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Journal articles on the topic 'BCR-ABL1 mutation'

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Published: 3 June 2025

Last updated: 31 July 2025

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1

Mian, Afsar Ali, Hadiqa Raees, Sujjawal Ahmad, Oliver Ottmann, and El-Nasir M. A. Lalani. "Arsenic Trioxide Suppresses Growth of BCR-ABL1 Positive Cells with "Gatekeeper" or Compound Mutation." Blood 138, Supplement 1 (2021): 4346. http://dx.doi.org/10.1182/blood-2021-154511.

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Abstract Introduction: Chronic myeloid leukemia (CML) and 30% of adult acute lymphatic leukemia (ALL) are characterized by the Philadelphia chromosome (Ph +), having a (9;22) chromosomal translocation. The BCR-ABL1 fusion protein is the hallmark of Ph + leukemia. BCR-ABL1 is characterized by constitutively activated ABL1 tyrosine kinase activity that determines its transformation potential. Tyrosine kinase inhibitors (TKI) have greatly improved the overall prognosis of these diseases. However, unsatisfactory responses in advanced disease stages, resistance and long-term tolerability of BCR-ABL

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2

Polivkova, Vaclava, Nikola Curik, Hana Zizkova, et al. "DNA Analysis of Mutations in the Kinase Domain of BCR-ABL1 By Allele-Specific Digital PCR Is Highly Sensitive and Refines Prediction of Kinetics of Resistant CML Clones." Blood 132, Supplement 1 (2018): 1743. http://dx.doi.org/10.1182/blood-2018-99-119710.

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Abstract Introduction: In chronic myeloid leukemia (CML) resistant to tyrosine kinase inhibitors (TKI), detection of mutations in the BCR-ABL1 kinase domain (KD) is routinely performed on transcript level. To determine the level of BCR-ABL1 KD mutation is important to follow kinetics of resistant CML cells and therapeutically prevent progression. However, the mutation types and levels are not always reliable predictors of subsequent dynamics of mutation-bearing clones and of corresponding clinical consequences (Willis, 2005; Khorashad, 2006; Preuner, 2012). DNA analysis enables more precise qu

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3

Chen, Jiaqi, Qihui Chen, Huan Hu, et al. "High-Accurate Third-Generation Sequencing to Comprehensively Decipher BCR::ABL1 TKIs in-Cis Resistant Mutations." Blood 144, Supplement 1 (2024): 3595. https://doi.org/10.1182/blood-2024-202681.

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Background Drug-resistant mutations in the ABL1 kinase domain (KD) of BCR::ABL1 are primary mechanisms of resistance to tyrosine kinase inhibitor (TKI) therapy in Ph-positive leukemia. These mutations alter the conformation of ABL1 within BCR::ABL1, impairing TKI and thus diminishing their anti-leukemia efficacy. Our previous studies, presented at the 61st and 62nd ASH Annual Meeting, demonstrated the superiority of next-generation sequencing (NGS) over Sanger sequencing for detecting BCR::ABL1-KD mutations. NGS offers higher sensitivity, accurate mutation frequency determination, and the abil

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4

Morishita, Soji, and Norio Komatsu. "Diagnosis- and Prognosis-Related Gene Alterations in BCR::ABL1-Negative Myeloproliferative Neoplasms." International Journal of Molecular Sciences 24, no. 16 (2023): 13008. http://dx.doi.org/10.3390/ijms241613008.

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BCR::ABL1-negative myeloproliferative neoplasms (MPNs) are a group of hematopoietic malignancies in which somatic mutations are acquired in hematopoietic stem/progenitor cells, resulting in an abnormal increase in blood cells in peripheral blood and fibrosis in bone marrow. Mutations in JAK2, MPL, and CALR are frequently found in BCR::ABL1-negative MPNs, and detecting typical mutations in these three genes has become essential for the diagnosis of BCR::ABL1-negative MPNs. Furthermore, comprehensive gene mutation and expression analyses performed using massively parallel sequencing have identif

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5

Li, Jin, Zhenyu Yan, Lin Shi, et al. "Abstract 341: Co-detection of BCR::ABL1 common and atypical fusion and mutation using a novel NGS assay, Dup-Seq BCR-ABL1." Cancer Research 84, no. 6_Supplement (2024): 341. http://dx.doi.org/10.1158/1538-7445.am2024-341.

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Abstract The clinical management of CML and Ph+ ALL patients requires the identification of BCR::ABL1 transcript variants and drug resistance mutations. Currently these assessments need to be performed using separate assays resulting in higher sample requirements, longer turnaround times and higher costs. In this study a custom NGS assay (Dup-Seq BCR-ABL1) was developed and validated that enables co-detection and identification of transcript variants (common and atypical) and resistance mutations. The assay design covers BCR exon 1 to ABL1 exon 10 and employs duplicate PCR amplification of BCR

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6

Liu, Hongxing, Jiaqi Chen, Fang Wang, et al. "NGS-Based Screening to Comprehensively Decipher TKIs Resistant Mutations in BCR-ABL1 Positive Leukemias." Blood 136, Supplement 1 (2020): 30. http://dx.doi.org/10.1182/blood-2020-140917.

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In BCR-ABL1 positive leukemia, mutations in the BCR-ABL1 kinase domain (KD) are the most common TKIs resistance mechanism. Sanger sequencing (SS) is currently the gold standard for detecting ABL1 KD mutations, but its low detection sensitivity cannot reveal mutations below 20% VAFs (variant allele frequency), and it is challenging to distinguish compound or polyclonal mutations. In recent years, the NGS-based BCR-ABL1 KD mutation screening protocol provides a powerful tool for deciphering complex patterns (compound or polyclonal mutations) and higher detection sensitivity (~2%, hotspot mutatio

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7

Li, Jin, Weihua Liu, Zhenyu Yan, et al. "Next-Generation Sequencing of the BCR-ABL1 Kinase Domain and Neighboring Domains Associated with Therapy Resistance." Blood 120, no. 21 (2012): 2549. http://dx.doi.org/10.1182/blood.v120.21.2549.2549.

