Multiplex PCR for simultaneous detection of the most frequent T cell receptor-δ gene rearrangements in childhood ALL

Taube, Tillmann; Seeger, K.; Beyermann, Birgit; Hänel, Claudia; Duda, Sabrina; Linderkamp, Christin; Henze, Günter

doi:10.1038/sj.leu.2400825

Cited by 16 publications

(13 citation statements)

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“…Identification of patient specific clonal gene rearrangements at initial and at relapse diagnosis of complete immunoglobulin heavy chain (IGH), the immunoglobulin light chain (IGK: VkKde, intron-Kde), T-cell receptor gamma (TRG: VG-JG1.3./2.3, VG-JG1.1/2.1), and complete and incomplete T-cell receptor delta (TRD: VD-(DD)-JD1, DD2-JD1, VD2-DD3, DD2-DD3), T-cell receptor Vdelta2-Jalpha(VD2-JA 9, 29, 30, 48, 54, 55, 58, 61) was performed for both BCP-and T-cell ALL as previously described in detail. [32][33][34][35] To confirm clonality of the identified product, homo-heteroduplex analysis was performed. 36 Clonal products were sequenced using the ABI PRISM one or multicapillary analyzer (Applied Biosystems, Darmstadt, Germany).…”

Section: 31mentioning

confidence: 99%

Very early/early relapses of acute lymphoblastic leukemia show unexpected changes of clonal markers and high heterogeneity in response to initial and relapse treatment

et al. 2011

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Minimal residual disease (MRD) quantified after induction treatment of childhood acute lymphoblastic leukemia (ALL) predicts risk of relapse. It has been assumed that early relapses derive from a residual population of leukemic cells, which is still present after induction and that relapsed disease will consequently be more resistant to treatment. To test these hypotheses, we performed a prospective study on patients treated according to the frontline-trial ALL-BFM 2000, which used MRD response for risk-group stratification. Patients (n ¼ 45) showed a median time to relapse of 1.5 years. In 89% of patients at least one T-cell-receptor/immunoglobulin gene rearrangement chosen for initial MRD quantification remained stable; however, at least one of the preferred markers for MRD stratification at relapse was different to diagnosis in 50% of patients. A similar proportion of very early, early and late relapses appeared to gain a marker at relapse although backtracking-analysis revealed that in 77% of cases, the gained markers were present as small sub-clones at initial diagnosis. Comparing initial and relapse MRD response to induction, 38% of patients showed a similar, 38% a better and 25% a poorer response after relapse. These data demonstrate an unexpectedly high clonal heterogeneity among very early/early relapses and challenge some current assumptions about relapsed ALL.

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Section: 31mentioning

confidence: 99%

Very early/early relapses of acute lymphoblastic leukemia show unexpected changes of clonal markers and high heterogeneity in response to initial and relapse treatment

et al. 2011

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“…Preparation of genomic DNA and PCR were performed as described previously (Taube et al, 1997). The following forward (F) and reverse (R) oligonucleotides (TIB Molbiol, Berlin, Germany) were used for detection of the HIF-1α gene (HIF1A):…”

Section: Dna Analysismentioning

confidence: 99%

Oxygen-regulated expression of the RNA-binding proteins RBM3 and CIRP by a HIF-1-independent mechanism

Wellmann

Bührer

Moderegger

et al. 2004

Journal of Cell Science

222

162

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The transcriptional regulation of several dozen genes in response to low oxygen tension is mediated by hypoxia-inducible factor 1 (HIF-1), a heterodimeric protein composed of two subunits, HIF-1α and HIF-1β. In the HIF-1α-deficient human leukemic cell line, Z-33, exposed to mild (8% O2) or severe (1% O2) hypoxia, we found significant upregulation of two related heterogenous nuclear ribonucleoproteins, RNA-binding motif protein 3 (RBM3) and cold inducible RNA-binding protein (CIRP), which are highly conserved cold stress proteins with RNA-binding properties. Hypoxia also induced upregulation of RBM3 and CIRP in the murine HIF-1β-deficient cell line, Hepa-1 c4. In various HIF-1 competent cells, RBM3 and CIRP were induced by moderate hypothermia (32°C) but hypothermia was ineffective in increasing HIF-1α or vascular endothelial growth factor (VEGF), a known HIF-1 target. In contrast, iron chelators induced VEGF but not RBM3 or CIRP. The RBM3 and CIRP mRNA increase after hypoxia was inhibited by actinomycin-D, and in vitro nuclear run-on assays demonstrated specific increases in RBM3 and CIRP mRNA after hypoxia, which suggests that regulation takes place at the level of gene transcription. Hypoxia-induced RBM3 or CIRP transcription was inhibited by the respiratory chain inhibitors NaN3 and cyanide in a dose-dependent fashion. However, cells depleted of mitochondria were still able to upregulate RBM3 and CIRP in response to hypoxia. Thus, RBM3 and CIRP are adaptatively expressed in response to hypoxia by a mechanism that involves neither HIF-1 nor mitochondria.

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“…In DNA from bone marrow samples of ALL patients taken at initial or relapse diagnosis immunoglobulin heavy and light chains (IgGH/IGK) gene rearrangements were identified using screening PCR reactions (144)(145)(146)(147). Clonality was assessed by homo-and hetero-duplex analysis (148).…”

Section: Immunoglobulin Gene Rearrangementsmentioning

confidence: 99%

Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia

et al. 2010

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Multiplex PCR for simultaneous detection of the most frequent T cell receptor-δ gene rearrangements in childhood ALL

Cited by 16 publications

References 1 publication

Very early/early relapses of acute lymphoblastic leukemia show unexpected changes of clonal markers and high heterogeneity in response to initial and relapse treatment

Very early/early relapses of acute lymphoblastic leukemia show unexpected changes of clonal markers and high heterogeneity in response to initial and relapse treatment

Oxygen-regulated expression of the RNA-binding proteins RBM3 and CIRP by a HIF-1-independent mechanism

Leukemia-associated genetic aberrations in mesenchymal stem cells of children with acute lymphoblastic leukemia

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