The partial tandem duplication of ALL1 (MLL) is consistently generated by Alu-mediated homologous recombination in acute myeloid leukemia.
about
The genomic region encompassing the nephropathic cystinosis gene (CTNS): complete sequencing of a 200-kb segment and discovery of a novel gene within the common cystinosis-causing deletionLeukemogenic rearrangements at the mixed lineage leukemia gene (MLL)-multiple rather than a single mechanismInflammation-induced cell proliferation potentiates DNA damage-induced mutations in vivoStructure of the MLT gene and molecular characterization of the genomic breakpoint junctions in the t(11;18)(q21;q21) of marginal zone B-cell lymphomas of MALT typeMolecular analysis of an unstable genomic region at chromosome band 11q23 reveals a disruption of the gene encoding the alpha2 subunit of platelet-activating factor acetylhydrolase (Pafah1a2) in human lymphomaRepair of double-strand breaks by homologous recombination in mismatch repair-defective mammalian cellsThe Structural Characterization of Tumor Fusion Genes and ProteinsBTECH: a platform to integrate genomic, transcriptomic and epigenomic alterations in brain tumorsGPHN, a novel partner gene fused to MLL in a leukemia with t(11;14)(q23;q24).Alu-associated interstitial deletions and chromosomal re-arrangement in 2 human multidrug-resistant cell lines.Telomerase deficiency affects the formation of chromosomal translocations by homologous recombination in Saccharomyces cerevisiae.RAD59 and RAD1 cooperate in translocation formation by single-strand annealing in Saccharomyces cerevisiaeRoles of retrotransposons in benign and malignant hematologic disease.Mll rearrangements in haematological malignancies: lessons from clinical and biological studies.Alu distribution and mutation types of cancer genes.The Alu-rich genomic architecture of SPAST predisposes to diverse and functionally distinct disease-associated CNV alleles.A mobile threat to genome stability: The impact of non-LTR retrotransposons upon the human genome.Characterization of the human and mouse genes for the alpha subunit of type II prolyl 4-hydroxylase. Identification of a previously unknown alternatively spliced exon and its expression in various tissues.Compound heterozygosity for a recurrent 16.5-kb Alu-mediated deletion mutation and single-base-pair substitutions in the ABCC6 gene results in pseudoxanthoma elasticumAll y'all need to know 'bout retroelements in cancer.More forks on the road to replication stress recoveryPAFc, a key player in MLL-rearranged leukemogenesis.Common themes in the pathogenesis of acute myeloid leukemia.DNA glycosylase activity and cell proliferation are key factors in modulating homologous recombination in vivo.Single-stranded annealing induced by re-initiation of replication origins provides a novel and efficient mechanism for generating copy number expansion via non-allelic homologous recombination.Estimating genomic instability mediated by Alu retroelements in breast cancer.MLL leukemia-associated rearrangements in peripheral blood lymphocytes from healthy individuals.Chromosomal rearrangements leading to MLL gene fusions: clinical and biological aspectsA novel selection system for chromosome translocations in Saccharomyces cerevisiae.Reciprocal translocations in Saccharomyces cerevisiae formed by nonhomologous end joining.The role of Alu repeat clusters as mediators of recurrent chromosomal aberrations in tumors.Chromosomal translocations involving the MLL gene: molecular mechanisms.Recombination between two chromosomes: implications for genomic integrity in mammalian cells.Regulatory mechanisms that prevent re-initiation of DNA replication can be locally modulated at origins by nearby sequence elements.Flt3 mutations and leukaemia.Origins of chromosome translocations in childhood leukaemia.Causes of oncogenic chromosomal translocation.An efficient method to generate chromosomal rearrangements by targeted DNA double-strand breaks in Drosophila melanogaster.The contribution of alu elements to mutagenic DNA double-strand break repair.Alu-mediated diverse and complex pathogenic copy-number variants within human chromosome 17 at p13.3.
