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Journal articles on the topic 'DNA translocation'

Author: Grafiati

Published: 4 June 2021

Last updated: 26 July 2025

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1

Huang, Stephanie, Kara Juneau, Patrick E. Bogard, et al. "Identifying Robertsonian Translocation Carriers by Microarray-Based DNA Analysis." Fetal Diagnosis and Therapy 40, no. 1 (2016): 59–62. http://dx.doi.org/10.1159/000441945.

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Objective: To develop a noninvasive prenatal testing improvement that allows identification of Robertsonian translocation carriers. Methods: Blood samples from 191 subjects, including 7 pregnant and 9 non-pregnant Robertsonian translocation carriers, were analyzed for fetal trisomy and Robertsonian translocation status. Digital Analysis of Selected Regions (DANSR™) assays targeting sequences common to the p arms of 5 acrocentric chromosomes were developed and added to existing DANSR assays. DANSR products were hybridized onto a custom DNA microarray for DNA analysis. The Fetal-Fraction Optimiz

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2

Chand, Mahesh Kumar, Vanessa Carle, K. G. Anuvind, and Kayarat Saikrishnan. "DNA-mediated coupling of ATPase, translocase and nuclease activities of a Type ISP restriction-modification enzyme." Nucleic Acids Research 48, no. 5 (2020): 2594–603. http://dx.doi.org/10.1093/nar/gkaa023.

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Abstract Enzymes involved in nucleic acid transactions often have a helicase-like ATPase coordinating and driving their functional activities, but our understanding of the mechanistic details of their coordination is limited. For example, DNA cleavage by the antiphage defense system Type ISP restriction-modification enzyme requires convergence of two such enzymes that are actively translocating on DNA powered by Superfamily 2 ATPases. The ATPase is activated when the enzyme recognizes a DNA target sequence. Here, we show that the activation is a two-stage process of partial ATPase stimulation

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3

Suma, Antonio, and Cristian Micheletti. "Pore translocation of knotted DNA rings." Proceedings of the National Academy of Sciences 114, no. 15 (2017): E2991—E2997. http://dx.doi.org/10.1073/pnas.1701321114.

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We use an accurate coarse-grained model for DNA and stochastic molecular dynamics simulations to study the pore translocation of 10-kbp–long DNA rings that are knotted. By monitoring various topological and physical observables we find that there is not one, as previously assumed, but rather two qualitatively different modes of knot translocation. For both modes the pore obstruction caused by knot passage has a brief duration and typically occurs at a late translocation stage. Both effects are well in agreement with experiments and can be rationalized with a transparent model based on the conc

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4

Wang, Xiaobin S., Demis Menolfi, Foon Wu-Baer, et al. "DNA damage–induced phosphorylation of CtIP at a conserved ATM/ATR site T855 promotes lymphomagenesis in mice." Proceedings of the National Academy of Sciences 118, no. 38 (2021): e2105440118. http://dx.doi.org/10.1073/pnas.2105440118.

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CtIP is a DNA end resection factor widely implicated in alternative end-joining (A-EJ)–mediated translocations in cell-based reporter systems. To address the physiological role of CtIP, an essential gene, in translocation-mediated lymphomagenesis, we introduced the T855A mutation at murine CtIP to nonhomologous end-joining and Tp53 double-deficient mice that routinely succumbed to lymphomas carrying A-EJ–mediated IgH-Myc translocations. T855 of CtIP is phosphorylated by ATM or ATR kinases upon DNA damage to promote end resection. Here, we reported that the T855A mutation of CtIP compromised th

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5

Weinstock, David M., Beth Elliott, and Maria Jasin. "A model of oncogenic rearrangements: differences between chromosomal translocation mechanisms and simple double-strand break repair." Blood 107, no. 2 (2006): 777–80. http://dx.doi.org/10.1182/blood-2005-06-2437.

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AbstractRecurrent reciprocal translocations are present in many hematologic and mesenchymal malignancies. Because significant sequence homology is absent from translocation breakpoint junctions, non-homologous end-joining (NHEJ) pathways of DNA repair are presumed to catalyze their formation. We developed translocation reporters for use in mammalian cells from which NHEJ events can be selected after precise chromosomal breakage. Translocations were efficiently recovered with these reporters using mouse cells, and their breakpoint junctions recapitulated findings from oncogenic translocations.

