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1. Full Text Long-range oncogenic activation of Igh-c-myc translocations by the Igh 3′ regulatory region
by Gostissa, Monica and Yan, Catherine T and Bianco, Julia M and Cogné, Michel and Pinaud, Eric and Alt, Frederick W
Nature, ISSN 0028-0836, 12/2009, Volume 462, Issue 7274, pp. 803 - 807
B-cell malignancies, such as human Burkitt's lymphoma, often contain translocations that link c-myc or other proto-oncogenes to the immunoglobulin heavy chain... 
B-CELL DEVELOPMENT | CHROMOSOMAL TRANSLOCATIONS | MECHANISM | MULTIDISCIPLINARY SCIENCES | V(D)J RECOMBINATION | GENE AMPLIFICATION | HEAVY-CHAIN LOCUS | CLASS-SWITCH RECOMBINATION | END | DNA BREAKS | TRANSGENIC MICE | Chromosome Breakpoints | Cells, Cultured | 3' Untranslated Regions - genetics | Mice, Transgenic | Lymphoma, B-Cell - genetics | Regulatory Sequences, Nucleic Acid - genetics | Animals | Genes, myc - genetics | Alleles | Lymphoma, B-Cell - pathology | Genes, Immunoglobulin Heavy Chain - genetics | Mice | Gene Rearrangement, B-Lymphocyte - genetics | Immunoglobulin Class Switching - genetics | Translocation, Genetic - genetics | Gene amplification | Lymphomas | Mutation | Genetic recombination | Tumors | Life Sciences | Immunology
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2. Full Text Role of genomic instability and p53 in AID-induced c-myc – Igh translocations
by McBride, Kevin M and Eisenreich, Thomas R and Ramiro, Almudena R and Nussenzweig, Andre and Lowe, Scott W and Nussenzweig, Michel C and Jankovic, Mila and Callen, Elsa and Chen, Hua-Tang and Chen, Junjie and Dickins, Ross A and Difilippantonio, Simone
Nature, ISSN 0028-0836, 03/2006, Volume 440, Issue 7080, pp. 105 - 109
Chromosomal translocations involving the immunoglobulin switch region are a hallmark feature of B-cell malignancies. However, little is known about the... 
B-CELLS | CHROMOSOMAL TRANSLOCATIONS | CYTIDINE DEAMINASE AID | ACTIVATION | SOMATIC HYPERMUTATION | 53BP1 | MULTIDISCIPLINARY SCIENCES | REGIONS | URACIL-DNA GLYCOSYLASE | CLASS-SWITCH RECOMBINATION | DEFICIENT MICE | Cell Line | Gene Expression | Cytidine Deaminase - genetics | Tumor Suppressor Protein p53 - metabolism | Mutation - genetics | Tumor Suppressor Protein p53 - genetics | Animals | Cytidine Deaminase - metabolism | Genes, myc - genetics | DNA Damage - genetics | Genes, Immunoglobulin Heavy Chain - genetics | Mice | Models, Genetic | Immunoglobulin Class Switching - genetics | B-Lymphocytes - metabolism | Genomic Instability - genetics | Translocation, Genetic - genetics | Enzymes | Acquired immune deficiency syndrome | Genomics | AIDS | Chromosomes | Cells | Tumors | Cancer
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3. Full Text MLL translocations, histone modifications and leukaemia stem-cell development
by Krivtsov, Andrei V and Armstrong, Scott A
Nature Reviews Cancer, ISSN 1474-175X, 11/2007, Volume 7, Issue 11, pp. 823 - 833
Translocations that involve the mixed lineage leukaemia (MLL) gene identify a unique group of acute leukaemias, and often predict a poor prognosis. The MLL... 
