Double-Gradient–Denaturing-Gradient Gel Electrophoresis for Mutation Screening of the BCR-ABL Tyrosine Kinase Domain in Chronic Myeloid Leukemia Patients

Sorel, Nathalie; Chazelas, Florence; Brizard, A.; Chomel, Jean‐Claude

doi:10.1373/clinchem.2004.047274

Cited by 24 publications

(9 citation statements)

References 15 publications

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“…3,4 NPM1-mutated AMLs have a distinctive gene expression profile characterized by up-regulation of genes involved in stem-cell maintenance. 5 We have observed rare cases of AML in which the blasts have prominent nuclear invaginations (so-called cuplike nuclei) similar to cases previously reported as AML with cuplike nuclear invaginations 6 or "myeloid/natural killer cell" acute leukemia. 7 AML with cuplike nuclei cases we have seen have immunophenotypic and cytogenetic features similar to NPM1-mutated AML.…”

Section: To the Editorsupporting

confidence: 72%

“…To determine the mechanism of IM resistance, we screened the BCR-ABL kinase domain for mutations by denaturing gradient gel electrophoresis (DGGE) as previously described. 5 At that time, the V379I mutation was detected by DGGE and characterized by direct sequencing. As shown in Figure 1, lane 3, the unmutated BCR-ABL allele was replaced by the mutated allele (band b).…”

Section: To the Editormentioning

confidence: 99%

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Sequential emergence of ABL-kinase mutations with loss of unmutated BCR-ABL allele during targeted therapies of CML

Sorel¹,

Martineau²,

Guilhot³

et al. 2006

Blood

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Section: To the Editorsupporting

confidence: 72%

Section: To the Editormentioning

confidence: 99%

Sequential emergence of ABL-kinase mutations with loss of unmutated BCR-ABL allele during targeted therapies of CML

Sorel¹,

Martineau²,

Guilhot³

et al. 2006

Blood

Self Cite

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“…This is consistent with the result obtained by Willis et al study, who did not detect these two mutations in 66 patients by using ASO-PCR technique (Willis et al, 2005). However, Sorel study detected the E255K mutation in only one out of 59 IM resistant patients by using Double-Gradient-Denaturing-Gradient Gel Electrophoresis (Sorel et al, 2005). Another study by Elass, Osman & AL-Gadir (2011) detected E255K in one patient from 50 IM resistant CML patients by using ASO-PCR technique.…”

Section: Discussionmentioning

confidence: 98%

Molecular Screening for E255K and F359V Mutations in Non-Responders Iraqi Chronic Myeloid Leukemia Patients to Imatinib Mesylate Therapy

Jamal¹,

Dhahi²,

Mattii³

2014

IJB

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Mutations in the kinase domain (KD) of BCR-ABL are the most prevalent mechanism of acquired resistance to first generation of tyrosine kinase inhibitor Imatinib Mesylate (IM) in chronic myeloid leukemia (CML) patients. Dasatinib and Nilotinib, the second generation of tyrosine kinase inhibitors (SGTKI), have been approved for second-line treatment of CML patients who demonstrate resistance to IM. The identification of E255K and F359Vmutations, which are considered highly resistant to SGTKI nilotinib, lead to a clear-cut decision in the choice of the appropriate SGTKI dasatinib. The aim of this study is to assess the frequency of mutations E255K and F359V in Iraqi CML patients who showed criteria of failure or suboptimal response to IM by using Allele Specific Oligonucleotid-Polymerase Chain Reaction (ASO-PCR). In this cross-section study, 70 patients were diagnosed clinically and hematologically as CML, who attended the Baghdad Medical City /Teaching Hospital/Hematology Unite, during the period between September 2011 to June 2012. They were on IM in different doses (400-800 mg/day) for at least one and a half year. Those patients were classified according to their responsiveness to IM into four groups according to European Leukemia Net. Also, 10 healthy age match subjects were included who served as technical negative control. Peripheral blood (PB) samples were taken from each subject. DNA was extracted using commercial available DNA extraction kit. Molecular screening for the presence of E255K and F359V mutations were done using ASO-PCR. The mean value of age of CML patients was 40.5 ± 2.56 years. Male to female ratio of CML patients was 1.12:1. The result of molecular screening for two mutations showed that all seventy CML patients were negative for both mutations. We conclude that the presence of other variants of studied mutations, another types of point mutations or other mechanisms for resistance to IM such as over expression of BCR-ABL, drug influx and efflux could be the causes of IM resistance.

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“…Les méthodes de balayage (DHPLC ou denaturing high performance liquid chromatography, DGGE ou denaturing gradient gel electrophoresis, HRM ou high-resolution melt curve analysis) permettent de mettre en évidence une anomalie inconnue à l'intérieur de la zone d'étude, ce qui autorise à ne séquen-cer que les échantillons présentant réellement une mutation (Fig. 14) [ [65][66][67]. Enfin, les méthodes de RT-PCR spécifiques d'allèles présentent une grande sensibilité mais ne permettent d'identifier qu'une seule mutation bien déterminée [68].…”

Section: Détection Des Mutations Du Domaine Kinase De Bcr-ablunclassified

Les syndromes myéloprolifératifs

Chomel

Sorel

Mayeur-Rousse

et al. 2009

Immuno-analyse & Biologie Spécialisée

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Double-Gradient–Denaturing-Gradient Gel Electrophoresis for Mutation Screening of the BCR-ABL Tyrosine Kinase Domain in Chronic Myeloid Leukemia Patients

Cited by 24 publications

References 15 publications

Sequential emergence of ABL-kinase mutations with loss of unmutated BCR-ABL allele during targeted therapies of CML

Sequential emergence of ABL-kinase mutations with loss of unmutated BCR-ABL allele during targeted therapies of CML

Molecular Screening for E255K and F359V Mutations in Non-Responders Iraqi Chronic Myeloid Leukemia Patients to Imatinib Mesylate Therapy

Les syndromes myéloprolifératifs

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