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6

Tennyson, Rachel B., Nathalie Ebran, Anissa E. Herrera, and Janet E. Lindsley. "A Novel Selection System for Chromosome Translocations in Saccharomyces cerevisiae." Genetics 160, no. 4 (2002): 1363–73. http://dx.doi.org/10.1093/genetics/160.4.1363.

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Abstract Chromosomal translocations are common genetic abnormalities found in both leukemias and solid tumors. While much has been learned about the effects of specific translocations on cell proliferation, much less is known about what causes these chromosome rearrangements. This article describes the development and use of a system that genetically selects for rare translocation events using the yeast Saccharomyces cerevisiae. A translocation YAC was created that contains the breakpoint cluster region from the human MLL gene, a gene frequently involved in translocations in leukemia patients,

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7

Lu, Zhengfei, Michael R. Lieber, Albert G. Tsai, et al. "Human Lymphoid Translocation Fragile Zones Are Hypomethylated and Have Accessible Chromatin." Molecular and Cellular Biology 35, no. 7 (2015): 1209–22. http://dx.doi.org/10.1128/mcb.01085-14.

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Chromosomal translocations are a hallmark of hematopoietic malignancies. CG motifs within translocation fragile zones (typically 20 to 600 bp in size) are prone to chromosomal translocation in lymphomas. Here we demonstrate that the CG motifs in human translocation fragile zones are hypomethylated relative to the adjacent DNA. Using a methyltransferase footprinting assay on isolated nuclei (in vitro), we find that the chromatin at these fragile zones is accessible. We also examinedin vivoaccessibility using cellular expression of a prokaryotic methylase. Based on this assay, which measures acc

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8

Lee, J. H., S. M. Kaeppler, R. A. Graybosch, and R. G. Sears. "A PCR assay for detection of a 2RL.2BS wheat–rye chromosome translocation." Genome 39, no. 3 (1996): 605–8. http://dx.doi.org/10.1139/g96-076.

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A 2RL.2BS wheat–rye translocation, present in the wheat germplasm line Hamlet, carries a gene for resistance to Hessian fly biotype L, one of the most virulent biotypes presently encountered in wheat production environments. Unlike several other wheat–rye chromosome translocations common in wheat breeding programs, 2RL lacks genes encoding storage proteins or other easily selected markers. Oligonucleotide primers synthesized from published sequences derived from the R173 family of moderately repetitive rye DNA were used in the DNA polymerase chain reaction (PCR) to identify specific markers fo

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9

Lomov, N. A., V. S. Viushkov, and M. A. Rubtsov. "Mechanisms for the development of therapy-related leukaemia caused by topoisomerase inhibitors." Биохимия 88, no. 7 (2023): 1101–22. http://dx.doi.org/10.31857/s0320972523070047.

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Leukemia is a blood cancer that originates in the blood and bone marrow. Therapy-related leukemia is a leukemia associated with prior chemotherapy. Cancer therapy with DNA-topoisomerase II inhibitors is one of the most effective among chemotherapies. However, its side effect can be the development of secondary leukemia, characterized by chromosomal rearrangements involving the AML1 or MLL gene. The set of recurrent translocations in such leukemia differs from the set of chromosomal rearrangements in other neoplasia. We review the factors that drive the translocations upon treatment of cells wi

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10

Roukos, Vassilis, Ty C. Voss, Christine K. Schmidt, Seungtaek Lee, Darawalee Wangsa, and Tom Misteli. "Spatial Dynamics of Chromosome Translocations in Living Cells." Science 341, no. 6146 (2013): 660–64. http://dx.doi.org/10.1126/science.1237150.

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Chromosome translocations are a hallmark of cancer cells. We have developed an experimental system to visualize the formation of translocations in living cells and apply it to characterize the spatial and dynamic properties of translocation formation. We demonstrate that translocations form within hours of the occurrence of double-strand breaks (DSBs) and that their formation is cell cycle–independent. Translocations form preferentially between prepositioned genome elements, and perturbation of key factors of the DNA repair machinery uncouples DSB pairing from translocation formation. These ob

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11

McKim, K. S., A. M. Howell, and A. M. Rose. "The effects of translocations on recombination frequency in Caenorhabditis elegans." Genetics 120, no. 4 (1988): 987–1001. http://dx.doi.org/10.1093/genetics/120.4.987.

