Identification of the human/mouse syntenic common fragile site FRA7K/Fra12C1—Relation of FRA7K and other human common fragile sites on chromosome 7 to evolutionary breakpoints

Helmrich, Anne; Stout-Weider, Karen; Matthaei, Anja; Hermann, K.; Heiden, Thomas

doi:10.1002/ijc.22049

Cited by 39 publications

(35 citation statements)

References 43 publications

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“…3). Additionally, 52 identified and in parts mapped FS were already published, but not included in the current genome browser versions (13,14,15,16,17,19,23,34). Most of these sites were confirmed in this study which underlines their eligibility to be appreciated as FS.…”

Section: ------------------------------------------------------------supporting

confidence: 50%

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Global screening and extended nomenclature for 230 aphidicolin-inducible fragile sites, including 61 yet unreported ones

Weise¹

2010

Int J Oncol

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Abstract. Since the first description of human fragile sites (FS) more than 40 years ago, a variety of substances were reported to induce chromosomal breaks at non-random, breakage-prone regions. According to information available from human genome browsers aphidicolin, an inhibitor of DNA replication induces 77 of 88 known common FS. However, in the literature additional FS are reported, which are also, at least in part, inducible by aphidicolin. To the best of our knowledge, here we present the first and largest ever done systematic, whole genome-directed and comprehensive screening for aphidicolin-inducible breakage-prone regions. The study was performed on stimulated peripheral blood lymphocytes of 3 unrelated healthy individuals. Twenty-five thousand metaphase spreads were analyzed and overall 22,537 FS located in 230 different loci were recorded. Sixtyone of those FS were never observed before and 52 were already previously reported but not included in genome browsers and yet verified. Interestingly, aphidicolin was able to induce all types of rare and common FS, suggesting that these breakage-prone regions are less dependent on the inducing chemicals than originally supposed. Overall, we provide the first comprehensive genome wide map for FS and studied possible correlations of chromosome length and GTG-banding level with FS-frequency. To handle FS better in future, an extension of the already existing alphabetical nomenclature for FS on single chromosomes is suggested.

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Section: ------------------------------------------------------------supporting

confidence: 50%

“…Additionally, differences in the observable FS-frequency within different individuals are well known (11,12). Besides these 88 official, database-annotated common FS others were observed and reported, including six recently reported new sites, particularly FRA4F (13), FRA7K (14), FRA6H (15), FRA9G (16), FRA13E (15) and FRA18C (17).…”

Section: Introductionmentioning

confidence: 94%

Global screening and extended nomenclature for 230 aphidicolin-inducible fragile sites, including 61 yet unreported ones

Weise¹

2010

Int J Oncol

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“…It appears, though, that they are densely packed in areas of high flexibility (Toledo et al, 2000). Notably, in a very recent study focusing on FS on chromosome 7, similar findings with regard to DNA-helix flexibility were drawn (Helmrich et al, 2007).…”

Section: Discussionmentioning

confidence: 60%

“…It appears that some CFSs contain flexibility peaks (Mishmar et al, 1998(Mishmar et al, , 1999Mimori et al, 1999;Zlotorynski et al, 2003), adenine-thymine runs (Zlotorynski et al, 2003) or an increased percentage of repetitive DNA (Morelli et al, 2002). Despite the usefulness of these sporadic observations, which generally concern the subset of the molecularly defined CFSs (Helmrich et al, 2007), a broad survey of the sequence characteristics of CFSs is missing.…”

Section: Introductionmentioning

confidence: 99%

Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study

et al. 2007

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Common fragile sites (CFSs) are regions of the genome prone to breakage by replication inhibitors (extrinsic replication stress). Recently, we and others observed that oncogene-induced replication stress (RS) induces DNA damage from the earliest stages of cancer. Our aim was to perform a genome-wide analysis in precancerous and cancerous experimental models to examine whether allelic imbalance occurs within CFSs. Subsequently, CFSs sequence characteristics were assessed. We used a growth-factor-induced human skin hyperplasia and a H-ras-induced mouse hyperplastic urothelium as preneoplastic models, along with an inducible U2OS-CDT1Tet-ON cancer cell line model, all bearing established oncogeneinduced RS stimuli. Human DNA was analysed with Affymetrix SNP microarrays, while mouse DNA was analysed with Nimblegen array CGH. We studied 56 aphidicolin-type CFSs and 1914 regions of control, nonfragile DNA. Our theoretical in silico analysis spanned 2.16 billion nonoverlapping bases on human chromosomes 1-22. Our results provide direct experimental evidence indicating that genomic alterations were more common within CFSs in epidermal and urothelial preneoplastic lesions as well as in cancer. CFSs were on average less flexible than nonfragile regions, contained more guanine-cytosine (GC) and Alu sequences. Importantly, regions with loss-of-heterozygosity were also less flexible and had a higher Alu percentage.

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“…Additionally, 2 integration sites were located in the mouse common fragile sites, Fra6B3 and Fra12C1 (17). Previous studies have revealed that common fragile sites are extremely unstable in the process of carcinogenesis and are always destroyed and rearranged in many tumor cells (18,19). Researchers have noted that most miRNAs play significant roles in tumorigenesis and metastasis (20).…”

Section: B Amentioning

confidence: 99%

Detection of SRS19-6MuLV in mouse dendritic cell sarcoma and its tumorigenesis

Liu

Bian

et al. 2011

Mol Med Report

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Abstract. SRS19-6MuLV is a member of the MuLV family originally isolated from the Tianjin-Shanghai-Zunyi complex of murine leukemia. A notable characteristic of this virus is that it induces tumors of multiple hematopoietic lineages, including myeloid, erythroid, T-lymphoid and B-lymphoid. In a previous study, a sequence with high homology to SRS19-6MuLV in a murine dendritic cell sarcoma (DCS) was identified through cDNA expression screening with mAb 983D4. To investigate the relationship between SRS19-6MuLV and DCS, the existence of a specific SRS19-6MuLV DNA fragment in DCS cells, 15 murine tumor cells, 2 murine tumor tissues, 12 normal murine cells/tissues, 11 human tumor cell lines and SRSV/3T3 (NIH/3T3 cells infected with SRS cell supernatant) was detected by PCR. The specific fragment of SRS19-6MuLV was detected in DCS, mouse fore-gastric cancer cells, LⅡ tumor tissue from which DCS is derived and SRSV/3T3. In addition, the integration sites of SRS19-6MuLV in the positive cells were examined by inverse PCR. Thus, 7 integration sites for SRS19-6MuLV were detected in DCS and 3 in SRSV/3T3. Analysis of sequences by BLAST revealed that some of the integration sites were associated with common fragile sites and some Ras-regulating miRNAs. Our results indicate that SRS19-6MuLV not only induced four types of leukemia, but also induced DCS. This virus does not infect human cells. Multiple integration of SRS19-6MuLV into chromosomes around fragile sites accounts for its carcinogenic effects.

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Identification of the human/mouse syntenic common fragile site FRA7K/Fra12C1—Relation of FRA7K and other human common fragile sites on chromosome 7 to evolutionary breakpoints

Cited by 39 publications

References 43 publications

Global screening and extended nomenclature for 230 aphidicolin-inducible fragile sites, including 61 yet unreported ones

Global screening and extended nomenclature for 230 aphidicolin-inducible fragile sites, including 61 yet unreported ones

Oncogene-induced replication stress preferentially targets common fragile sites in preneoplastic lesions. A genome-wide study

Detection of SRS19-6MuLV in mouse dendritic cell sarcoma and its tumorigenesis

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