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Abstract Abstract 2549 Background: BCR-ABL1 mutation testing is recommended for CML and Ph+ ALL patients who fail first line tyrosine kinase inhibitor (TKI) therapy or who have a suboptimal response to therapy. BCR-ABL1 mutations in the kinase domain (KD) of ABL1 account for at least 40–50% of all TKI resistant cases. Rare mutations such as E123Q and T212R in the regulatory domain of ABL upstream of the kinase domain have also been reported to lead to resistance to imatinib. The current gold standard for BCR-ABL1 mutation detection is Sanger sequencing, which has an analytical sensitivity of ∼

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8

Santos, Fabio P. S., Jorge Cortes, Charles Koller, and Elias Jabbour. "Combination Therapy with Tyrosine Kinase Inhibitors and Agents with Different Mechnisms of Actions Is Effective in a Patient with Chronic Myeloid Leukemia Harboring the T315l BCR - ABL1 Mutation." Blood 114, no. 22 (2009): 4282. http://dx.doi.org/10.1182/blood.v114.22.4282.4282.

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Abstract Abstract 4282 Mutations of BCR-ABL1 have been observed in 50% of patients with chronic myeloid leukemia (CML) who develop resistance to imatinib. The gate-keeper mutation T315I is one of the mutations with universal resistance to imatinib and to the second-generation tyrosine kinase inhibitors (TKI) that are approved for the treatment of patients with imatinib failure. The use of new kinase inhibitors with in vitro activity against T315I mutation as well as other agents with different mechanisms of actions is being evaluated in clinical trials. We report the case of a 57-year old man

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9

Baer, Constance Regina, Claudia Haferlach, Wolfgang Kern, and Torsten Haferlach. "Prospective Next-Generation Sequencing of Mutations in the ABL1 Kinase Domain in CML Patients Lacking Optimal Response According to ELN Guidelines." Blood 128, no. 22 (2016): 3100. http://dx.doi.org/10.1182/blood.v128.22.3100.3100.

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Abstract Background: In chronic myeloid leukemia (CML), mutations in the ABL1 kinase domain cause resistance to tyrosine kinase inhibitors (TKIs), and require therapy intervention. According to ELN guidelines (Baccarani et al., 2013), ABL1 sequencing is recommended for cases of progression, failure and warning. Failure and warning apply to patients, who did not reach treatment milestones or had shown response and subsequently lost it. An increase in BCR-ABL1/ABL1 ratio can be regarded as first alert. Failure is then defined as loss of major molecular response (BCR-ABL1/ABL1 <0.1%) if confir

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10

Soverini, Simona, Caterina De Benedittis, Luca Zazzeroni, et al. "In Chronic Myeloid Leukemia Patients on 2nd-Line Tyrosine Kinase Inhibitor Therapy, Deep Sequencing at the Time of Warning May Allow Sensitive Detection of Emerging BCR-ABL1 Mutants." Blood 124, no. 21 (2014): 815. http://dx.doi.org/10.1182/blood.v124.21.815.815.

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Abstract Background and Aims: Next generation amplicon-based deep sequencing (DS) on the Roche, Illumina or Ion Torrent instruments is becoming accessible to a wider and wider number of diagnostic laboratories. Although conventional sequencing is still the gold standard, DS has been hailed by many as the future of diagnostic BCR-ABL1 kinase domain (KD) mutation screening. BCR-ABL1 KD mutations are infrequent in newly diagnosed chronic myeloid leukemia (CML) patients (pts) receiving 1st-line TKI therapy, but remain a challenge in relapsed pts, who usually display a greater genetic instability.

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11

Kim, Soo-Hyun, Soo Young Choi, Sung-Eun Lee, et al. "Dynamics and Characteristics of BCR-ABL1 Multiple Mutations in Tyrosine Kinase Inhibitor Resistant CML." Blood 120, no. 21 (2012): 1677. http://dx.doi.org/10.1182/blood.v120.21.1677.1677.

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Abstract Abstract 1677 Background: BCR-ABL1 kinase domain (KD) point mutation causes resistance to tyrosine kinase inhibitors (TKI) in CML patients through impaired binding of TKI to the target site. One of the characteristics of patients with BCR-ABL1 kinase domain point mutations is the fact that some patients have multiple mutations. However there have not been many studies showing that data about clinical relevance or dynamics of multiple mutation during CML treatment. Methods: Since 2002, 414 CML patients were screened for mutation analysis due to sign of resistance to TKI including imati

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Grossmann, Vera, Melanie Wild, Susanne Schnittger, et al. "Ultra-Deep Next-Generation Sequencing (NGS) Detects BCR-ABL1 Kinase Domain Mutations with High Sensitivity and Allows to Monitor the Composition of Distinct Subclones During Tyrosine Kinase Inhibitor Treatment." Blood 116, no. 21 (2010): 2268. http://dx.doi.org/10.1182/blood.v116.21.2268.2268.

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Abstract Abstract 2268 Since the introduction of imatinib mesylate for treating patients with chronic myeloid leukemia (CML) data has shown that a small proportion of patients in chronic phase experience refractoriness to kinase inhibitor treatment due to mutations in the ABL1 domain. A variety of molecular methods provide a clinically feasible workflow to detect these mutations but have both strengths and weaknesses: e.g. direct sequencing of nested PCR assays amplifying the ABL1 part of BCR-ABL1 fusion transcript has a low diagnostic detection sensitivity of 10%; and more sensitive methods s

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13

Li, Jin, Zhenyu Yan, Agus Darwanto, et al. "Phasing Analysis Of TKI Resistance Mutations In The BCR-ABL1 Kinase Domain and Neighboring Domains Using Next-Generation Sequencing." Blood 122, no. 21 (2013): 3817. http://dx.doi.org/10.1182/blood.v122.21.3817.3817.

