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GENE:

ABL1 (ABL proto-oncogene 1)

i
Other names: ABL proto-oncogene 1, ABL, c-ABL, JTK7, p150, ABL1
1d
ASC4KIDS: Study to Determine the Dose and Safety of Asciminib in Pediatric Patients With Chronic Myeloid Leukemia (clinicaltrials.gov)
P1/2, N=34, Recruiting, Novartis Pharmaceuticals | Trial completion date: Jan 2031 --> Nov 2031
Trial completion date
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
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Scemblix (asciminib)
2d
The initial molecular response predicts the deep molecular response but not treatment-free remission maintenance in a real-world chronic myeloid leukemia cohort. (PubMed, Haematologica)
We obtained similar results when patients were divided in subgroups by first-line treatment (imatinib vs second generation TKI, 2G-TKI)...In conclusion, this first comparative study of early therapeutic response parameters showed that they are excellent indicators of TKI efficacy (BCR::ABL1 transcript reduction) and best responders. Conversely, they did not predict the achievement of the TKI discontinuation criteria and TFR maintenance, suggesting that other parameters are involved in TFR maintenance.
Journal • Real-world evidence • Real-world
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ABL1 (ABL proto-oncogene 1)
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imatinib
4d
Multilineage involvement in KMT2A-rearranged B acute lymphoblastic leukaemia: cell-of-origin, biology, and clinical implications. (PubMed, Histopathology)
In summary, multilineage involvement is common in both BCR::ABL1-rearranged and KMT2A-rearranged B-ALL, which should be taken into consideration when interpreting the disease burden during the clinical course.
Journal
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ABL1 (ABL proto-oncogene 1) • KMT2A (Lysine Methyltransferase 2A)
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MLL rearrangement • ABL1 fusion
6d
Asciminib for third-line treatment of chronic myeloid leukemia: Cost-effectiveness analysis based on treatment-free remission approach. (PubMed, Farm Hosp)
Asciminib broadens therapeutic choices for patient's refractory or intolerant to 2 prior lines of treatment in a cost-effectiveness manner. The costs of drugs significantly impact the overall cost of the disease, emphasizing the importance of the selected discount rates for each drug. Given the relatively low incidence of CML, the introduction of asciminib has a limited budgetary impact, warranting individualized decisions based on patient`s clinical characteristics.
Journal • HEOR • Cost-effectiveness • Cost effectiveness
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
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BCR-ABL1 fusion
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imatinib • Iclusig (ponatinib) • Bosulif (bosutinib) • Scemblix (asciminib)
7d
Identification of Ureidocoumarin-Based Selective Discoidin Domain Receptor 1 (DDR1) Inhibitors via Drug Repurposing Approach, Biological Evaluation, and In Silico Studies. (PubMed, Pharmaceuticals (Basel))
Molecular docking and MD simulations disclosed the putative binding mode of this coumarin chemotype and provided insights for further optimization of this scaffold. The present findings collectively supported the potential improvement of ureidocoumarins 3i and 3q for cancer treatment.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • DDR2 (Discoidin domain receptor 2)
7d
Ponatinib Induces a Procoagulant Phenotype in Human Coronary Endothelial Cells via Inducing Apoptosis. (PubMed, Pharmaceutics)
In addition, these changes were associated with an increased ratio of Bax and Bcl-xL proteins in the presence of the decreased THBD mRNA level. Overall, ponatinib enhances the procoagulant activity of ECs via inducing apoptosis, which may contribute to thrombotic events.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • BCL2L1 (BCL2-like 1) • VCAM1 (Vascular Cell Adhesion Molecule 1)
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Iclusig (ponatinib)
7d
ADAMTS13, von Willebrand Factor, Platelet Microparticles, Factor VIII, and Impact of Somatic Mutations in the Pathogenesis of Splanchnic Vein Thrombosis Associated with BCR-ABL-Negative Myeloproliferative Neoplasms. (PubMed, Life (Basel))
The significant increase in circulating MV, VWF, and FVIII:C in the MPN patients and in the patients with thrombosis supports the role of endothelium damage in promoting thrombotic events. In particular, a significant increase in VWF and FVIII:C levels was found in the MPN patients with SVT.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • JAK2 (Janus kinase 2) • CALR (Calreticulin)
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JAK2 V617F • JAK2 mutation
7d
Oxidative Stress and Chronic Myeloid Leukemia: A Balance between ROS-Mediated Pro- and Anti-Apoptotic Effects of Tyrosine Kinase Inhibitors. (PubMed, Antioxidants (Basel))
The ideal environment for tyrosine kinase inhibitor therapy is produced by a favorable oxidative status. We discuss the latest studies that aim to manipulate the redox system to alter the apoptosis of cancerous cells.