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Abstract In the nematode Caenorhabditis elegans, recombination suppression in translocation heterozygotes is severe and extensive. We have examined the meiotic properties of two translocations involving chromosome I, szT1(I;X) and hT1(I;V). No recombination was observed in either of these translocation heterozygotes along the left (let-362-unc-13) 17 map units of chromosome I. Using half-translocations as free duplications, we mapped the breakpoints of szT1 and hT1. The boundaries of crossover suppression coincided with the physical breakpoints. We propose that DNA sequences at the right end o

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12

Hernández-Ainsa, Silvia, Nicholas A. W. Bell, Vivek V. Thacker, et al. "DNA Origami Nanopores for Controlling DNA Translocation." ACS Nano 7, no. 7 (2013): 6024–30. http://dx.doi.org/10.1021/nn401759r.

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13

Greisman, Harvey A., Hye Son Yi, and Noah G. Hoffman. "transCGH: Rapid Identification and High-Resolution Mapping of Balanced IgH Translocations in Archival DNA Using Custom Oligonucleotide Arrays." Blood 110, no. 11 (2007): 459. http://dx.doi.org/10.1182/blood.v110.11.459.459.

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Abstract Array based comparative genomic hybridization (CGH) has revolutionized the study of chromosomal imbalances but generally is incapable of detecting balanced genomic rearrangements like reciprocal translocations, which play central roles in the pathogenesis and diagnosis of lymphomas, leukemias and other tumors. The precise identification of immunoglobulin heavy chain (IgH) translocation partners, for example, is essential for the classification of B cell lymphomas and for predicting prognosis in plasma cell neoplasms like multiple myeloma. Using IgH translocations as a model for balanc

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14

Schwer, Bjoern, Pei-Chi Wei, Amelia N. Chang, et al. "Transcription-associated processes cause DNA double-strand breaks and translocations in neural stem/progenitor cells." Proceedings of the National Academy of Sciences 113, no. 8 (2016): 2258–63. http://dx.doi.org/10.1073/pnas.1525564113.

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High-throughput, genome-wide translocation sequencing (HTGTS) studies of activated B cells have revealed that DNA double-strand breaks (DSBs) capable of translocating to defined bait DSBs are enriched around the transcription start sites (TSSs) of active genes. We used the HTGTS approach to investigate whether a similar phenomenon occurs in primary neural stem/progenitor cells (NSPCs). We report that breakpoint junctions indeed are enriched around TSSs that were determined to be active by global run-on sequencing analyses of NSPCs. Comparative analyses of transcription profiles in NSPCs and B

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15

Fonseca, Rafael, Carina S. Debes-Marun, Elisa B. Picken, et al. "The recurrent IgH translocations are highly associated with nonhyperdiploid variant multiple myeloma." Blood 102, no. 7 (2003): 2562–67. http://dx.doi.org/10.1182/blood-2003-02-0493.

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Abstract Aneuploid is ubiquitous in multiple myeloma (MM), and 4 cytogenetic subcategories are recognized: hypodiploid (associated with a shorter survival), pseudodiploid, hyperdiploid, and near-tetraploid MM. The hypodiploid, pseudodiploid, and near-tetraploid karyotypes can be referred to as the nonhyperdiploid MM. Immunoglobulin heavy-chain (IgH) translocations are seen in 60% of patients. We studied the relation between aneuploidy and IgH translocations in MM. Eighty patients with MM and abnormal metaphases were studied by means of interphase fluorescent in situ hybridization (FISH) to det

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16

Hein, Daniel, Karin Dreisig, Shai Izraeli, Kjeld Schmiegelow, Arndt Borkhardt, and Ute Fischer. "Determination of the Origin of the t(1;19) TCF3-PBX1 Fusion By Genomic Inverse PCR for Exploration of Ligated Breakpoints (GIPFEL)." Blood 132, Supplement 1 (2018): 4093. http://dx.doi.org/10.1182/blood-2018-99-110521.