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Abstract Background Many CML patients treated with tyrosine kinase inhibitors (TKIs) eventually develop resistance as a result of ABL1 kinase domain (KD) mutations, and sequential treatment with different TKIs may select for multiple BCR-ABL1 mutations. Whether multiple mutations arise in distinct clones (in trans, or polyclonal mutations) or instead are present within the same BCR-ABL1 molecule (in cis, or compound mutations), has been shown to have important implications with respect to TKI sensitivities (Eide, C.A. et al., Blood 2011). Distinguishing between polyclonal and compound mutation

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Saglio, Giuseppe, and Carmen Fava. "BCR-ABL1 mutation ≠ ponatinib resistance." Blood 127, no. 6 (2016): 666–67. http://dx.doi.org/10.1182/blood-2015-12-685149.

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15

Chen, Jiaqi, Hongxing Liu, Fang Wang, et al. "Dynamic Evolution of Ponatinib Resistant BCR-ABL1 T315 and Compound Mutations." Blood 134, Supplement_1 (2019): 3796. http://dx.doi.org/10.1182/blood-2019-129579.

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The third-generation tyrosine kinase inhibitor (TKI) ponatinib exhibits activity against all common BCR-ABL1 kinase domain (KD) single mutations, including the highly resistant gatekeeper T315I. However, the drug response is variable and the clinical resistance mutations may still befall with few reports to date. We performed next-generation sequencing (NGS) detection of BCR-ABL1 KD mutations in sequential samples of three BCR-ABL1-positive leukemia patients who developed clinical resistance to ponatinib, to explore the dynamic evolution of ponatinib mutations. Case 1 was diagnosed as chronic

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Schnittger, Susanne, Tamara Alpermann, Wolfgang Kern, Torsten Haferlach, and Claudia Haferlach. "Response to Imatinib Mesylate In CML Patients as Assessed by Quantitative Real Time PCR Can Predict the Probability for Resistance Mutations In the BCR-ABL1 Kinase Domain." Blood 116, no. 21 (2010): 3420. http://dx.doi.org/10.1182/blood.v116.21.3420.3420.

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Abstract Abstract 3420 The introduction of imatinib into the treatment of patients with chronic myeloid leukemia (CML) resulted in a seven year event free survival of 81% (IRIS trial). Quantitative BCR-ABL1 monitoring to control for therapy response has been recommended every three months. Major molecular response (MMR) was defined as reduction of the %BCR-ABL1/ABL1 to ≤0.1 after the first year of treatment (European LeukemiaNet, ELN, Baccarani et al., JCO 2009). However, a small proportion of patients in chronic phase experience refractoriness to kinase inhibitor treatment. As a major cause o

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Vannuffel, Pascal, Barbara Cauwelier, Céline De Rop, and Friedel Nollet. "Detection and Monitoring of BCR-ABL1 Kinase Domain Mutations By Next Generation Sequencing." Blood 126, no. 23 (2015): 4042. http://dx.doi.org/10.1182/blood.v126.23.4042.4042.

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Abstract Background. Among myeloproliferative diseases, development of chronic myeloid leukaemia (CML) is associated with the emergence of the fusion oncogene BCR-ABL1 resulting from a t(9,22) chromosomal translocation (Philadelphia chromosome). Mutations of the BCR-ABL1 kinase domain constitute a major cause of treatment failure in CML patients receiving tyrosine kinase inhibitor (TKI) treatment. Moreover, the occurrence of cells with multiple mutations is frequently associated with a higher resistance rate to the different TKI (Imatinib, Dasatinib or Nilotinib). So far, the gold standard pro

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Martin-Cabrera, Pedro, Claudia Haferlach, Torsten Haferlach, Wolfgang Kern, and Susanne Schnittger. "Co-Occurrence of Separate BCR-ABL1-Positve and JAK2V617F-Positive Clones in 23 Patients Reveals Biologic and Clinical Importance." Blood 124, no. 21 (2014): 3175. http://dx.doi.org/10.1182/blood.v124.21.3175.3175.

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Abstract Background: The simultaneous detection of a BCR-ABL1 rearrangement and a JAK2V617F mutation in the same patient is a very rare event and has previously been described in case reports or very small series of cases only. Aim: 1) To establish the incidence of cases with concurrent BCR-ABL1 rearrangement and JAK2V617F mutation. 2) Evaluate whether one clone harbours both mutations or whether there are two independent clones. 3) Establish whether these patients have additional concurrent gene mutations and how they influence the evolution of both diseases. Patients and Methods: A total of

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Tauchi, Tetsuzo, Seiichiro Katagiri, Seiichi Okabe, et al. "Combined Effects of a Pan-ABL1 Kinase Inhibitor, Ponatinib and Dasatinib Against T315I Mutant Forms of BCR-ABL1: In Vitro and In Vivo Studies." Blood 118, no. 21 (2011): 2482. http://dx.doi.org/10.1182/blood.v118.21.2482.2482.

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Abstract Abstract 2482 Ponatinib is a third-generation ABL1 kinase inhibitor optimized using structure-based drug design to bind the inactive, DFG-out conformation of wild-type (WT)-BCR-ABL1 and T315I BCR-ABL1. Ponatinib provides an effective in minimizing resistance, however, certain BCR-ABL1 compound mutations such as Y235H/T315I and E255K/T315I are predicted to be recalcitrant to ponatinib. Combining ponatinib and dasatinib may provide several advantages, including enhanced efficacy and the potential to reduce the emergence of new resistant compound mutations. In the present study, we inves

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Borisevich, M. V., and T. V. Savitskaya. "F359C mutation of the BCR-ABL1 gene in adolescent with chronic myeloid leukemia. Case report." Russian Journal of Pediatric Hematology and Oncology 6, no. 2 (2019): 72–75. http://dx.doi.org/10.21682/2311-1267-2019-6-2-72-75.

