tandem duplication


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tandem duplication

a MUTATION or RECOMBINATION event producing identical adjacent segments. For example, A B C D E becomes A B C D B C D E.
References in periodicals archive ?
According to the company, gilteritinib is an investigational compound that has demonstrated inhibitory activity against FLT3 internal tandem duplication (ITD) as well as FLT3 tyrosine kinase domain (TKD), two common types of FLT3 mutations seen in one-third of patients with AML.
GSTKa and GSTKb are located on the same genome region, suggesting the segmental duplication or tandem duplication origin.
It will investigate the compound's potency over a period of two years following hematopoietic stem cell transplant (HCT) in patients with FLT3 internal tandem duplication (ITD) mutation-positive (FLT3/ITD+) acute myeloid leukemia (AML) who are in remission after induction therapy.
The molecular aberrations that have been previously studied [sup][3] in CN-AML patients include internal tandem duplications of the fms -related tyrosine kinase 3 gene ( FLT3-ITD ),[sup][4],[5],[6] the nucleophosmin gene ( NPM1 ) mutations,[sup][7] MLL partial tandem duplication ( MLL-PTD ),[sup][5],[8] E-26 transformation-specificrelated gene ( ERG) [sup][9],[10] and brain and acute leukemia, cytoplasmic ( BAALC ) expression levels.
Cases with two bands were considered positive for ITD: the lower band corresponded to the normal c-kit gene while the upper band corresponded to the c-kit gene containing the internal tandem duplication (LONDON et al.
This strategy will exploit the characteristic of tandem duplication (two identical contiguous sequences) and will result in the deletion or inversion of the mutation restoring the dystrophin expression.
Internal tandem duplication (ITD) mutations of FLT3 are present in approximately 20% of patients with AML, in 28% to 34% of patients with AML with normal cytogenetics, and in 40% of patients with AML with concurrent NPM1 mutation.
3] Pfeiffer et al (1992) reported de novo inverted tandem duplication of 12pl1.
These mutations were shown to be internal tandem duplication (ITDs), mainly involving a tyrosine rich stretch at the end of exon 14 (587-NEYFYVDFREYEYD-560), coding for the juxtamembrane (JM) domain of the receptor (Fig.
Moreover, this cluster of genes was proposed to have arisen by tandem duplication of ancestral beta-globin genes, with the first duplication occurring 200 to 155 MYBP just prior to a period in mammalian evolution when eutherians and marsupials diverged from a common ancestor (22).
RT-PCR was performed to identify PML/RAR [alpha], AML1/ETO, CBF [beta]/MYH11 and FLT3 internal tandem duplication (ITD).