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Abstract Pediatric acute lymphoblastic leukemia (ALL) is characterized by recurrent chromosomal translocations. The translocation t(1;19) that fuses the gene encoding the basic helix-loop-helix transcription factor TCF3 with the gene encoding the homeodomain protein PBX1 is the second most common one occurring in approximately 5-10% of precursor B ALL cases. Backtracking of clonotypic TCF3-PBX1 translocations that were identified in leukemia patients by PCR amplification of Guthrie cards from these individuals provided weak evidence for a prenatal origin of a minority of TCF3-PBX1 translocatio

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17

Lomov, Nikolai A., Vladimir S. Viushkov, Sergey V. Ulianov, et al. "Recurrent Translocations in Topoisomerase Inhibitor-Related Leukemia Are Determined by the Features of DNA Breaks Rather Than by the Proximity of the Translocating Genes." International Journal of Molecular Sciences 23, no. 17 (2022): 9824. http://dx.doi.org/10.3390/ijms23179824.

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Topoisomerase inhibitors are widely used in cancer chemotherapy. However, one of the potential long-term adverse effects of such therapy is acute leukemia. A key feature of such therapy-induced acute myeloid leukemia (t-AML) is recurrent chromosomal translocations involving AML1 (RUNX1) or MLL (KMT2A) genes. The formation of chromosomal translocation depends on the spatial proximity of translocation partners and the mobility of the DNA ends. It is unclear which of these two factors might be decisive for recurrent t-AML translocations. Here, we used fluorescence in situ hybridization (FISH) and

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18

Moorefield, Beth. "DNA translocation hinges on cohesin." Nature Structural & Molecular Biology 28, no. 11 (2021): 874. http://dx.doi.org/10.1038/s41594-021-00688-1.

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19

Lowe, J., T. H. Massey, C. P. Mercogliano, M. D. Allen, I. Grainge, and D. J. Sherratt. "DNA translocation by hexameric FtsK." Acta Crystallographica Section A Foundations of Crystallography 64, a1 (2008): C134. http://dx.doi.org/10.1107/s0108767308095676.

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20

Fan, Rong, Rohit Karnik, Min Yue, Deyu Li, Arun Majumdar, and Peidong Yang. "DNA Translocation in Inorganic Nanotubes." Nano Letters 5, no. 9 (2005): 1633–37. http://dx.doi.org/10.1021/nl0509677.

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21

Merchant, Chris. "DNA Translocation Through Graphene Nanopores." Biophysical Journal 100, no. 3 (2011): 521a. http://dx.doi.org/10.1016/j.bpj.2010.12.3046.

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22

Merchant, Christopher A., Ken Healy, Meni Wanunu, et al. "DNA Translocation through Graphene Nanopores." Nano Letters 10, no. 8 (2010): 2915–21. http://dx.doi.org/10.1021/nl101046t.

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23

Schneider, Grégory F., Stefan W. Kowalczyk, Victor E. Calado, et al. "DNA Translocation through Graphene Nanopores." Nano Letters 10, no. 8 (2010): 3163–67. http://dx.doi.org/10.1021/nl102069z.

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24

Welker, D. L., and K. L. Williams. "TRANSLOCATIONS IN DICTYOSTELIUM DISCOIDEUM." Genetics 109, no. 2 (1985): 341–64. http://dx.doi.org/10.1093/genetics/109.2.341.

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ABSTRACT Fourteen translocations of independent origin were identified in Dictyostelium discoideum on the basis of segregation anomalies of diploids heterozygous for these chromosome rearrangements, all of which led to the cosegregation of unlinked markers. Many of these translocations were discovered in strains mutagenized with MNNG or in strains carrying mutations affecting DNA repair; however, spontaneous translocations were also obtained. Haploid mitotic recombinants of the rearranged linkage groups were produced from diploids heterozygous for the translocations at frequencies of up to 5%

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25

Cheong, Taek-Chin, Qi Wang, Ahram Jang, Elif Karaca-Atabay, and Roberto Chiarle. "Abstract 403: APOBEC3 enzymes induce chromosomal translocations in solid cancer." Cancer Research 84, no. 6_Supplement (2024): 403. http://dx.doi.org/10.1158/1538-7445.am2024-403.