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Chronic myeloid leukemia (CML) in children is rare, less than 3 % of all cases of leukemia in pediatric practice. Along with the successes achieved in the treatment of CML with imatinib, it’s necessary to study of molecular factors in predicting resistance to therapy. According to the literature, about 30 % of adult patients with imatinib resistance have point mutations in the kinase domain of BCR-ABL1 gene. The number of reports about mutation spectrum of the BCR-ABL1 gene in children with resistant forms of CML is limited. This article describes the clinical case of secondary resistance to i

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Boucher, Lara, Nathalie Sorel, Christophe Desterke, et al. "Deciphering Potential Molecular Signatures to Differentiate Acute Myeloid Leukemia (AML) with BCR::ABL1 from Chronic Myeloid Leukemia (CML) in Blast Crisis." International Journal of Molecular Sciences 24, no. 20 (2023): 15441. http://dx.doi.org/10.3390/ijms242015441.

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Acute myeloid leukemia (AML) with BCR::ABL1 has recently been recognized as a distinct subtype in international classifications. Distinguishing it from myeloid blast crisis chronic myeloid leukemia (BC-CML) without evidence of a chronic phase (CP), remains challenging. We aimed to better characterize this entity by integrating clonal architecture analysis, mutational landscape assessment, and gene expression profiling. We analyzed a large retrospective cohort study including CML and AML patients. Two AML patients harboring a BCR::ABL1 fusion were included in the study. We identified BCR::ABL1

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Gruber, Tanja, Mi Sook Chang, Richard Sposto, and Markus Müschen. "Activation-Induced Cytidine Deaminase Accelerates Clonal Evolution of BCR-ABL1-Driven B Cell Lineage Acute Lymphoblastic Leukemia." Blood 114, no. 22 (2009): 181. http://dx.doi.org/10.1182/blood.v114.22.181.181.

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Abstract Abstract 181 Activation-Induced Cytidine Deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center (GC) B cells. Occasionally, AID can target non-Ig genes and thereby promote GC B cell lymphomagenesis. We recently demonstrated that the oncogenic BCR-ABL1 kinase induces aberrant expression of AID in pre-B acute lymphoblastic leukemia (ALL). Compared to other ALL subtypes, BCR-ABL1 ALL is considered high risk and is characterized by a high degree of genetic instability. Because aberrant mutational activity of AID is assoc

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Baccarani, Michele, Simona Soverini, and Caterina De Benedittis. "Molecular Monitoring and Mutations in Chronic Myeloid Leukemia: How to Get the Most out of Your Tyrosine Kinase Inhibitor." American Society of Clinical Oncology Educational Book, no. 34 (May 2014): 167–75. http://dx.doi.org/10.14694/edbook_am.2014.34.167.

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The course of chronic myeloid leukemia (CML) and the response to treatment with tyrosine kinase inhibitors (TKIs) are best monitored and assessed using two molecular tests: the first is real-time quantitative reverse transcription-polymerase chain reaction (RQ-PCR), which measures the size of residual disease that is expressed as BCR-ABL1% (the ratio between BCR-ABL1 and a control gene) and the other is mutational analysis by Sanger sequencing, which checks for the presence of BCR-ABL1 kinase domain point mutations. Both tests are technically demanding and require a high level of specializatio

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Tirrò, Elena, Stefania Stella, Michele Massimino, et al. "Colony-Forming Cell Assay Detecting the Co-Expression of JAK2V617F and BCR-ABL1 in the Same Clone: A Case Report." Acta Haematologica 141, no. 4 (2019): 261–67. http://dx.doi.org/10.1159/000496821.

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BCR-ABL1-negative myeloproliferative disorders and chronic myeloid leukaemia are haematologic malignancies characterised by single and mutually exclusive genetic alterations. Nevertheless, several patients co-expressing the JAK2V617F mutation and the BCR-ABL1 transcript have been described in the literature. We report the case of a 61-year-old male who presented with an essential thrombocythaemia phenotype and had a subsequent diagnosis of chronic phase chronic myeloid leukaemia. Colony-forming assays demonstrated the coexistence of 2 different haematopoietic clones: one was positive for the J

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Soverini, Simona, Caterina De Benedittis, Cristina Papayannidis, et al. "Backtracking BCR-ABL1 Mutants in Philadelphia-Positive Acute Lymphoblastic Leukemia Patients Relapsing on Tyrosine Kinase Inhibitors with Deep Sequencing: Implications for Routine Mutation Testing." Blood 124, no. 21 (2014): 2259. http://dx.doi.org/10.1182/blood.v124.21.2259.2259.

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Abstract Background: With the release of benchtop next-generation sequencers allowing to conjugate assay sensitivity and throughput with affordability, it was envisioned that NGS could soon replace conventional methods in the routine diagnostic identification of mutations relevant for diagnostication, prognostication and therapeutic tailoring. Having recently implemented and optimized a strategy for BCR-ABL1 kinase domain (KD) mutation screening based on the Roche-454 NGS technology, we decided to take advantage of its unique capability to capture the complexity and the clonal relationships of

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Soverini, Simona, Luana Bavaro, Caterina De Benedittis, et al. "Prospective assessment of NGS-detectable mutations in CML patients with nonoptimal response: the NEXT-in-CML study." Blood 135, no. 8 (2020): 534–41. http://dx.doi.org/10.1182/blood.2019002969.