Review • Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
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fenretinide nanoparticle (ST-001 nanoFenretinide)
7d
Variable characteristics overlooked in human K-562 leukemia cell lines with a common signature. (PubMed, Sci Rep)
Furthermore, our data could serve as a reference for evaluating other K-562 sublines, facilitating the discovery of new K-562 sublines with distinct characteristics. This approach results in the accumulation of K-562 sublines with diverged characteristics and expands the options available, which may help in selecting the most suitable K-562 subline for each experiment.
Preclinical • Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
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BCR-ABL1 fusion
8d
High Level of CD8+PD-1+ Cells in Patients with Chronic Myeloid Leukemia Who Experienced Loss of MMR after Imatinib Discontinuation. (PubMed, Cells)
Interestingly, at 3 months of TFR, patients with the e13a2 transcript had a significantly higher proportion of the PD-1-expressing immune cells compared to patients with the e14a2. Our results suggest the important involvement of CD8+PD-1+ cells in the success of TFR and may help in identifying a group of patients who could successfully discontinue imatinib.
Journal • PD(L)-1 Biomarker • IO biomarker
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ABL1 (ABL proto-oncogene 1) • CD8 (cluster of differentiation 8) • PD-1 (Programmed cell death 1)
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PD-1 expression
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imatinib
8d
Journal
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TP53 (Tumor protein P53) • ABL1 (ABL proto-oncogene 1) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • JAK2 (Janus kinase 2) • RUNX1 (RUNX Family Transcription Factor 1) • ASXL1 (ASXL Transcriptional Regulator 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • SETBP1 (SET Binding Protein 1) • CALR (Calreticulin)
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TP53 mutation • DNMT3A mutation • ASXL1 mutation • TET2 mutation • SRSF2 mutation • U2AF1 mutation
9d
Mutation analysis of BCR-ABL1 kinase domain in chronic myeloid leukemia patients with tyrosine kinase inhibitors resistance: a Malaysian cohort study. (PubMed, BMC Res Notes)
Additionally, the use of NGS is advised for accurately determining the mutation status of BCR::ABL1 KD, particularly in cases where the allele frequency is low, and for identifying mutations across multiple exons simultaneously. Therefore, the utilization of NGS as a diagnostic platform for this test is very promising to guide therapeutic decision-making.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
10d
Trial initiation date
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ABL1 (ABL proto-oncogene 1) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • PDGFRA (Platelet Derived Growth Factor Receptor Alpha) • CD19 (CD19 Molecule) • PDGFRB (Platelet Derived Growth Factor Receptor Beta) • CSF1R (Colony stimulating factor 1 receptor)
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CD19 expression
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TruSight RNA Pan-Cancer Panel
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dasatinib • imatinib • cytarabine • doxorubicin hydrochloride • cyclophosphamide • Blincyto (blinatumomab) • methotrexate • vincristine • daunorubicin • leucovorin calcium • Oncaspar liquid (pegaspargase) • mercaptopurine • Asparlas (calaspargase pegol-mknl) • thioguanine • Starasid (cytarabine ocfosfate)
11d
Exploring hematological alterations and genetics linked to SNV rs10974944 in myeloproliferative neoplasms among Amazon patients. (PubMed, Sci Rep)
Associations were observed between rs10974944 and the JAK2 V617F, in which the G allele (OR 3.4; p < 0.0001) and GG genotype (OR 4.9; p = 0.0016) were associated with JAK2 V617F + and an increase in variant allele frequency (GG: OR 15.8; p =  < 0.0001; G: OR 6.0; p = 0.0002). These results suggest an association between rs10974944 (G) and a status for JAK2 V617F, JAK2 V617F + _VAF ≥ 50%, and laboratory alterations in the erythroid lineage.