CHROMOSOMAL TRANSLOCATIONS | ONCOLOGY | GENE-EXPRESSION | METHYLTRANSFERASE ACTIVITY | ALL-1 GENE | ACUTE MYELOID-LEUKEMIA | FUSION PARTNERS | HOX EXPRESSION | BREAKPOINT CLUSTER REGION | PARTIAL TANDEM DUPLICATION | HEMATOPOIETIC STEM | Protein Methyltransferases | Neoplastic Stem Cells - cytology | Prognosis | Humans | Myeloid-Lymphoid Leukemia Protein - deficiency | Infant | Myeloid-Lymphoid Leukemia Protein - chemistry | Epigenesis, Genetic - physiology | Oncogene Proteins, Fusion - physiology | Oncogene Proteins, Fusion - chemistry | Myeloid-Lymphoid Leukemia Protein - physiology | Cell Transformation, Neoplastic - genetics | Gene Expression Regulation, Developmental | Adult | Child | Leukemia - genetics | Chromatin - ultrastructure | Histone-Lysine N-Methyltransferase - genetics | Gene Expression Regulation - genetics | Gene Expression Regulation - physiology | Hematopoietic Stem Cells - metabolism | Cell Division - physiology | Animals | Histone Methyltransferases | Epigenesis, Genetic - genetics | Myeloid-Lymphoid Leukemia Protein - genetics | Oncogene Proteins, Fusion - genetics | Hematopoietic Stem Cells - cytology | Mice | Protein Processing, Post-Translational | Histones - metabolism | Methylation | Histone-Lysine N-Methyltransferase - physiology | Leukemia | Stem cells | Histones | Physiological aspects | Genetic aspects | Research | Gene expression
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4. Telomeres and Chromosomal Translocations There's a Ligase at the End of the Translocation
by Baird, DM and Hendrickson, EA
2018, Advances in Experimental Medicine and Biology, Volume 1044, 24
Chromosomal translocations are now well understood to not only constitute signature molecular markers for certain human cancers but often also to be causative... 
MEDICINE, RESEARCH & EXPERIMENTAL | A-NHEJ | STRAND BREAK REPAIR | LIGIV | PROTEIN-KINASE | HUMAN-CELLS | JOINING PATHWAYS | EARLY-STAGE | LIGIII | CELL BIOLOGY | EXCISION-REPAIR | GENETIC INSTABILITY | BACKUP PATHWAYS | Chromosomal translocations | HDR | GENETICS & HEREDITY | CHRONIC LYMPHOCYTIC-LEUKEMIA | DNA LIGASES | C-NHEJ | DNA DSB Repair
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5. Full Text Alternative end-joining is suppressed by the canonical NHEJ component Xrcc4-ligase IV during chromosomal translocation formation
by Simsek, Deniz and Jasin, Maria
Nature Structural and Molecular Biology, ISSN 1545-9993, 04/2010, Volume 17, Issue 4, pp. 410 - 416
Chromosomal translocations in hematologic and mesenchymal tumors form overwhelmingly by nonhomologous end-joining (NHEJ). Canonical NHEJ, essential for the... 
XRCC4 | BIOCHEMISTRY & MOLECULAR BIOLOGY | DOUBLE-STRAND BREAKS | MECHANISMS | MAMMALIAN-CELLS | CELL BIOLOGY | REPAIR | BIOPHYSICS | PATHWAY | GENE AMPLIFICATION | HOMOLOGOUS RECOMBINATION | PROTEINS | DNA-LIGASE-IV | DNA-Binding Proteins - metabolism | Translocation, Genetic | DNA Repair | Humans | DNA Ligase ATP | DNA-Binding Proteins - genetics | DNA Ligases - metabolism | Physiological aspects | Genetic aspects | Research | Translocation (Genetics) | Ligases | Stem cells | Cell division | Chromosomes | ligase IV | alternative NHEJ | DNA double-strand break | nonhomologous end-joining | Xrcc4 | chromosomal translocation
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6. Full Text MYC translocation partner gene determines survival of patients with large B‐cell lymphoma with MYC‐ or double‐hit MYC/BCL2 translocations
by Pedersen, Mette Ø and Gang, Anne O and Poulsen, Tim S and Knudsen, Helle and Lauritzen, Anne F and Nielsen, Signe L and Klausen, Tobias W and Nørgaard, Peter
European Journal of Haematology, ISSN 0902-4441, 01/2014, Volume 92, Issue 1, pp. 42 - 48
In large B‐cell lymphoma ( LBCL ) MYC ‐ and MYC / BCL 2 double‐hit ( DH ) translocations have been associated with inferior survival. We hypothesised that the... 