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Abstract In chronic myeloid leukemia (CML) patients, tyrosine kinase inhibitors (TKIs) may select for drug-resistant BCR-ABL1 kinase domain (KD) mutants. Although Sanger sequencing (SS) is considered the gold standard for BCR-ABL1 KD mutation screening, next-generation sequencing (NGS) has recently been assessed in retrospective studies. We conducted a prospective, multicenter study (NEXT-in-CML) to assess the frequency and clinical relevance of low-level mutations and the feasibility, cost, and turnaround times of NGS-based BCR-ABL1 mutation screening in a routine setting. A series of 236 con

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Liu, Hongxing, Ping Zhu, Chunrong Tong, et al. "Clonal Evolution of BCR-ABL1 Kinase Domain Mutation In Tyrosine Kinase Inhibitor Treatment Patient." Blood 116, no. 21 (2010): 597. http://dx.doi.org/10.1182/blood.v116.21.597.597.

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Abstract Abstract 597 Resistance against tyrosine kinase inhibitors (TKI) has been an important issue in treatment for chronic myeloid leukemia (CML) and Ph-positive acute lymphoblastic leukemia (ALL), and it mainly result from BCR-ABL1 kinase domain mutation. Many studies have focused on the issue, however, characteristics of origin and evolution of BCR-ABL1 mutant clones remains unclear. In this study, we analyzed BCR-ABL1 mutations within the kinase domain for 189 bone marrow or peripheral blood samples, which were collected from 151 cases of CML or Ph-positive ALL. All samples were taken p

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Nardi, Valentina, Joshua Schwieterman, Zachary Kincaid, et al. "A Novel BCR::ABL1 Rearrangement Harboring the Gatekeeper Mutation Drives Hyper-Kinase Activity Conferring Resistance to Ponatinib and Asciminib Combination Therapy." Blood 144, Supplement 1 (2024): 4541. https://doi.org/10.1182/blood-2024-211279.

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Targeted inhibition of BCR::ABL1 by tyrosine kinase inhibitors (TKIs) has demonstrated remarkable clinical efficacy in chronic myeloid leukemia (CML) and Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia (Ph+ B-ALL). However, the emergence of resistant mutations undermines treatment response. These resistant mutants prevent drug binding either by steric blockade or by altering the conformational dynamics, called as conformational escape variants. Notably, the gatekeeper mutation (T315I) confers resistance through both mechanisms. To address this challenge, a combination ther

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Batar, Peter, Gabriella Mezei, and Arpad Illes. "Treatment-Emergent Resistance to Asciminib in Chronic Myeloid Leukemia Patients Due to Myristoyl-Binding Pocket-Mutant of BCR::ABL1/A337V Can Be Effectively Overcome with Dasatinib Treatment." Current Oncology 32, no. 2 (2025): 97. https://doi.org/10.3390/curroncol32020097.

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Despite the groundbreaking success of tyrosine kinase inhibitor therapy, the management of chronic myeloid leukemia patients is often impaired by resistance due to specific point mutations in the BCR::ABL1 oncogene. Upon classical ATP-competitive inhibitor treatment, these single nucleotide variants occur in the tyrosine kinase domain of ABL1. The novel allosteric BCR::ABL1 inhibitor asciminib was developed to treat CML patients alone or in combination to overcome or potentially prevent these treatment-emergent TKD mutations. Here, we present a case of a patient undergoing first-line asciminib

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Machnicki, Marcin M., Monika Pepek, Iwona Solarska, et al. "ASXL1 Mutations Detectable at Diagnosis May Predict Response to Imatinib in Patients with Chronic Myeloid Leukemia." Blood 134, Supplement_1 (2019): 4148. http://dx.doi.org/10.1182/blood-2019-129834.

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Clinical resistance to tyrosine kinase inhibitors (TKI) remains a significant problem in the therapy of patients with chronic myeloid leukemia (CML). Although BCR-ABL1-kinase domain mutations are the major cause of resistance to TKI, some patients manifest primary or develop secondary resistance to TKI without detectable BCR-ABL1 mutations. We aimed to assess the prevalence of additional gene mutations in a group of 50 patients with primary (n = 26) or secondary resistance (n = 24) to TKI, in most cases to imatinib (n = 49) and in one to dasatinib. We employed ~1000 genes custom target enrichm

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Miller, ChristoPher B., Charles G. Mullighan, Xiaoping Su, et al. "Pax5 Haploinsufficiency Cooperates with BCR-ABL1 to Induce Acute Lymphoblastic Leukemia." Blood 112, no. 11 (2008): 293. http://dx.doi.org/10.1182/blood.v112.11.293.293.

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Abstract Genes regulating B lymphoid development are somatically mutated in over 40% of B-progenitor acute lymphoblastic leukemia (ALL) cases, with the most common targets being the transcription factors PAX5, IKZF1 (encoding Ikaros), and EBF1. Notably, BCR-ABL1 ALL is characterized by a high frequency of mutations of IKZF1 (85%), PAX5 (55%), and CDKN2A/B (encoding INK4/ARF, 55%), suggesting that these lesions cooperate with BCR-ABL1 in lymphoid leukemogenesis. To examine cooperativity between Pax5 haploinsufficiency and BCR-ABL1, we transplanted Pax5+/+ and Pax5+/− bone marrow cells transduce

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Yeung, David T., Naranie Shanmuganathan, Agnes S. M. Yong, et al. "Update of the Ascend-CML Study of Frontline Asciminib: High Rate of Optimal Response and Resistance Due to Mutations Is Rare." Blood 144, Supplement 1 (2024): 476. https://doi.org/10.1182/blood-2024-201218.