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Abstract Introduction: Chromosomal translocations are common oncogenic drivers in human cancers, and an increasing number of translocations are being considered as crucial diagnostic and prognostic markers in clinics. In B-cell lymphoma, a number of chromosomal translocations are directed by the off-target activity of the activation-induced cytidine deaminase (AID; a B-cell specific apolipoprotein B mRNA-editing enzyme, catalytic polypeptode-like (APOBEC) family enzyme). However, in solid tumors, no such enzymes capable of directing chromosomal translocations have been identified. Given recent

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Kolaris, Christos P., Diana J. Slater, Anna Sechser Perl, Eric F. Rappaport, Neil Osheroff, and Carolyn A. Felix. "DNA Topoisomerase II Poisons and the Etiology of Acute Leukemia in Infants." Blood 106, no. 11 (2005): 2850. http://dx.doi.org/10.1182/blood.v106.11.2850.2850.

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Abstract Background: Chromosomal translocations leading to MLL chimeric oncoproteins are the primary aberrations in infant acute leukemias, but how these translocations are created has not been established. A Children’s Oncology Group population epidemiology study recently validated that maternal consumption of dietary items containing topoisomerase II interacting compounds during pregnancy increases the risk of infant AML with MLL translocations. An inactivating polymorphism in the gene encoding NQO1, which detoxifies the topoisomerase II poison p-benzoquinone, also is associated with an incr

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Ren, Rongqin, Jennifer Jackson, Jacob Kames, et al. "Abstract 5452: Complimentary use of DNA- and RNA-based NGS assays optimizes detection of clinically relevant translocations for comprehensive genomic profiling." Cancer Research 83, no. 7_Supplement (2023): 5452. http://dx.doi.org/10.1158/1538-7445.am2023-5452.

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Abstract Introduction: Detection of gene translocations is a key component of clinical diagnostics to enable precision medicine in oncology. Several methods such as fluorescence in situ hybridization or RT-PCR have historically been employed, however, next-generation sequencing (NGS)-based comprehensive genomic profiling (CGP) including DNA and RNA sequencing approaches have been validated for this purpose. Here we explore the complimentary nature of these methods to enable detection of clinically relevant translocations to guide patient care. Methods: We utilized Endeavor, a 505 gene DNA-base

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28

Meeker, TC, JC Grimaldi, R. O'Rourke, E. Louie, G. Juliusson, and S. Einhorn. "An additional breakpoint region in the BCL-1 locus associated with the t(11;14)(q13;q32) translocation of B-lymphocytic malignancy." Blood 74, no. 5 (1989): 1801–6. http://dx.doi.org/10.1182/blood.v74.5.1801.1801.

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Abstract The t(11;14)(q13;q32) translocation is associated with human B- lymphocytic malignancy. This translocation divides the IgH locus on chromosome 14q32 and may activate a postulated proto-oncogene, bcl–1, located on chromosome 11q13. Two samples of chronic lymphocytic leukemia with the t(11;14)(q32;q13) translocation were studied. The break in one sample was shown to join Jh sequences with the previously described bcl–1 major translocation cluster. DNA blots of the second sample suggested that Jh sequences were joined to a different breakpoint region on chromosome 11. This translocation

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Meeker, TC, JC Grimaldi, R. O'Rourke, E. Louie, G. Juliusson, and S. Einhorn. "An additional breakpoint region in the BCL-1 locus associated with the t(11;14)(q13;q32) translocation of B-lymphocytic malignancy." Blood 74, no. 5 (1989): 1801–6. http://dx.doi.org/10.1182/blood.v74.5.1801.bloodjournal7451801.

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The t(11;14)(q13;q32) translocation is associated with human B- lymphocytic malignancy. This translocation divides the IgH locus on chromosome 14q32 and may activate a postulated proto-oncogene, bcl–1, located on chromosome 11q13. Two samples of chronic lymphocytic leukemia with the t(11;14)(q32;q13) translocation were studied. The break in one sample was shown to join Jh sequences with the previously described bcl–1 major translocation cluster. DNA blots of the second sample suggested that Jh sequences were joined to a different breakpoint region on chromosome 11. This translocation was clone

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30

Fitzgerald, TJ, GA Neale, SC Raimondi, and RM Goorha. "c-tal, a helix-loop-helix protein, is juxtaposed to the T-cell receptor- beta chain gene by a reciprocal chromosomal translocation: t(1;7)(p32;q35)." Blood 78, no. 10 (1991): 2686–95. http://dx.doi.org/10.1182/blood.v78.10.2686.2686.