P2860
Q24624725-C49CE8C9-6AC9-4584-ABBA-0A8C7C5A7548Q26830271-A948CAB0-8646-49C4-BB6F-FD83905A4113Q27311572-DDE122D4-252A-4B1B-9D86-29579A6FA039Q28143157-BF8007B4-BF53-4869-8F51-D6DFE9F0A1D9Q28199129-924E9619-F971-4DBC-8776-B8EBEF18F877Q28209896-F1E245AD-B3AF-4745-AFA3-A46840682095Q28386511-296F8EE4-93E0-4BB2-B7B6-39DD6A3BF8B1Q30484798-BE111DBF-57DF-4BA5-A969-85E0DA688029Q30727023-E6CFC234-BEFE-4349-9B02-C9F0973E266EQ30868385-1E850D30-B8DC-4145-83F4-3E5AB5A29A28Q33373337-BF86B745-9B1B-4D18-8C4A-9BC5CCA39D95Q33599063-A01A66DD-648E-4038-95C7-B6DA9DC39378Q33697456-E134FD9A-0003-46C8-9A7F-02ACA1B69065Q33723613-A4C09BA9-C813-4638-9F85-663594C967A6Q33853323-2D0CDB3B-1729-49AA-8002-F94304D826DAQ34030743-86BA4BEF-3F36-4BD3-948A-21A7FCE84B38Q34077410-7B531CE3-7EDC-4C46-A2DD-6BD541F2EF4AQ34095530-A8449E73-9DCA-40FB-833B-D1C48A385224Q34113251-5DF7EC0D-A18F-45F5-BF59-A973EAC908A8Q34143181-13363A4F-32A9-4578-9D4B-0170CD5761EDQ34161464-E210CD69-A530-4163-A400-19D6D72D1C73Q34245737-60D24508-731B-4315-A81F-3CF284F12CD9Q34405458-3F50CEFD-C1A0-4D6E-9F12-E89350A20D6AQ34434917-834E8C00-9E84-4CC4-BF4C-4D79CB37B9A4Q34539939-7D28E442-6D52-4820-8C09-8FAB0574264CQ34548438-EF6754BB-A689-421B-A189-0F8DA16163A8Q34565527-3BEB544E-75F0-46FA-B334-C3413445F822Q34601806-87603D39-B728-499D-A188-5B8E1A5DC99CQ34614824-20CEE04B-3686-422E-93A7-40B4CEB7ACE6Q34643637-E5C746A5-EC7A-436A-B611-E0785BAAD83CQ34804028-94733C93-4D92-433B-AEEE-369F488973E4Q35128590-6EC5550F-4647-4521-AE04-FE16D00734FFQ35132661-6DA1B461-4C6C-46A6-9FE8-9ABA754F4C6DQ35191354-A8833D98-1A32-4DF3-9EA2-184D103435BDQ35192266-C9A6C97F-46F8-4630-8C17-CCB808B22A29Q35210004-73EF4116-E49F-4EA3-9BD2-1A34B0F7D457Q35570942-4307E98F-9607-4E64-B6DE-339751FEA67FQ35574304-35E1E65C-D5C8-4A98-95C9-397883CF8747Q35575274-CAE0919D-B4F2-4015-B533-C413E690BCC4Q35766412-6E325B74-CC4E-4985-9255-BBFC351F333C
P2860
The partial tandem duplication of ALL1 (MLL) is consistently generated by Alu-mediated homologous recombination in acute myeloid leukemia.
description
1998 nî lūn-bûn
@nan
1998 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
1998 թվականի մարտին հրատարակված գիտական հոդված
@hy
1998年の論文
@ja
1998年論文
@yue
1998年論文
@zh-hant
1998年論文
@zh-hk
1998年論文
@zh-mo
1998年論文
@zh-tw
1998年论文
@wuu
name
The partial tandem duplication ...... ion in acute myeloid leukemia.
@ast
The partial tandem duplication ...... ion in acute myeloid leukemia.
@en
The partial tandem duplication of ALL1
@nl
type
label
The partial tandem duplication ...... ion in acute myeloid leukemia.
@ast
The partial tandem duplication ...... ion in acute myeloid leukemia.
@en
The partial tandem duplication of ALL1
@nl
prefLabel
The partial tandem duplication ...... ion in acute myeloid leukemia.
@ast
The partial tandem duplication ...... ion in acute myeloid leukemia.
@en
The partial tandem duplication of ALL1
@nl
P2093
P2860
P356
P1476
The partial tandem duplication ...... ion in acute myeloid leukemia.
@en
P2093
G Marcucci
M A Caligiuri
M P Strout
P2860
P304
P356
10.1073/PNAS.95.5.2390
P407
P577
1998-03-01T00:00:00Z