Journal
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ABL1 (ABL proto-oncogene 1) • JAK2 (Janus kinase 2)
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JAK2 V617F
11d
Integrated drug profiling and CRISPR screening identify BCR::ABL1-independent vulnerabilities in chronic myeloid leukemia. (PubMed, Cell Rep Med)
We employ genome-wide CRISPR-Cas9 screening for six drugs, and mediator complex, apoptosis, and erythroid-lineage-related genes are identified as key resistance hits for TKIs, whereas the Wee1 inhibitor AZD1775 and mepacrine exhibit distinct resistance profiles. KCTD5, a consistent TKI-resistance-conferring gene, is found to mediate TKI-induced BCR::ABL1 ubiquitination. In summary, we delineate potential mechanisms for primary TKI resistance and non-BCR::ABL1-targeting drugs, offering insights for optimizing CML treatment.
Journal
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ABL1 (ABL proto-oncogene 1) • CD34 (CD34 molecule)
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adavosertib (AZD1775)
11d
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
11d
Kinase activities in pancreatic ductal adenocarcinoma with prognostic and therapeutic avenues. (PubMed, Mol Oncol)
Subtype-associated activity profiles can guide therapeutic combination approaches in tumor and stroma-enriched tissues, and emphasize the critical role of parallel signaling pathways. In addition, kinase activity profiling identifies potential disease markers with prognostic significance.
Journal
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EGFR (Epidermal growth factor receptor) • ABL1 (ABL proto-oncogene 1) • CDK7 (Cyclin Dependent Kinase 7) • IR (Insulin receptor) • PAK2 (P21 (RAC1) Activated Kinase 2) • MYLK (Myosin Light Chain Kinase) • PTK6 (Protein Tyrosine Kinase 6)
12d
Chronic neutrophilic leukemia and atypical chronic myeloid leukemia: 2024 update on diagnosis, genetics, risk stratification, and management. (PubMed, Am J Hematol)
Most commonly used agents include hydroxyurea, interferon, Janus kinase inhibitors, and hypomethylating agents, though none are disease-modifying. Actionable mutations (NRAS/KRAS, ETNK1) have also been identified, supporting novel agents targeting involved pathways. Preclinical and clinical studies evaluating new drugs (e.g., fedratinib, phase 2) and combinations are detailed.
Review • Journal
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KRAS (KRAS proto-oncogene GTPase) • ABL1 (ABL proto-oncogene 1) • NRAS (Neuroblastoma RAS viral oncogene homolog) • ASXL1 (ASXL Transcriptional Regulator 1) • TET2 (Tet Methylcytosine Dioxygenase 2) • SRSF2 (Serine and arginine rich splicing factor 2) • CSF3R (Colony Stimulating Factor 3 Receptor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • SETBP1 (SET Binding Protein 1) • ETNK1 (Ethanolamine Kinase 1)
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KRAS mutation • NRAS mutation • ASXL1 mutation • TET2 mutation • EZH2 mutation • SRSF2 mutation • U2AF1 mutation • CSF3R T618I • CSF3R mutation • ETNK1 mutation
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hydroxyurea • Inrebic (fedratinib)
13d
BCR::ABL1 Kinase N-lobe Mutants Confer Moderate to High Degrees of Resistance to Asciminib. (PubMed, Blood)
Molecular dynamics simulations of the M244V substitution implicate stabilization of an active kinase conformation through impact on the -C helix as a mechanism of resistance. These N-lobe mutations may compromise the clinical activity of ongoing combination studies of asciminib with ATP-competitive TKIs.
Journal
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ABL1 (ABL proto-oncogene 1)
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Scemblix (asciminib)
16d
IKZF1PLUS alterations contribute to outcome disparities in Hispanic/Latino children with B-lymphoblastic leukemia. (PubMed, Pediatr Blood Cancer)
Our study shows enrichment of high-risk genetic variants in H/L B-ALL and raises consideration for novel therapeutic targets.