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Abstract Studies on nonrandom chromosomal translocations have been important for the identification of genes potentially involved in the malignant transformation of cells. The most widely studied translocations, involving members of the Ig supergene family, have shown juxtapositions of proto-oncogenes with the rearranging loci. Such translocations can inappropriately activate expression of the proto-oncogenes and thereby play a role in tumorigenesis. Because the cytogenetic analysis of a bone marrow sample from a child with T-cell acute lymphoblastic leukemia showed a (1;7)(p32;q35) translocat

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31

Fitzgerald, TJ, GA Neale, SC Raimondi, and RM Goorha. "c-tal, a helix-loop-helix protein, is juxtaposed to the T-cell receptor- beta chain gene by a reciprocal chromosomal translocation: t(1;7)(p32;q35)." Blood 78, no. 10 (1991): 2686–95. http://dx.doi.org/10.1182/blood.v78.10.2686.bloodjournal78102686.

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Studies on nonrandom chromosomal translocations have been important for the identification of genes potentially involved in the malignant transformation of cells. The most widely studied translocations, involving members of the Ig supergene family, have shown juxtapositions of proto-oncogenes with the rearranging loci. Such translocations can inappropriately activate expression of the proto-oncogenes and thereby play a role in tumorigenesis. Because the cytogenetic analysis of a bone marrow sample from a child with T-cell acute lymphoblastic leukemia showed a (1;7)(p32;q35) translocation, we s

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32

Felix, Carolyn A., Marie L. Carillo, Karen A. Urtishak, et al. "Mechanisms in Leukemia-Associated Chromosomal Translocations: Novel, High-Throughput Sequencing Method to Detect Topoisomerase II (TOP2) Cleavage Complexes Genome-Wide with Exact Base Resolution,." Blood 118, no. 21 (2011): 3445. http://dx.doi.org/10.1182/blood.v118.21.3445.3445.

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Abstract Abstract 3445 Associations of chemotherapeutic TOP2 poisons with secondary leukemia have implicated TOP2-mediated DNA damage in balanced chromosomal translocations underlying many common forms of leukemia. “TOP2 poisons” convert native TOP2 into a cellular toxin by disrupting the cleavage/re-ligation equilibrium, either by decreasing the reverse rate of re-ligation or increasing the forward rate of cleavage, thus increasing cleavage complexes and causing DNA strand breaks that can promote recombination or initiate apoptosis. Besides anticancer chemotherapy, several dietary substances

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Li, Wanlong, Ghana S. Challa, Huilan Zhu, and Wenjie Wei. "Recurrence of Chromosome Rearrangements and Reuse of DNA Breakpoints in the Evolution of the Triticeae Genomes." G3 Genes|Genomes|Genetics 6, no. 12 (2016): 3837–47. http://dx.doi.org/10.1534/g3.116.035089.

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Abstract Chromosomal rearrangements (CRs) play important roles in karyotype diversity and speciation. While many CR breakpoints have been characterized at the sequence level in yeast, insects, and primates, little is known about the structure of evolutionary CR breakpoints in plant genomes, which are much more dynamic in genome size and sequence organization. Here, we report identification of breakpoints of a translocation between chromosome arms 4L and 5L of Triticeae, which is fixed in several species, including diploid wheat and rye, by comparative mapping and analysis of the draft genome a

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Emmanuel, Akinola, Marei Dose, Shilpa Keerthivasan, Katayoun Aghajani та Fotini Gounari. "β-Catenin induces T-cell transformation by promoting genomic instability (HEM4P.237)". Journal of Immunology 192, № 1_Supplement (2014): 116.13. http://dx.doi.org/10.4049/jimmunol.192.supp.116.13.

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Abstract Deregulated activation of β-catenin has been correlated with genomic instability in cancer. During thymocyte development β-catenin activates transcription in partnership with Tcf-1, an essential T-cell specific DNA-binding protein. We previously reported that targeted activation of β-catenin in thymocytes (CAT mice) induces lymphomas that depend on recombination-activating-gene (RAG) and c-Myc activities. Here we show that these lymphomas have recurring Tcra/Myc translocations that resulted from illegitimate RAG-recombination events and resembled oncogenic translocations in ponies. We

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Goodenow, Donna, Henry Thompson, Elizabeth Toufekoulas, Heather Derby, and Christine Richardson. "Abstract B015: Identification of novel natural compounds that induce DNA damage and chromosomal translocations." Cancer Research 84, no. 1_Supplement (2024): B015. http://dx.doi.org/10.1158/1538-7445.dnarepair24-b015.

