BCR-ABL kinase domain mutations in tyrosine kinase inhibitors-naïve and -exposed Southeast Asian chronic myeloid leukemia patients

Wongboonma, Wanwisa; Thongnoppakhun, Wanna; Auewarakul, Chirayu

doi:10.1016/j.yexmp.2012.01.007

Cited by 24 publications

(20 citation statements)

References 47 publications

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“…20µl water solution of cDNA (9.65 ng/µl) and 3.8 µM photosensitizer Radachlorin (Rada-Pharma Co, Ltd., Moscow, Russia) in individual tubes was prepared. This solution was irradiated with 662 nm laser «LAHTA -MILON» (MILON Laser, St. Petersburg, Russia) at power density I = 50 mW/cm 2 with energy doses: 2. and reverse (5'-GTTCCCGTAGGTCATGAACTCAG-3') primers [7], Taq polymerase (1.25 units per reaction), dNTP (200 µM) and 10х Mg 2+ Tris-HCl buffer («Sileks», Russia). Used primers were specific to the BCR-ABL gene fragment of cDNA.…”

Section: Ssdna Damage By Singlet Oxygenmentioning

confidence: 99%

ssDNA damage dependence from singlet oxygen concentration at photodynamic interaction

Клименко

Kaydanov

Anton

et al. 2017

J. Phys.: Conf. Ser.

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Abstract. Single stranded DNA damage at photodynamic treatment with Radachlorin photosensitizer was investigated. Chemical trap method was used to evaluate generation of singlet oxygen in water solution. Interaction of singlet oxygen with ssDNA resulted into decrease of the replication activity of ssDNA. DNA stopped replicating during PCR at irradiation doses greater than 15 J/cm 2 and concentration of photosensitizer [PS] = 3.8 µM. The dependence of replication activity of ssDNA on generated singlet oxygen concentration was identified.

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Section: Ssdna Damage By Singlet Oxygenmentioning

confidence: 99%

ssDNA damage dependence from singlet oxygen concentration at photodynamic interaction

Клименко

Kaydanov

Anton

et al. 2017

J. Phys.: Conf. Ser.

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“…DNA was extracted from PB using commercial available DNA extraction Kit (Promega, USA) following manufacture instructions. ASO-PCR was performed in 30µl reaction (Kang et al, 2006;Wongboonma et al, 2012). Briefly, three master mixes were prepared, one for T315I mutation detection, the second for F317L mutation detection and the third one for wild type bcr-abl detection (WT).…”

Section: Aso-pcrmentioning

confidence: 99%

Molecular Screening for T315I and F317L Resistance Mutations in Iraqi Chronic Myeloid Leukemia Non-Responders Patients to Imatinib

Dhahi¹,

Matti²,

Fadel³

2013

CCO

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The development of Imatinib Mesylate (IM), the first generation specific tyrosine kinase inhibitor (TKI) of BCR-ABL, has had a major impact in patients with Chronic Myeloid Leukemia (CML), establishing IM as the standard therapy for CML. Despite the clinical success obtained with the use of IM, primary resistance to IM and molecular evidence of persistent disease has been observed in 20-25% of IM treated patients. The existence of second generation TKIs (SGTKIs), which are effective in patients with IM resistance, makes identification of predictors of resistance to IM an important goal in CML. The aim of this prospective study was to determine prevalence of T315I, which confers full resistance to all available tyrosine-kinase inhibitors, and F317l mutations, which classified as resistant mutation to IM and dasatinib but sensitive to nilotinb, in IM non-responder CML patients from Iraq with highly sensitive Allele-Specific Oligonucleotide-PCR assay (ASO-PCR). Forty four CML patients were recruited from Baghdad Teaching Hospitalet-Hematology Unite from Feb. 2009 to Feb. 2013. Those patients were followed up (hematological, cytogenetically, and molecularly). At the time of sampling, thirty four CML patients in advance phase(accelerated phase(AP) or blast crisis(BC)) or loss their cytogenetic response were IM non-responders while ten CML patients in CP were IM responder, considered as T315I and F317 L mutations negative control group. Ten IM non-responders patients out of those 34 patients were recruited to SGTKIs (Dasatinib and/or Nilotinib). The results shown that only T315I mutation was detected in one IM non-responder CML patient (3%). Although relation between response to SGTKIs and mutation status was non-significance (P= 0.100), mutation is limited to only one patient who did not respond to either treatment forms. In conclusion, the uses of bcr-abl mutation screening test for T315I and F317L mutations in CML patients may influences the choice of specific SGTKIs after treatment with IM has failed.