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Asciminib, a Myristoyl Pocket BCR::ABL1 inhibitor, recently demonstrated its safety and efficacy in newly diagnosed CP-CML in the Phase III ASC4FIRST (Hochhaus, 2024), and the phase II ALLG CML13 ASCEND studies. Here, we update the ASCEND trial outcomes out to 24 months (mos) including molecular response and outcomes in patients (pts) failing asciminib or with suboptimal responses, and those with BCR::ABL1 mutations. In ASCEND, pts started asciminib (ASC) 40mg twice a day (BID) at diagnosis and switched to 80 mg daily after 12 mos. Pts with treatment failure (BCR::ABL1 &gt;10% at 3 or 6 mo

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Giudice, Valentina, Andrea Ghelli Luserna di Rorà, Bianca Serio, et al. "Axitinib in Ponatinib-Resistant B-Cell Acute Lymphoblastic Leukemia Harboring a T315L Mutation." International Journal of Molecular Sciences 21, no. 24 (2020): 9724. http://dx.doi.org/10.3390/ijms21249724.

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Adult acute lymphoblastic leukemia (ALL) with BCR-ABL1 rearrangement (Philadelphia chromosome, Ph) is a hematological aggressive disease with a fatal outcome in more than 50% of cases. Tyrosine kinase inhibitors (TKIs) targeting the activity of BCR-ABL1 protein have improved the prognosis; however, relapses are frequent because of acquired somatic mutations in the BCR-ABL1 kinase domain causing resistance to first, second and third generation TKIs. Axitinib has shown in vitro and ex vivo activity in blocking ABL1; however, clinical trials exploring its efficacy in ALL are missing. Here, we pre

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De, Benedittis Caterina, Cristina Papayannidis, Claudia Venturi, et al. "The clonal evolution of two distinct T315I-positive BCR-ABL1 subclones in a Philadelphia-positive acute lymphoblastic leukemia failing multiple lines of therapy: a case report." BMC Cancer 17, no. 1 (2017): 523. https://doi.org/10.1186/s12885-017-3511-2.

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<strong>Background: </strong>The treatment of Philadelphia chromosome-positive Acute Lymphoblastic Leukemia (Ph+ ALL) patients who harbor the T315I BCR-ABL1 mutation or who have two or more mutations in the same BCR-ABL1 molecule is particularly challenging since first and second-generation Tyrosine Kinase Inhibitors (TKIs) are ineffective. Ponatinib, blinatumomab, chemotherapy and transplant are the currently available options in these cases.<strong>Case presentation: </strong>We here report the case of a young Ph+ ALL patient who relapsed on front-line dasatinib therapy because of two indepe

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Guerineau, Hippolyte, Jean-Michel Cayuela, Stéphanie Dulucq, et al. "Mutation of Epigenetic Regulators at Diagnosis Is an Independent Predictor of Tyrosine Kinase Inhibitor Treatment Failure: A Report from the Residiag Study." Blood 142, Supplement 1 (2023): 4540. http://dx.doi.org/10.1182/blood-2023-186271.

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Introduction Additional mutations at chronic myeloid leukemia (CML) diagnosis have been shown to variably affect tyrosine kinase inhibitor (TKI) response and were inconstantly detected at loss of response. Contradictory observations may have resulted from difficulties in reliably inferring CML clonal architecture from mutations quantified by NGS, BCR::ABL1 by qRT-PCR, ABL1-TK by RNA-Seq. The RESIDIAG study was designed to identify at diagnosis molecular markers predictive of TKI treatment failure and analyze the clonal dynamics using asymmetric capture sequencing (aCAP-Seq). Methods DNA sample

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Erbilgin, Yucel, Ahmet Emre Eskazan, Ozden Hatirnaz Ng, et al. "Next-Generation Sequencing Of The BCR-ABL1 Kinase Domain May Be Beneficial In Decision Making Among Chronic Myeloid Leukemia Patients With Tyrosine Kinase Inhibitor Resistance." Blood 122, no. 21 (2013): 384. http://dx.doi.org/10.1182/blood.v122.21.384.384.

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Abstract Background and Aim BCR-ABL1 mutation testing is recommended for chronic myeloid leukemia (CML) patients who have suboptimal response and/or treatment failure with tyrosine kinase inhibitor (TKI) therapy. BCR-ABL1 mutations in the kinase domain (KD) of ABL1 account for at least 40-50% of all TKI resistant cases. Thus, detection of low-level mutations after development of resistance may offer critical information to guide subsequent therapy selection. The current gold standard for BCR-ABL1 mutation detection is Sanger sequencing (SS), which has an analytical sensitivity of approximately

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Deininger, Michael W., Jane F. Apperley, Christopher Kevin Arthur, et al. "Post Hoc Analysis of Responses to Ponatinib in Patients with Chronic-Phase Chronic Myeloid Leukemia (CP-CML) By Baseline BCR-ABL1 Level and Baseline Mutation Status in the Optic Trial." Blood 138, Supplement 1 (2021): 307. http://dx.doi.org/10.1182/blood-2021-145995.

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Abstract Introduction: Ponatinib is a third-generation, pan-inhibitory tyrosine kinase inhibitor (TKI) designed to potently inhibit BCR-ABL1 with or without any single resistance mutation, including T315I. Patients (pts) with resistant disease or with T315I BCR-ABL1 mutations respond inadequately to earlier-generation BCR-ABL1 TKIs, leading to poor survival outcomes. OPTIC (Optimizing Ponatinib Treatment in CP-CML, NCT02467270; ongoing) is a phase 2 trial evaluating the safety and efficacy of ponatinib in pts with CP-CML whose disease is resistant to 2 or more TKIs or who have a T315I mutation

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Porretto, Ferdinando. "Nilotinib early switch efficacy in non-optimal responder CML patient after first line imatinib treatment." Clinical Management Issues 5, no. 6S (2015): 11–16. http://dx.doi.org/10.7175/cmi.v5i6s.1133.