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Abstract Background: Etoposide is a well-characterized chemotherapeutic that promotes DNA double-strand breaks (DSBs) and is associated with therapy-related chromosomal translocations and leukemias. Natural compounds including bioflavonoids, which are found in food as well as in dietary supplements, have been shown by our lab to induce DSBs and promote genome rearrangements. Given the potential for bioflavonoids to cause these harmful effects, we are investigating the potential for a wide array of other natural compounds and environmental agents to also induce DNA DSBs and chromosomal transloc

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Canoy, Reynand Jay, Anna Shmakova, Anna Karpukhina, Mikhail Shepelev, Diego Germini, and Yegor Vassetzky. "Factors That Affect the Formation of Chromosomal Translocations in Cells." Cancers 14, no. 20 (2022): 5110. http://dx.doi.org/10.3390/cancers14205110.

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Chromosomal translocations are products of the illegitimate repair of DNA double-strand breaks (DSBs). Their formation can bring about significant structural and molecular changes in the cell that can be physiologically and pathologically relevant. The induced changes may lead to serious and life-threatening diseases such as cancer. As a growing body of evidence suggests, the formation of chromosomal translocation is not only affected by the mere close spatial proximity of gene loci as potential translocation partners. Several factors may affect formation of chromosomal translocations, includi

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Han, Cai, Lin-Yu Sun, Wen-Tao Wang, Yu-Meng Sun, and Yue-Qin Chen. "Non-coding RNAs in cancers with chromosomal rearrangements: the signatures, causes, functions and implications." Journal of Molecular Cell Biology 11, no. 10 (2019): 886–98. http://dx.doi.org/10.1093/jmcb/mjz080.

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Abstract Chromosomal translocation leads to the juxtaposition of two otherwise separate DNA loci, which could result in gene fusion. These rearrangements at the DNA level are catastrophic events and often have causal roles in tumorigenesis. The oncogenic DNA messages are transferred to RNA molecules, which are in most cases translated into cancerous fusion proteins. Gene expression programs and signaling pathways are altered in these cytogenetically abnormal contexts. Notably, non-coding RNAs have attracted increasing attention and are believed to be tightly associated with chromosome-rearrang

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Li, Hong-Jie, Bei-Hai Guo, Yi-Wen Li, Li-Qun Du, Xu Jia, and Chih-Ching Chu. "Molecular cytogenetic analysis of intergeneric chromosomal translocations between wheat (Triticum aestivum L.) and Dasypyrum villosum arising from tissue culture." Genome 43, no. 5 (2000): 756–62. http://dx.doi.org/10.1139/g00-020.

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Fluorescence in situ hybridization (FISH) was applied with total genomic DNA extracted from Dasypyrum villosum (L.) Candargy as a probe to characterize chromosome translocations arising from tissue culture in hybrids of Triticum aestivum × (T. durum - D. villosum, amphiploid). Chromosome translocations between wheat and D. villosum occurred in callus cells at an average frequency of 1.9%. Translocations existed not only in callus cells but also in regenerants. Three plants with translocation chromosomes were characterized among 66 regenerants of T. aestivum 'Chinese Spring' × 'TH1W' and 'NPFP'

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Jensen, Taylor J., Sung K. Kim, Dirk van den Boom, Cosmin Deciu, and Mathias Ehrich. "Noninvasive Detection of a Balanced Fetal Translocation from Maternal Plasma." Clinical Chemistry 60, no. 10 (2014): 1298–305. http://dx.doi.org/10.1373/clinchem.2014.223198.