Journal
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ABL1 (ABL proto-oncogene 1) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • RUNX1 (RUNX Family Transcription Factor 1) • ETV6 (ETS Variant Transcription Factor 6) • CRLF2 (Cytokine Receptor Like Factor 2) • IKZF1 (IKAROS Family Zinc Finger 1) • CDKN2B (Cyclin Dependent Kinase Inhibitor 2B) • P2RY8 (P2Y Receptor Family Member 8) • DUX4 (Double Homeobox 4)
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CDKN2A deletion • IKZF1 deletion • CRLF2 rearrangement
16d
Does presence of complex translocations involving BCR::ABL1 in chronic myeloid leukemia affect the response rate to tyrosine kinase inhibitors? A systematic review of the literature. (PubMed, Ann Diagn Pathol)
Based on the inclusion criteria, a total of 15 studies were included from which a total of 87 cases were covered. Overall, we identified 38 unique complex three- and four-way translocations across 87 Ph-positive cases and found that 85 patients with complex Ph-positive cytogenetics achieved complete remission upon treatment and did not appear to have a lesser response to TKI therapy.
Review • Journal
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ABL1 (ABL proto-oncogene 1)
16d
Allogeneic hematopoietic cell transplantation for acute myeloid leukemia with BCR::ABL1 fusion. (PubMed, EJHaem)
In conclusion, our results suggest that pre-transplant TKI could improve disease status before allo-HCT. Moreover, allo-HCT resulted in high OS, high LFS, low relapse, and low NRM rates in patients with AML with BCR::ABL1.
Journal
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ABL1 (ABL proto-oncogene 1)
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ABL1 fusion
16d
Inotuzumab Ozogamicin and Frontline Chemotherapy in Treating Young Adults With Newly Diagnosed B Acute Lymphoblastic Leukemia (clinicaltrials.gov)
P3, N=310, Suspended, Alliance for Clinical Trials in Oncology | Trial completion date: Aug 2024 --> Aug 2025 | Trial primary completion date: Mar 2024 --> Mar 2025
Trial completion date • Trial primary completion date
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • CD20 (Membrane Spanning 4-Domains A1) • CD22 (CD22 Molecule) • ITGB1 (Integrin Subunit Beta 1)
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CD20 positive • CD22 positive
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Rituxan (rituximab) • cytarabine • doxorubicin hydrochloride • cyclophosphamide • Besponsa (inotuzumab ozogamicin) • vincristine • daunorubicin • Oncaspar liquid (pegaspargase) • mercaptopurine • thioguanine
17d
FL118 Is a Potent Therapeutic Agent against Chronic Myeloid Leukemia Resistant to BCR-ABL Inhibitors through Targeting RNA Helicase DDX5. (PubMed, Int J Mol Sci)
Furthermore, FL118 potently induced apoptosis not only in Ba/F3 cells expressing BCR-ABL, but also in those expressing the BCR-ABL T315I mutant, which is resistant to BCR-ABL inhibitors. Collectively, these results revealed that DDX5 is a critical therapeutic target in CML and that FL118 is an effective candidate compound for the treatment of BCR-ABL inhibitor-resistant CML.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • BIRC5 (Baculoviral IAP repeat containing 5) • CASP3 (Caspase 3) • DDX5 (DEAD-Box Helicase 5)
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BIRC5 expression • BCR expression
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FL118
18d
Unveiling IL6R and MYC as Targeting Biomarkers in Imatinib-Resistant Chronic Myeloid Leukemia through Advanced Non-Invasive Apoptosis Detection Sensor Version 2 Detection. (PubMed, Cells)
This study contributes to understanding the mechanisms of Imatinib resistance in CML, proposing IL6R and MYC as pivotal targets for therapeutic strategies. Moreover, the utilization of NIADS v2 enhances our capability to analyze apoptosis and drug responses, contributing to a deeper understanding of CML pathogenesis and treatment options.
Journal • Metastases
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ABL1 (ABL proto-oncogene 1) • IL7R (Interleukin 7 Receptor) • IL6R (Interleukin 6 receptor)
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MYC expression • IL7R expression
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imatinib
20d
What is new in acute myeloid leukemia classification? (PubMed, Blood Res)
AML cases defined by differentiation (WHO2022) and AML not otherwise specified (ICC) are categorized as lacking specific defining genetic abnormalities, WHO2022 labels this as a myeloid neoplasm post cytotoxic therapy (MN-pCT), described as an appendix after specific diagnosis. Similarly, in ICC, it can be described as "therapy-related", without a separate AML category.