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We report a case of a patient with chronic myeloid leukemia in chronic phase who was treated with Imatinib as first line therapy. He showed a suboptimal response by 2006 ELN criteria after six months, for this reason we performed a mutational analysis that showed the mutation F486S. Due to this finding we made an early switch to Nilotinib (Nil); patients started Nil at 300 bid mg/day obtaining at six month a complete cytogenetic response (CCyR) and a MMolR (RQ-PCR ratio BCR-ABL1/ABL1%IS: 0.05). The patient is now on 24 months Nil treatment showing a RQ-PCR ratio BCR-ABL1/ABL1%IS: 0.004.

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Branford, Susan. "Molecular monitoring in chronic myeloid leukemia—how low can you go?" Hematology 2016, no. 1 (2016): 156–63. http://dx.doi.org/10.1182/asheducation-2016.1.156.

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Abstract Molecular monitoring of BCR-ABL1 transcripts for patients with chronic myeloid leukemia (CML) is now used to assess response to tyrosine kinase inhibitors (TKIs), including treatment failure that mandates a change of therapy. Therefore, many centers have adopted the molecular technique for measuring BCR-ABL1 and rely on conversion of values to the international reporting scale for appropriate clinical interpretation. However, the technique has a degree of inherent variability despite standardized procedures, which means care should be taken by the clinician when assessing response bas

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Catalano, Gianfranco, Pasquale Niscola, Cristina Banella, et al. "NPM1 MUTATED, BCR-ABL1 POSITIVE MYELOID NEOPLASMS: REVIEW OF LITERATURE." Mediterranean Journal of Hematology and Infectious Diseases 12, no. 1 (2020): e2020083. http://dx.doi.org/10.4084/mjhid.2020.083.

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Break point cluster region - Abelson (BCR-ABL1) chimeric protein and mutated Nucleophosmin (NPM1) are often present in hematological cancers, but they rarely coexist in the same disease. Both anomalies are considered founder mutations causing inhibition of differentiation and apoptosis, but BCR-ABL1 could act as a secondary mutation conferring a proliferative advantage to a pre-neoplastic clone. The 2016 World Health Organization (WHO) classification lists the provisional acute myeloid leukemia (AML) with BCR-ABL1, which must be diagnosed differentially from the rare blast phase (BP) onset of

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Soverini, Simona, Caterina De Benedittis, Claudia Venturi, et al. "Clinical Relevance of Low Burden BCR-ABL1 Mutations Detectable By Amplicon Deep Sequencing (DS) in Philadelphia-Positive (Ph+) Acute Lymphoblastic Leukemia (ALL) Patients (pts): The Type of Mutation Matters." Blood 126, no. 23 (2015): 2489. http://dx.doi.org/10.1182/blood.v126.23.2489.2489.

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Abstract Background and Aims- In Ph+ ALL pts treated with tyrosine kinase inhibitors (TKIs), the likelihood of acquiring TKI-insensitive mutations and the striking incidence of highly resistant T315I and compound mutants underscore the importance of BCR-ABL1 kinase domain (KD) sequence surveillance for timely and rational therapeutic reassessment. We used an amplicon DS strategy of the BCR-ABL1 KD to assess the following issues: i) whether DS allows earlier detection of emerging TKI-insensitive mutations in pts undergoing BCR-ABL1 KD mutation screening for minimal residual disease (MRD) persis

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Xiao, Hongli, Heng Wang, Jin Lou, Weihong Chen, Qiaoxia Zhang, and Xin Du. "Ultra-Deep Sequencing Leads to Earlier and More Sensitive Detection of Known or Novel Mutations of BCR-ABL1 in Chronic Myeloid Leukemia." Blood 132, Supplement 1 (2018): 5429. http://dx.doi.org/10.1182/blood-2018-99-113728.

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Abstract Detection of BCR-ABL1 mutations that inhibit tyrosine kinase inhibitors is important for the treatment of CML patients. Sanger sequencing (SS) technique is considered the gold standard for mutation detection in a clinical laboratory. We analyzed 40 clinical samples from 22 CML patients with TKI resistance by ultra-deep sequencing (UDS) and compared the results with classical SS-based tests. UDS facilitates the detection of low levels of mutations (<20% allele frequencies) that SS does not detect. In subgroups of cases with multiple mutations, UDS was also able to determine whether

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Ramachandran, Krishna C., Geetha Narayanan, Sreejith G. Nair, et al. "Isodicentric Philadelphia Chromosome: A Rare Chromosomal Aberration in Imatinib-Resistant Chronic Myelogenous Leukemia Patients - Case Report with Review of the Literature." Cytogenetic and Genome Research 150, no. 3-4 (2016): 273–80. http://dx.doi.org/10.1159/000458164.

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The BCR-ABL1 fusion gene derived from the Philadelphia chromosome, resulting from a classical translocation event t(9;22)(q34.13;q11.23), is responsible for the pathogenesis of chronic myeloid leukemia (CML) in more than 90% of the patients. The isoderivative chromosome 22, ider(22), and relative amplification or duplication of the BCR-ABL1 gene have been considered as one of the major reasons associated with the resistance to chemotherapy with imatinib mesylate, but the data remain unclear. GTG-banding together with FISH were performed to identify the presence of the ider(22) chromosome. Reve

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Hanan, A., J. Safdar, A. Khan, et al. "Myeloid neoplasm with concurrent BCR::ABL1 translocation, and JAK2 and SF3B1 co-mutations with severe fibrosis: a case report." American Journal of Clinical Pathology 162, Supplement_1 (2024): S88—S89. http://dx.doi.org/10.1093/ajcp/aqae129.197.