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Abstract BACKGROUND Massively parallel sequencing of circulating cell free (ccf) DNA from maternal plasma has been demonstrated to be a powerful method for the detection of fetal copy number variations (CNVs). Although the detection of CNVs has been described by multiple independent groups, genomic aberrations resulting in copy number–neutral events including balanced translocations have proven to be more challenging to detect noninvasively from ccf DNA. METHODS Data modeling was initially performed to evaluate multiple methods, ultimately leveraging the short length of ccf DNA and paired-end

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Keller-Seitz, Monika U., Ulrich Certa, Christian Sengstag, Friedrich E. Würgler, Mingzeng Sun, and Michael Fasullo. "Transcriptional Response of Yeast to Aflatoxin B1: Recombinational Repair InvolvingRAD51andRAD1." Molecular Biology of the Cell 15, no. 9 (2004): 4321–36. http://dx.doi.org/10.1091/mbc.e04-05-0375.

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The potent carcinogen aflatoxin B1is a weak mutagen but a strong recombinagen in Saccharomyces cerevisiae. Aflatoxin B1exposure greatly increases frequencies of both heteroallelic recombination and chromosomal translocations. We analyzed the gene expression pattern of diploid cells exposed to aflatoxin B1using high-density oligonucleotide arrays comprising specific probes for all 6218 open reading frames. Among 183 responsive genes, 46 are involved in either DNA repair or in control of cell growth and division. Inducible growth control genes include those in the TOR signaling pathway and SPO12

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Qi, Y., K. Nam, M. C. Spong, et al. "Strandwise translocation of a DNA glycosylase on undamaged DNA." Proceedings of the National Academy of Sciences 109, no. 4 (2012): 1086–91. http://dx.doi.org/10.1073/pnas.1111237108.

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Kolaris, Christos P., Mingli Liu, Katie Foote, et al. "NUP98 Translocation Breakpoints in Treatment-Related MDS Are Drug-Stimulated DNA Topoisomerase II Cleavage Sites." Blood 104, no. 11 (2004): 1970. http://dx.doi.org/10.1182/blood.v104.11.1970.1970.

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Abstract Chemotherapeutic DNA topoisomerase II (top2) poisons (i.e. agents that stabilize the top2 covalent complex and have the overall effect of increasing cleavage complexes) have been implicated in the treatment complication of leukemia characterized by balanced translocations, among which are translocations of the NUP98 gene at chromosome band 11p15. NUP98, which encodes a 98-kd docking protein in the nuclear pore complex, is disrupted by translocations in de novo and chemotherapy-related leukemias and has ~15 partner genes encoding proteins of diverse function. There have been no studies

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Yang, Wayne, Boya Radha, Adnan Choudhary, et al. "Translocation of DNA through Ultrathin Nanoslits." Advanced Materials 33, no. 11 (2021): 2007682. http://dx.doi.org/10.1002/adma.202007682.

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Plesa, C., N. van Loo, and C. Dekker. "DNA nanopore translocation in glutamate solutions." Nanoscale 7, no. 32 (2015): 13605–9. http://dx.doi.org/10.1039/c5nr02793d.

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Balasubramanian, Ramkumar, Sohini Pal, Himanshu Joshi, et al. "DNA Translocation through Hybrid Bilayer Nanopores." Journal of Physical Chemistry C 123, no. 18 (2019): 11908–16. http://dx.doi.org/10.1021/acs.jpcc.9b00399.

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Dreiseikelmann, B. "Translocation of DNA across bacterial membranes." Microbiological Reviews 58, no. 3 (1994): 293–316. http://dx.doi.org/10.1128/mmbr.58.3.293-316.1994.

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Dreiseikelmann, B. "Translocation of DNA across bacterial membranes." Microbiological Reviews 58, no. 3 (1994): 293–316. http://dx.doi.org/10.1128/mr.58.3.293-316.1994.

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Chen, Lei, and A. T. Conlisk. "DNA nanowire translocation phenomena in nanopores." Biomedical Microdevices 12, no. 2 (2009): 235–45. http://dx.doi.org/10.1007/s10544-009-9378-5.

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Zhao, Xiaojing, Yue Zhao, Yunsheng Deng, et al. "DNA translocation through solid-state nanopore." Journal of Micro-Bio Robotics 14, no. 1-2 (2018): 35–40. http://dx.doi.org/10.1007/s12213-018-0104-3.

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Raghavan, Sathees C., and Michael R. Lieber. "DNA structures at chromosomal translocation sites." BioEssays 28, no. 5 (2006): 480–94. http://dx.doi.org/10.1002/bies.20353.

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