BMC Genomics ◽  
2009 ◽  
Vol 10 (1) ◽  
pp. 59 ◽  
Author(s):  
Allison A Burrow ◽  
Laura E Williams ◽  
Levi CT Pierce ◽  
Yuh-Hwa Wang

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