On the frequency of chromosome exchanges in a control population measured by chromosome painting

Tucker, James D.; Lee, Denise A.; Ramsey, Marilyn J.; Briner, Jane; Olsen, Letha; Moore, Dan H.

doi:10.1016/0165-1161(94)90049-3

Cited by 102 publications

(42 citation statements)

References 33 publications

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“…Loss of MMR activity leads to increased mutation rates, associated microsatellite instability, and the accumulation of mutations that play a role in carcinogenesis and are characterized by a mutator phenotype (12,13). Aged cells showed significantly higher rates of microsatellite instability (17)(18)(19)(20), which is likely to be responsible for a predisposition to cancer in the elderly, particularly in view of the role of genetic instability in carcinogenesis. Therefore, the MMR system may show reduced functionality with age.…”

Section: Introductionmentioning

confidence: 99%

Senescence-Dependent MutSα Dysfunction Attenuates Mismatch Repair

Chang¹,

Jin

Yoon

et al. 2008

Molecular Cancer Research

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DNA damage and mutations in the genome increase with age. To determine the potential mechanisms of senescence-dependent increases in genomic instability, we analyzed DNA mismatch repair (MMR) efficiency in young and senescent human colonic fibroblast and human embryonic lung fibroblast. It was found that MMR activity is significantly reduced in senescent cells. Western blot and immunohistochemistry analysis revealed that hMSH2 and MSH6 protein (MutSA complex), which is a known key component in the MMR pathway, is markedly down-regulated in senescent cells. Moreover, the addition of purified MutSA to extracts from senescent cells led to the restoration of MMR activity. Semiquantitative reverse transcription-PCR analysis exhibited that MSH2 mRNA level is reduced in senescent cells. In addition, a decrease in E2F transcriptional activity in senescent cells was found to be crucial for MSH2 suppression. E2F1 small interfering RNA expression reduced hMSH2 expression and MMR activity in young human primary fibroblast cells. Importantly, expression of E2F1 in quiescent cells restored the MSH2 expression as well as MMR activity, whereas E2F1-infected senescent cells exhibited no restoration of MSH2 expression and MMR activity. These results indicate that the suppression of E2F1 transcriptional activity in senescent cells lead to stable repression of MSH2, followed by a induction of MutSA dysfunction, which results in a reduced cellular MMR capacity in senescent cells. (Mol Cancer Res 2008;6(6):978 -89)

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Section: Introductionmentioning

confidence: 99%

Senescence-Dependent MutSα Dysfunction Attenuates Mismatch Repair

Chang¹,

Jin

Yoon

et al. 2008

Molecular Cancer Research

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“…Giemsa-detected aberrations are mainly transient markers of cytogenetic damage, which are not perpetuated in subsequent cell divisions. Stable aberrations persist through multiple cell divisions, and can accumulate over time with continued exposure; therefore, they are inherently more sensitive measures of continuous low-dose exposure than Giemsa-detected aberrations [Tucker et al, 1994;Ramsey et al, 1995;Ellard et al, 1996;Marshall and Obe, 1998]. The lack of correlation between stable and Giemsa-detected aberration frequencies is biologically plausible, as they are measuring two different types of aberrations, which is exemplified in the data shown in Tables I and II.…”

Section: Discussionmentioning

confidence: 95%

“…Traditional cytogenetic methods of measuring chromosome aberrations rely on nonbanded Giemsa-stained preparations, and thus are unable to detect most stable aberrations such as deletions and translocations. It is these stable aberrations that are most closely associated with cancer risk, as unstable aberrations are lethal and not perpetuated [Tucker et al, 1994;Ramsey et al, 1995;Ellard et al, 1996;Marshall and Obe, 1998]. Until the development of FISH, unstable aberrations, detected by Giemsa-staining, were used as an indicator of levels of chromosome breakage.…”

Section: Introductionmentioning

confidence: 99%

Fluorescence in situ hybridization is necessary to detect an association between chromosome aberrations and polycyclic aromatic hydrocarbon exposure in utero and reveals nonrandom chromosome involvement

Bocskay

Orjuela

Tang

et al. 2007

Environ and Mol Mutagen

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Chromosome aberrations are associated with environmental exposures in infants and children. Recently we reported that prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) was significantly (P < 0.01) associated with stable aberration frequencies in cord blood from a subset of 60 newborns from the Columbia Center for Children's Environmental Health Prospective Cohort Study (Bocskay K et al. [2005]: Cancer Epidemiol Biomarkers Prev 14:506-511). To determine whether the environmental exposures may be targeting specific chromosomes and to compare various methods for measuring chromosome aberrations, we further evaluated this same subset of subjects composed of African-American and Dominican nonsmoking mother-newborn pairs residing in low-income neighborhoods of New York City, and exposed to varying levels of airborne PAHs. Chromosome aberrations were measured in cord blood lymphocytes, both by whole chromosome probe (WCP) fluorescence in situ hybridization (FISH) and traditional Giemsa-staining. Prenatal exposures were assessed by personal air monitoring. Breaks in chromosomes 1-6, as detected by WCP FISH, were nonrandomly distributed, underscoring the importance of appropriate chromosome probe selection to capture cytogenetic damage in response to exposure. FISH for stable aberrations was found to be a more sensitive method for detecting aberration frequencies associated with environmental exposures, when compared with FISH for unstable aberrations or Giemsa-staining for aberrations. Together, these results suggest that PAHs may be targeting specific chromosomes and highlight the importance of using the more sensitive detection methods to assess risk in populations with low levels of exposure.

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“…It is suitable mainly for detection of structural rearrangement, especially for analysis of induced translocations (Pinkel et al 1988;Natarajan et al 1991;Tucker et al 1993Tucker et al , 1994Tucker et al , 1995.…”

Section: Whole Chromosomal Painting Probes (Fish-wcp)mentioning

confidence: 99%

Fluorescence in situ hybridisation

Lakatosova

Holečková

2007

Biologia

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Fluorescence in situ hybridisation (FISH) is a rapid and reliable technique for chromosomal investigations that is used for a wide variety of cytogenetic purposes at present. This molecular-cytogenetic method has been developed continuously for many years. As a consequence, various modifications with different kinds of fluorescently labelled probes have been introduced to optimise the detection of DNA and RNA sequences. This review articlepaper presents the general principles of in situ hybridisation, probe labelling and examples of proper use of different kinds of probes. In addition, some newer FISH methods and their usefulness in human molecular cytogenetics are described.

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On the frequency of chromosome exchanges in a control population measured by chromosome painting

Cited by 102 publications

References 33 publications

Senescence-Dependent MutSα Dysfunction Attenuates Mismatch Repair

Senescence-Dependent MutSα Dysfunction Attenuates Mismatch Repair

Fluorescence in situ hybridization is necessary to detect an association between chromosome aberrations and polycyclic aromatic hydrocarbon exposure in utero and reveals nonrandom chromosome involvement

Fluorescence in situ hybridisation

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