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Abstract Introduction/Objective Myeloproliferative neoplasms (MPNs) arise from hematopoietic stem cells with somatically altered tyrosine kinase signaling. Classification of MPNs is based on hematologic, histopathologic and molecular characteristics including the presence of BCR::ABL1 and JAK2 V617F. Methods/Case Report We present a 72-year-old male with a myeloid neoplasm and severe fibrosis, with concurrent BCR::ABL1 translocation, and co-mutations in JAK2 and SF3B1. Initially, the patient was diagnosed with anemia, thrombocytosis and folic acid deficiency and was prescribed supplemental fol

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Sanders, Mathijs A., Anikó Szabó, Carla Exalto, et al. "Extensive RAG-Mediated Rearrangements and Mutations in BCR-ABL1 and BCR-ABL1-like Adult Acute Lymphoblastic Leukemia." Blood 128, no. 22 (2016): 4067. http://dx.doi.org/10.1182/blood.v128.22.4067.4067.

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Abstract BCR-ABL1 and BCR-ABL1-like acute lymphoblastic leukemia (ALL) are two major pre-B cell acute leukemia subtypes characterized by genetic alterations affecting lymphoid-specific transcription factors. Studies examining the chain of genetic events necessary to develop leukemia established that the BCR-ABL1 fusion gene and kinase-activating BCR-ABL1-like lesions are initiating events, however, insufficient for leukemia development. Secondary genetic events targeting B cell development genes are therefore an essential requirement for overt ALL. A recent study (Papaemmanuil et al, Nat. Gene

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Shabih Haider, Asad Mahmood, Fahim AKhtar, Rafia Mahmood, Saadia Muzafar, and Maliha Batool. "BCR-ABL1 Gene Mutation in Acute Lymphoblastic Leukemia." Annals of PIMS-Shaheed Zulfiqar Ali Bhutto Medical University 18, no. 3 (2022): 181–85. http://dx.doi.org/10.48036/apims.v18i3.629.

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Objective: Determination of frequency of BCR-ABL1 gene mutation in Acute Lymphoblastic Leukemia. Methodology: This cross sectional study was carried out at the Department of Molecular Haematology, Armed Forces Institute of Pathology between January 2018 to March 2021. All newly diagnosed patients of Acute Lymphoblastic Leukemia were included in the study while patients already on treatment and with secondary leukemia were excluded from the study. Blood counts were done and various parameters such as total leukocyte count, hemoglobin, and platelet count were calculated. Results: 623 patients we

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Schneeweiss, Mathias A., Konstantin Byrgazov, Chantal B. Lucini, et al. "Hydroxyurea Induces Growth Inhibition in BCR-ABL1 T315I+ Clones and Synergizes with Ponatinib in Killing TKI-Resistant CML Cells." Blood 128, no. 22 (2016): 5425. http://dx.doi.org/10.1182/blood.v128.22.5425.5425.

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Abstract In chronic myeloid leukemia (CML), the occurrence of BCR-ABL1 T315I is associated with resistance against first- and second-generation BCR-ABL1 tyrosine kinase inhibitors (TKI). Ponatinib is a third generation TKI that exerts strong anti-neoplastic effects in advanced CML and is capable of suppressing the kinase activity of BCR-ABL1 T315I. However, therapy with ponatinib is associated with potentially severe side effects. In addition, resistance against ponatinib may develop in sub-clones carrying multiple (compound) mutations in BCR-ABL1. In addition, BCR-ABL1-independent oncogenic p

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Xue, Mengxing, Zhao Zeng, Qinrong Wang, et al. "Mutational Profiles during the Progression of Chronic Myeloid Leukemia." Blood 138, Supplement 1 (2021): 3596. http://dx.doi.org/10.1182/blood-2021-154273.

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Abstract Background: Despite significant improvements in the prognosis of chronic myeloid leukemia (CML) achieved by targeted therapy with tyrosine kinase inhibitors (TKIs), a small proportion of cases may not respond to TKIs or may relapse after an initial response, and then progress from chronic phase (CP) to blastic crisis (BC), characterized by a dismal prognosis. It remained uncertain whether the genetic lesions in addition to the BCR-ABL1 fusion could predict clinical outcomes of CML in the TKI era. Aim: To study the mutational profiles at each stage of CML and the prognostic significanc

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Marin, Anelis Maria, Denise Kusma Wosniaki, Heloisa Bruna Soligo Sanchuki, et al. "Molecular BCR::ABL1 Quantification and ABL1 Mutation Detection as Essential Tools for the Clinical Management of Chronic Myeloid Leukemia Patients: Results from a Brazilian Single-Center Study." International Journal of Molecular Sciences 24, no. 12 (2023): 10118. http://dx.doi.org/10.3390/ijms241210118.

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Chronic myeloid leukemia (CML) is a well-characterized oncological disease in which virtually all patients possess a translocation (9;22) that generates the tyrosine kinase BCR::ABL1 protein. This translocation represents one of the milestones in molecular oncology in terms of both diagnostic and prognostic evaluations. The molecular detection of the BCR::ABL1 transcription is a required factor for CML diagnosis, and its molecular quantification is essential for assessing treatment options and clinical approaches. In the CML molecular context, point mutations on the ABL1 gene are also a challe

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SOARE, Dan-Sebastian, Georgiana Elena ENE, Daniela DIACONESCU, et al. "Philadelphia chromosome positive de novo AML or blast phase CML?" Documenta Haematologica - Revista Romana de Hematologie 1, no. 1 (2023): 25–31. http://dx.doi.org/10.59854/dhrrh.2023.1.1.25.

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The BCR::ABL1 translocation and the accompanying Philadelphia chromosome represents the first mutation which defined a disease, chronic myeloid leukemia. It also represents the first druggable target for which a specific compound was developed and accepted in current clinic practice, imatinib. Despite these, there are still areas in which the diagnosis and the best treatment sequence still needs investigation. One such context is the diagnosis and management of BCR::ABL1 positive myeloid neoplasms with ≥20% blasts, more specifically the differentiation between myeloid blast phase chronic myelo

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