Review • Journal
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TP53 (Tumor protein P53) • ABL1 (ABL proto-oncogene 1) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • STAG2 (Stromal Antigen 2) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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TP53 mutation • U2AF1 mutation • CEBPA mutation
21d
A novel fluorescent probe based imprinted polymer-coated magnetite for the detection of imatinib leukemia anti-cancer drug traces in human plasma samples. (PubMed, Spectrochim Acta A Mol Biomol Spectrosc)
Owing to these merits, the proposed fluorescence sensor was utilized to detect IMB in drug tablets and human plasma, and satisfactory results (99.3-100.4 %) were obtained. Thus, the synthesized fluorescence sensor is a promising platform for IMB sensing in various applications.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
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imatinib
21d
Asciminib Maintains Antibody-Dependent Cellular Cytotoxicity against Leukemic Blasts. (PubMed, Cancers (Basel))
The introduction of rituximab has improved the outcomes in CD20 positive cases. Other monoclonal antibodies, such as tafasitamab (anti-CD19), obinutuzumab (anti-CD20) and epratuzumab (anti-CD22) have been tested in trials (NCT05366218, NCT04920968, NCT00098839)...In contrast to ATP site inhibitors such as dasatinib and ponatinib, the novel first-in-class selective allosteric ABL myristoyl pocket (STAMP) inhibitor asciminib did not significantly impact ADCC in our settings. Our results suggest that asciminib should be considered in clinical trials.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
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BCR-ABL1 fusion • CD20 positive
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dasatinib • Rituxan (rituximab) • Iclusig (ponatinib) • Gazyva (obinutuzumab) • Scemblix (asciminib) • Monjuvi (tafasitamab-cxix) • Epratucyn (epratuzumab)
22d
The molecular basis of Abelson kinase regulation by its αI-helix. (PubMed, Elife)
It was recently established that binding of type II ATP site inhibitors, such as imatinib, generates a force from the KD N-lobe onto the SH3 domain and in consequence disassembles the core. In contrast, the allosteric inhibitor asciminib strongly reduces Abl's activity by fixating the αI-helix and reducing the force onto the SH2 domain. These observations are explained by a simple mechanical model of Abl activation involving forces from the KD N-lobe and the αI-helix onto the KD/SH2SH3 interface.
Journal
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ABL1 (ABL proto-oncogene 1)
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imatinib • Scemblix (asciminib)
22d
Journal
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TP53 (Tumor protein P53) • ABL1 (ABL proto-oncogene 1) • KMT2A (Lysine Methyltransferase 2A)
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MLL rearrangement
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Besponsa (inotuzumab ozogamicin)
23d
Chronic myeloid leukaemia: Biology and therapy. (PubMed, Blood Rev)
Which TKI is the best initial therapy for which persons and what depth and duration of molecular remission is needed to achieve TFR are controversial. In this review we discuss these issues and suggest future research directions.
Review • Journal
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ABL1 (ABL proto-oncogene 1)
23d
CCN2/CTGF expression does not correlate with fibrosis in myeloproliferative neoplasms, consistent with noncanonical TGF-β signaling driving myelofibrosis. (PubMed, Virchows Arch)
Remarkably, CCN2 expression did not correlate with fibrosis or other disease parameters such as platelet count or thrombovascular events, neither in this subgroup nor in the whole study group. This suggests that in BM of MPN patients other, CCN2-independent pathways (such as noncanonical TGF-β signaling) may be more important for the development of fibrosis.
Journal
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ABL1 (ABL proto-oncogene 1) • TGFB1 (Transforming Growth Factor Beta 1) • CTGF (Connective tissue growth factor)
23d
Myeloid neoplasms in inflammatory bowel disease: A case series and review of the literature. (PubMed, Leuk Res Rep)
No IBD characteristic was found to associate with MN disease severity, including the previously-identified association between MNs and thiopurine exposure. Of the somatic mutations identified in out cohort's MN, mutations in TET2 were most prevalent, followed by FLT3-ITD, BCR-ABL, and NPM1 mutations.
