A 700-kb physical and transcription map of the cervical cancer tumor suppressor gene locus on chromosome 11q13

Zainabadi, Kayvan; Benyamini, Payam; Chakrabarti, Rita; Veena, Mysore S.; Chandrasekharappa, Settara C.; Gatti, Richard A.; Srivatsan, Eri S.

doi:10.1016/j.ygeno.2005.02.014

Cited by 24 publications

(36 citation statements)

References 43 publications

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“…FRA11A, a rare folate-sensitive fragile site has been mapped to the interval between D11S913 and ACTN3 in band 11q13.2 (Zainabadi et al, 2005). In our study, three of the BAC clones (692F22, 380K11, and 527H7) that were used to map the amplicon covered the FRA11A locus.…”

Section: Discussionmentioning

confidence: 88%

Molecular cytogenetic characterization of the 11q13 amplicon in head and neck squamous cell carcinoma

Jin¹,

Jin²,

Gisselsson³

et al. 2006

Cytogenet Genome Res

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Amplification of 11q13 DNA sequences and overexpression of CCND1 are common findings in head and neck squamous cell carcinoma (HNSCC), identified in about 30% of the cases. However, little is known about initiation of the amplification and the organization of the amplicon. In order to study the structure of the amplicon in more detail and to learn more about the mechanisms involved in its initiation, prometaphase, metaphase, and anaphase fluorescence in situ hybridization (FISH) with 40 BAC clones spanning a 16-Mb region in chromosome bands 11q12.2 to 11q13.5 was performed in nine HNSCC cell lines with homogeneously staining regions. FISH analysis showed that the size of the amplicon varied among the nine cell lines, the smallest being 2.12 Mb and the largest 8.97 Mb. The smallest overlapping region of amplification was approximately 1.61 Mb, covering the region from BAC 729E14 to BAC 102B19. This region contained several genes previously shown to be amplified and overexpressed in HNSCC, including CCDN1, CTTN, SHANK2, and ORAOV1. The cell lines were also used to study the internal structure of the amplicon. Various patterns of amplified DNA sequences within the amplicon were found among the nine cell lines. Even within the same cell line, different amplicon structures could be found in different cell populations, indicating that the mechanisms involved in the development of the amplicons in HNSCC were more complex than previously assumed. The frequent finding of inverted repeats within the amplicons, however, suggests that breakage-fusion-bridge cycles are important in the initiation, but the fact that such repeats constituted only small parts of the amplicons indicate that they are further rearranged during tumor progression.

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Section: Discussionmentioning

confidence: 88%

Molecular cytogenetic characterization of the 11q13 amplicon in head and neck squamous cell carcinoma

Jin¹,

Jin²,

Gisselsson³

et al. 2006

Cytogenet Genome Res

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“…Gray spots, moving average ratio of 10 adjacent clones and a smoothing algorithm (black vertical lines ). Gains and losses are marked using the aCGH-Smooth software (http://www.few.vu.nl/~vumarray/) with default settings, apart from the E-variable set to 5. has been found to contain mutations in cancer (30 [31][32][33][34]. Interestingly, all except one of the fragile sites that coincide with the asbestosassociated regions have been implicated in bladder cancer (35) that is also associated with asbestos exposure (36).…”

Section: Resultsmentioning

confidence: 99%

Identification of Specific Gene Copy Number Changes in Asbestos-Related Lung Cancer

et al. 2006

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Asbestos is a well-known lung cancer-causing mineral fiber. In vitro and in vivo experiments have shown that asbestos can cause chromosomal damage and aberrations. Lung tumors, in general, have several recurrently amplified and deleted chromosomal regions. To investigate whether a distinct chromosomal aberration profile could be detected in the lung tumors of heavily asbestos-exposed patients, we analyzed the copy number profiles of 14 lung tumors from highly asbestosexposed patients and 14 matched tumors from nonexposed patients using classic comparative genomic hybridization (CGH). A specific profile could lead to identification of the underlying genes that may act as mediators of tumor formation and progression. In addition, array CGH analyses on cDNA microarrays (13,000 clones) were carried out on 20 of the same patients. Classic CGH showed, on average, more aberrations in asbestos-exposed than in nonexposed patients, and an altered region in chromosome 2 seemed to occur more frequently in the asbestos-exposed patients. Array CGH revealed aberrations in 18 regions that were significantly associated with either of the two groups. The most significant regions were 2p21-p16.3, 5q35.3, 9q33.3-q34.11, 9q34.13-q34.3, 11p15.5, 14q11.2, and 19p13.1-p13.3 (P < 0.005). Furthermore, 11 fragile sites coincided with the 18 asbestos-associated regions (P = 0.08), which may imply preferentially caused DNA damage at these sites. Our findings are the first evidence, indicating that asbestos exposure may produce a specific DNA damage profile. (Cancer Res 2006; 66(11): 5737-43)

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“…is located immediately upstream of all the amplicons ( Figure 3) (Buttel et al, 2004;Zainabadi et al, 2005). Based on the Breakage-Fusion-Bridge theory of gene amplification (Coquelle et al, 1997), FRA11A together with other downstream fragile sequences may contribute to the establishment of the CoAA amplicon boundaries.…”

Section: Coaa Gene Amplification In Human Cancersmentioning

confidence: 99%

Gene amplification and associated loss of 5′ regulatory sequences of CoAA in human cancers

et al. 2006

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A 700-kb physical and transcription map of the cervical cancer tumor suppressor gene locus on chromosome 11q13

Cited by 24 publications

References 43 publications

Molecular cytogenetic characterization of the 11q13 amplicon in head and neck squamous cell carcinoma

Molecular cytogenetic characterization of the 11q13 amplicon in head and neck squamous cell carcinoma

Identification of Specific Gene Copy Number Changes in Asbestos-Related Lung Cancer

Gene amplification and associated loss of 5′ regulatory sequences of CoAA in human cancers

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