Characterization of the common fragile site FRA9E and its potential role in ovarian cancer

@article{Callahan2003CharacterizationOT,
  title={Characterization of the common fragile site FRA9E and its potential role in ovarian cancer},
  author={Gwen Callahan and Stacy R. Denison and Leslie A Phillips and Viji Shridhar and David I. Smith},
  journal={Oncogene},
  year={2003},
  volume={22},
  pages={590-601}
}
Common fragile sites (CFSs) are regions of profound genomic instability that have been hypothesized to play a role in cancer. The major aim of this study was to locate a fragile region associated with ovarian cancer. Differential display (DD)-PCR analysis comparing normal ovarian epithelial cultures and ovarian cancer cell lines identified pregnancy-associated plasma protein-A (PAPPA) because of its frequent loss of expression (LOE) in ovarian cancer cell lines. PAPPA is localized to human… 

Molecular characterization of the human common fragile site FRA1H

TLDR
The FRA1H DNA sequence was analyzed to identify coding sequences, the AT content, the type and quantity of the DNA repeats, the CpG islands, the matrix attachment regions, and the number and distribution of high‐flexibility regions and a 120 kb long sequence was identified that may be involved in inducing fragility in the surrounding regions.

Relationship between FRA11F and 11q13 gene amplification in oral cancer

TLDR
Findings suggest that gene amplification involving chromosomal band 11q13 in OSCC may be initiated by breakage at FRA11F, a nonstaining gaps or breaks in chromosomes that are expressed under conditions inducing replicative stress.

A selected group of large common fragile site genes have decreased expression in oropharyngeal squamous cell carcinomas

TLDR
The results suggest that this selected group of large genes might serve as potential tumor suppressors involved in the development of OPSCCs, and are located within the two most frequently expressed CFSs.

Characterization of FRA6E and its potential role in autosomal recessive juvenile parkinsonism and ovarian cancer

Characterization of FRA6E (6q26), the third most frequently observed common fragile site (CFS) in the human population, determined that aphidicolin‐induced instability at FRA6E extends over a very

Common Fragile Sites: Genomic Hotspots of DNA Damage and Carcinogenesis

TLDR
Recent studies of FATS (for Fragile-site Associated Tumor Suppressor), a new CACG at FRA10F, reveal an active role of this CACGs in regulating DNA damage checkpoints and suppressing tumorigenesis.

Molecular characterization of common fragile sites as a strategy to discover cancer susceptibility genes

TLDR
The cytogenetic hypothesis that common fragile sites (cFSs) are hotspots of cancer breakpoints is increasingly supported by recent data from whole-genome profiles of different cancers, and emphasis is put on less-studied cFS genes as potential contributors to cancer development.

Short communication Biallelic deletion and loss of expression analysis of genes at FRA2G common fragile site in tumor-derived cell lines

TLDR
It is found that Burkitt lymphoma-derived cell line DAUDI has a biallelic deletion of eight of the nine analyzed genes, and loss of expression of the DHRS9 gene (alias RDHL), one of the deleted genes in the DAUDi cell line, is observed in MOLT- 14 and Raji cell lines derived from BurkITT lymphoma and from T-cell acute lymphoblastic leukemia.
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The hypothesis that common fragile sites and their associated genes are, in general, unstable in some cancer cells is supported, including FRAXB, which is not associated with any known tumor suppressor genes or activity.

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TLDR
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Data is provided to suggest that several of the genes mapped to common fragile sites within CFSs may be inactivated in ovarian cancer.

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TLDR
FISH-based analysis of three overlapping P1 clones reveals that aphidicolin-induced breakage in the FRA7G region occurs over a region of at least 300 Kb in length and there is an association with both spcDNAs and hot-spots for viral integration.

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TLDR
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TLDR
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TLDR
The homozygous deletion of WWOX exons from ovarian cancer cells and three different tumor cell lines is demonstrated and evidence strengthens the case for WWOX as a tumor suppressor gene in ovarian cancer and other tumor types.

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