A DNA damage repair mechanism is involved in the origin of chromosomal translocations t(4;11) in primary leukemic cells.
about
Panhandle and reverse-panhandle PCR enable cloning of der(11) and der(other) genomic breakpoint junctions of MLL translocations and identify complex translocation of MLL, AF-4, and CDK6.Systematic Classification of Mixed-Lineage Leukemia Fusion Partners Predicts Additional Cancer PathwaysMolecular Process Producing Oncogene Fusion in Lung Cancer Cells by Illegitimate Repair of DNA Double-Strand BreaksTranslin binds to the sequences adjacent to the breakpoints of the TLS and CHOP genes in liposarcomas with translocation t(12;6)GPHN, a novel partner gene fused to MLL in a leukemia with t(11;14)(q23;q24).Regulation of pairing between broken DNA-containing chromatin regions by Ku80, DNA-PKcs, ATM, and 53BP1Diagnostic tool for the identification of MLL rearrangements including unknown partner genesDNA polymerase mu, a candidate hypermutase?Near-precise interchromosomal recombination and functional DNA topoisomerase II cleavage sites at MLL and AF-4 genomic breakpoints in treatment-related acute lymphoblastic leukemia with t(4;11) translocationMLL-SEPTIN6 fusion recurs in novel translocation of chromosomes 3, X, and 11 in infant acute myelomonocytic leukaemia and in t(X;11) in infant acute myeloid leukaemia, and MLL genomic breakpoint in complex MLL-SEPTIN6 rearrangement is a DNA topoisomHeterogeneous duplications in patients with Pelizaeus-Merzbacher disease suggest a mechanism of coupled homologous and nonhomologous recombination.The landscape of somatic mutations in infant MLL-rearranged acute lymphoblastic leukemiasA novel selection system for chromosome translocations in Saccharomyces cerevisiae.Methylenetetrahydrofolate reductase (MTHFR) polymorphisms and risk of molecularly defined subtypes of childhood acute leukemiaNucleotide-resolution mapping of topoisomerase-mediated and apoptotic DNA strand scissions at or near an MLL translocation hotspotChromosomal translocations in human cells are generated by canonical nonhomologous end-joining.Haplotypes of DNA repair and cell cycle control genes, X-ray exposure, and risk of childhood acute lymphoblastic leukemia.Induction of chromosomal translocations in mouse and human cells using site-specific endonucleases.CD8 Memory Cells Develop Unique DNA Repair Mechanisms Favoring Productive DivisionProspective tracing of MLL-FRYL clone with low MEIS1 expression from emergence during neuroblastoma treatment to diagnosis of myelodysplastic syndromeThe molecular biology of mixed lineage leukemia.The role of mechanistic factors in promoting chromosomal translocations found in lymphoid and other cancers.MLL-SEPTIN gene fusions in hematological malignancies.Pathogenetic, Clinical, and Prognostic Features of Adult t(4;11)(q21;q23)/MLL-AF4 Positive B-Cell Acute Lymphoblastic Leukemia.Current evidence for an inherited genetic basis of childhood acute lymphoblastic leukemia.Breakpoints of t(4;11) translocations in the human MLL and AF4 genes in ALL patients are preferentially clustered outside of high-affinity matrix attachment regions.Genome-wide TOP2A DNA cleavage is biased toward translocated and highly transcribed loci.Coupled homologous and nonhomologous repair of a double-strand break preserves genomic integrity in mammalian cellsLoss of drug-stimulated topoisomerase II DNA breaks in living cells is different at two unrelated loci.Cleavage of the MLL gene by activators of apoptosis is independent of topoisomerase II activity.Molecular characterization of a myelodysplasia-associated chromosome 7 inversion.Expression of MLL-AF4 or AF4-MLL fusions does not impact the efficiency of DNA damage repair.Molecular characterization of identical, novel MLL-EPS15 translocation and individual genomic copy number alterations in monozygotic infant twins with acute lymphoblastic leukemia.A model of oncogenic rearrangements: differences between chromosomal translocation mechanisms and simple double-strand break repair.Genomic anatomy of the specific reciprocal translocation t(15;17) in acute promyelocytic leukemia.Distribution of genomic breakpoints in chronic myeloid leukemia: analysis of 308 patients.Double-strand DNA break formation mediated by flap endonuclease-1.Biased distribution of chromosomal breakpoints involving the MLL gene in infants versus children and adults with t(4;11) ALL.Clustering of genomic breakpoints at the MLL locus in therapy-related acute leukemia with t(4;11)(q21;q23).Transcription linked to recombination: a gene-internal promoter coincides with the recombination hot spot II of the human MLL gene
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P2860
A DNA damage repair mechanism is involved in the origin of chromosomal translocations t(4;11) in primary leukemic cells.
description
1999 nî lūn-bûn
@nan
1999年の論文
@ja
1999年学术文章
@wuu
1999年学术文章
@zh
1999年学术文章
@zh-cn
1999年学术文章
@zh-hans
1999年学术文章
@zh-my
1999年学术文章
@zh-sg
1999年學術文章
@yue
1999年學術文章
@zh-hant
name
A DNA damage repair mechanism is involved in the origin of chromosomal translocations t
@nl
A DNA damage repair mechanism ...... 11) in primary leukemic cells.
@en
type
label
A DNA damage repair mechanism is involved in the origin of chromosomal translocations t
@nl
A DNA damage repair mechanism ...... 11) in primary leukemic cells.
@en
prefLabel
A DNA damage repair mechanism is involved in the origin of chromosomal translocations t
@nl
A DNA damage repair mechanism ...... 11) in primary leukemic cells.
@en
P2093
P2860
P356
P1433
P1476
A DNA damage repair mechanism ...... 11) in primary leukemic cells.
@en
P2093
A Borkhardt
F Griesinger
I Breitenlohner
P2860
P2888
P304
P356
10.1038/SJ.ONC.1202842
P407
P577
1999-08-01T00:00:00Z