double‐hit | translocation partner genes | genes | MYC | BCL | diffuse large B‐cell lymphoma | 2 genes | chromosomal translocation | MYC genes | BCL2 genes | Double-hit | Chromosomal translocation | MYC translocation partner genes | Diffuse large B-cell lymphoma | RITUXIMAB PLUS CYCLOPHOSPHAMIDE | DOXORUBICIN | diffuse large B-cell lymphoma | double-hit | PREDNISONE | VINCRISTINE | BCL2 | HEMATOLOGY | EXPRESSION | Translocation, Genetic | Lymphoma, Large B-Cell, Diffuse - drug therapy | Prognosis | Humans | Middle Aged | Male | Genes, bcl-2 | Genes, myc | Lymphoma, Large B-Cell, Diffuse - mortality | Lymphoma, Large B-Cell, Diffuse - diagnosis | Aged, 80 and over | Aged | Neoplasm Staging | Lymphoma, Large B-Cell, Diffuse - genetics | Chemotherapy | Immunoglobulins | Patient outcomes | Genes | Lymphomas | Genetic aspects | Cancer
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7. Short Article - Isolated cell translocations: are they significant?
by Devi, R. R and Sayee, R
Short Article - Isolated cell translocations: are they significant?, 12/2005
BACKGROUND: Cytogenetics study using cultured T-lymphocytes derived from peripheral blood is the easiest way to study human chromosome complement and it is... 
translocation | T-lymphocyte | GTG banding | Chromosomal abnormality
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8. Full Text Detecting DNA double-stranded breaks in mammalian genomes by linear amplification-mediated high-throughput genome-wide translocation sequencing
by Hu, Jiazhi and Meyers, Robin M and Dong, Junchao and Panchakshari, Rohit A and Alt, Frederick W and Frock, Richard L
Nature Protocols, ISSN 1754-2189, 05/2016, Volume 11, Issue 5, pp. 853 - 871
Unbiased, high-throughput assays for detecting and quantifying DNANA double-stranded breaks (DSBs) across the genome in mammalian cells will facilitate basic... 
B-CELLS | SYSTEM | CHROMOSOMAL TRANSLOCATIONS | RECOMBINATION | READ ALIGNMENT | INSTABILITY | BIOCHEMICAL RESEARCH METHODS | CRISPR-CAS9 | REARRANGEMENTS | PCR | REVEALS | Mammals - genetics | Translocation, Genetic | Computational Biology - methods | Reproducibility of Results | Gene Library | Cells, Cultured | DNA Breaks, Double-Stranded | Polymerase Chain Reaction - methods | Deoxyribonucleases - genetics | Animals | Chromosomes - genetics | Mice | DNA, Single-Stranded | Genome | High-Throughput Nucleotide Sequencing - methods | Animal genetics | Ionizing radiation | DNA binding proteins | Research
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9. Full Text Mechanisms of oncogenic chromosomal translocations
by Byrne, Michael and Wray, Justin and Reinert, Brian and Wu, Yuehan and Nickoloff, Jac and Lee, Suk‐Hee and Hromas, Robert and Williamson, Elizabeth
Annals of the New York Academy of Sciences, ISSN 0077-8923, 03/2014, Volume 1310, Issue 1, pp. 89 - 97
Chromosome translocations are caused by inappropriate religation of two DNA double‐strand breaks (DSBs) in heterologous chromosomes. These DSBs can be... 
DNA end‐joining repair | DNA repair | oncogenesis | chromosomal translocation | Oncogenesis | Chromosomal translocation | DNA end-joining repair | TOTAL-BODY IRRADIATION | CYTIDINE DEAMINASE AID | END-JOINING PATHWAY | MAJOR BREAKPOINT REGION | DOUBLE-STRAND BREAKS | T(14/18) TRANSLOCATION | CELL BIOLOGY | GENOMIC INSTABILITY | ONCOLOGY | INTERSPERSED REPEAT ELEMENTS | CLASS-SWITCH RECOMBINATION | TOXICOLOGY | DNA-REPAIR | Deoxyribonucleases - genetics | Animals | Poly(ADP-ribose) Polymerases - genetics | Cell Transformation, Neoplastic - genetics | Humans | DNA Repair - physiology | DNA End-Joining Repair - physiology | Poly (ADP-Ribose) Polymerase-1 | Poly(ADP-ribose) Polymerases - physiology | Receptors, Immunologic - genetics | DNA Breaks, Double-Stranded | Translocation, Genetic - genetics | Nuclear radiation | Chromosomes | DNA damage | Deoxyribonucleic acid--DNA
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10. Mobile genetic elements
by Shapiro, James Allen
1983, ISBN 0126386803, xvi, 688 p., [2] p. of plates
ADN extrachromosomique | Hérédité cytoplasmique | Translocation (Génétique) | Mobile genetic elements
Book
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11. Full Text CRISPR-Cas9-guided oncogenic chromosomal translocations with conditional fusion protein expression in human mesenchymal cells
by Vanoli, Fabio and Tomishima, Mark and Feng, Weiran and Lamribet, Khadija and Babin, Loelia and Brunet, Erika and Jasin, Maria
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 04/2017, Volume 114, Issue 14, pp. 3696 - 3701
Gene editing techniques have been extensively used to attempt to model recurrent genomic rearrangements found in tumor cells. These methods involve the... 