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“…t (9;22) occurs in the juxtaposition of the Abelson (ABL1) oncogene, a tyrosine kinase (TK) located on chromosome 9, to the breakpoint cluster region (BCR) gene located on chromosome 22, leading to aberrantly increased TK activity (3,4). Mechanisms that have been attributed to BCR-ABL-positive cells and been implicated in the pathogenesis of CML include increased proliferation, increased resistance to apoptosis, and an alteration of cell adhesion properties (1).…”

Section: Introductionmentioning

confidence: 99%

“…Previous studies have reported that ~20% of patients fail therapy with imatinib mesylate due to point mutations within the BCR/ABL KD (11). The emergence of point mutations in the BCR-ABL KD is a primary cause of imatinib resistance in patients with CML, and >90 types of KD mutations have been reported, particularly in the accelerated and blast crisis phases (4,8,12). These mutations may alter the BCR-ABL KD structure and impair the imatinib-binding affinity (4,12).…”

Section: Introductionmentioning

confidence: 99%

“…The emergence of point mutations in the BCR-ABL KD is a primary cause of imatinib resistance in patients with CML, and >90 types of KD mutations have been reported, particularly in the accelerated and blast crisis phases (4,8,12). These mutations may alter the BCR-ABL KD structure and impair the imatinib-binding affinity (4,12). Point mutations in the KD occur in 30-90% of patients who develop resistance to the drug (13).…”

Section: Introductionmentioning

confidence: 99%

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Molecular screening and the clinical impacts of BCR‑ABL KD mutations in patients with imatinib‑resistant chronic myeloid leukemia

et al. 2017

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Abstract. The present study aimed to detect the frequency of kinase domain (KD) mutations in order to evaluate their clinical significance and functional importance in 45 patients with chronic myeloid leukemia (CML) who were resistant to imatinib therapy. Sanger sequencing was used (45 patients), along with allele-specific oligonucleotide polymerase chain reaction (ASO-PCR; 3 patients), for the screening of mutations. BCR/ABL KD was amplified by nested PCR and sequencing was performed. Secondly, ASO-PCR was performed to confirm the results of the sequence analysis for E255K mutations. Mutations were detected in 11/45 patients (24.44%) via Sanger sequencing. D241G (4.4%), C369C (4.4%), K285N (2.2%), A380T (2.2%) and A366V (2.2%) mutations were detected. E255K (8.8%) was detected by ASO-PCR and Sanger sequencing. Mutations are a primary reason for suboptimal responses, loss of response and resistance to imatinib. In particular, the E255K mutation, which is characterized by resistance to imatinib and nilotinib, was detected in four patients. Analyzing the mutations and monitoring patients with CML may improve their prognosis and survival rate. ASO-PCR assays will be beneficial for the routine monitoring of mutations.

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BCR-ABL kinase domain mutations in tyrosine kinase inhibitors-naïve and -exposed Southeast Asian chronic myeloid leukemia patients

Cited by 24 publications

References 47 publications

ssDNA damage dependence from singlet oxygen concentration at photodynamic interaction

ssDNA damage dependence from singlet oxygen concentration at photodynamic interaction

Molecular Screening for T315I and F317L Resistance Mutations in Iraqi Chronic Myeloid Leukemia Non-Responders Patients to Imatinib

Molecular screening and the clinical impacts of BCR‑ABL KD mutations in patients with imatinib‑resistant chronic myeloid leukemia

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