DSRCT | EWSR1-WT1 | Chromosomal translocation | CRISPR-Cas9 | Homology-directed repair | STEM-CELLS | MULTIDISCIPLINARY SCIENCES | ZINC-FINGER | DOUBLE-STRAND BREAKS | CANCER TRANSLOCATIONS | MAMMALIAN-CELLS | chromosomal translocation | TALE NUCLEASES | IN-VIVO | PAIRED NICKS | HOMOLOGOUS RECOMBINATION | homology-directed repair | EWS-WT1 GENE FUSION | Promoter Regions, Genetic | Translocation, Genetic | Mesenchymal Stromal Cells - cytology | Oncogene Proteins, Fusion - genetics | Humans | RNA-Binding Protein EWS - genetics | CRISPR-Cas Systems | Mesenchymal Stromal Cells - metabolism | Gene Editing - methods | DNA Breaks, Double-Stranded | WT1 Proteins - genetics | Translocation (Genetics) | Stem cells | Genetic aspects | Nucleotide sequencing | Observations | Methods | DNA sequencing | Biological Sciences | EWSR1–WT1
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12. Full Text Chromosomal translocations in black flies (Diptera: Simuliidae) - Facilitators of adaptive radiation?
by Adler, Peter H and Yadamsuren, Oyunchuluun and Procunier, William S
PLoS ONE, ISSN 1932-6203, 06/2016, Volume 11, Issue 6, p. e0158272
A macrogenomic investigation of a Holarctic clade of black flies-the Simulium cholodkovskii lineage-provided a platform to explore the implications of a... 
REPRODUCTIVE ISOLATING MECHANISM | GROUP DIPTERA-SIMULIIDAE | CYTOTAXONOMY | SPECIATION | MULTIDISCIPLINARY SCIENCES | MEIOSIS | SALIVARY-GLAND CHROMOSOMES | INTERCHANGE | IDENTIFICATION | CYTOLOGICAL DESCRIPTION | VECTOR | Translocation, Genetic | Polytene Chromosomes | Radiation Tolerance - genetics | Male | Chromosome Mapping | Phylogeny | Biological Evolution | Simuliidae - genetics | Animals | Chromosomes, Insect | Simuliidae - radiation effects | Female | Simuliidae - classification | Genetic Linkage | Translocation (Genetics) | Analysis | Radiation | Influence | Genetic aspects | Research | Diptera | Adaptive structures | Sex chromosomes | Hybrids | Spermatogenesis | Taxonomy | Zoology | Sex | Heterozygotes | Polytene | Black flies | Males | Taxa | Adaptive radiation | Evolution | Chromosomes | Species | Speciation | Translocation | Reproductive isolation | Sympatric populations | Gene expression | Progeny | Chromosome translocations | Disjunction | Spermatogonia | Structure-function relationships
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13. Full Text Translocation-related sarcomas
by Nakano, Kenji and Nakano, Kenji and Takahashi, Shunji
International Journal of Molecular Sciences, ISSN 1661-6596, 12/2018, Volume 19, Issue 12, p. 3784
Chromosomal translocations are observed in approximately 20% of soft tissue sarcomas (STS). With the advances in pathological examination technology, the... 
Chromosomal translocation | Ewing sarcoma breakpoint region 1 | Transcription factor E3 | Forkhead box transcription factor O | Soft tissue sarcoma | Translocation-related sarcoma | Anaplastic lymphoma kinase | Neurotrophic tyrosine kinase | forkhead box transcription factor O | SSX FUSION TYPE | BIOCHEMISTRY & MOLECULAR BIOLOGY | anaplastic lymphoma kinase | IN-SITU HYBRIDIZATION | CLEAR-CELL SARCOMA | OPEN-LABEL | translocation-related sarcoma | CHEMISTRY, MULTIDISCIPLINARY | chromosomal translocation | EWING SARCOMA | PHASE-III TRIAL | PRIMITIVE NEUROECTODERMAL TUMOR | transcription factor E3 | INFLAMMATORY MYOFIBROBLASTIC TUMOR | SOFT-TISSUE SARCOMA | neurotrophic tyrosine kinase | PART SARCOMA
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