Review • Journal
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FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • NPM1 (Nucleophosmin 1) • TET2 (Tet Methylcytosine Dioxygenase 2)
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FLT3-ITD mutation • NPM1 mutation • TET2 mutation
24d
A review of immunotargeted therapy for Philadelphia chromosome positive acute lymphoblastic leukaemia: making progress in chemotherapy-free regimens. (PubMed, Hematology)
Since 2000, targeted therapy combined with chemotherapy, represented by the tyrosine kinase inhibitor Imatinib, has become the first-line treatment for PH + ALL...More recently, some innovative immune-targeted therapy greatly improved the prognosis of PH + ALL, such as Blinatumomab and Inotuzumab Ozogamicin...These new therapeutic interventions are changing the treatment landscape for PH + ALL. In summary, this review discusses the current advancements in targeted therapeutic agents shift in the treatment strategy of PH + ALL towards using more tolerable chemotherapy-free induction and consolidation regimens confers better disease outcomes and might obviate the need for HSCT.
Review • Journal • IO biomarker
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ABL1 (ABL proto-oncogene 1)
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imatinib • Blincyto (blinatumomab) • Besponsa (inotuzumab ozogamicin)
24d
Chronic myeloproliferative neoplasms with concomitant CALR mutation and BCR::ABL1 translocation: diagnostic and therapeutic implications of a rare hybrid disease. (PubMed, Front Cell Dev Biol)
The presence of BCR::ABL1 translocation with a coexisting CALR mutation is even more uncommon. Herein, starting from a routinely diagnosed case of CALR-mutated primary myelofibrosis subsequently acquiring BCR::ABL1 translocation, we performed a comprehensive review of the literature, discussing the clinicopathologic and molecular features, as well as the outcome and treatment of cases with BCR::ABL1 and CALR co-occurrence.
Review • Journal
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ABL1 (ABL proto-oncogene 1) • JAK2 (Janus kinase 2) • CALR (Calreticulin)
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JAK2 mutation • CALR mutation
25d
Real-world data of cardio-oncologic interventions for cardiovascular adverse events with oral oncolytics. (PubMed, Cardiooncology)
Pre-existing CVD or CV risk factors predispose oncology patients to CV adverse events. Real-world practice reveals that CV adverse events require temporary interruption of treatment and initiation of pharmacologic treatment. A multidisciplinary, patient-centered approach that includes discussion of risks/benefits of treatment continuation, and initiation of guideline-directed treatment is recommended until high-quality, drug-specific data for monitoring and treatment become available.
Journal • Adverse events • Real-world evidence • Real-world
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase)
25d
Ponatinib and STAT5 Inhibitor Pimozide Combined Synergistic Treatment Applications Potentially Overcome Drug Resistance via Regulating the Cytokine Expressional Network in Chronic Myeloid Leukemia Cells. (PubMed, J Interferon Cytokine Res)
Therefore, pimozide could be a promising agent to support TKI therapies in ponatinib resistance. This research would help to clarify the role of cytokines in ponatinib resistance and advance the development of new therapeutics to utilize the STAT5 inhibitor pimozide in combination with TKIs.
Journal
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ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • IFNG (Interferon, gamma) • IL6 (Interleukin 6) • CXCL8 (Chemokine (C-X-C motif) ligand 8) • IL2 (Interleukin 2) • IL10 (Interleukin 10) • IL18 (Interleukin 18) • IL1A (Interleukin 1, alpha) • IL15 (Interleukin 15) • STAT5A (Signal Transducer And Activator Of Transcription 5A)
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Iclusig (ponatinib)
25d
Journal
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ABL1 (ABL proto-oncogene 1) • ITGA6 (Integrin, alpha 6) • ITGB1 (Integrin Subunit Beta 1) • ITGB4 (Integrin Subunit Beta 4)
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ABL1 T315I
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imatinib
25d
Combination of dasatinib and venetoclax in newly diagnosed chronic phase chronic myeloid leukemia. (PubMed, Cancer)
Treatment with dasatinib and venetoclax was safe and effective in CML-CP. The cumulative response rates with the combination were similar to those with single-agent dasatinib. Further follow-up is needed to evaluate the rates of durable deep molecular response and treatment-free remission.
Journal
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ABL1 (ABL proto-oncogene 1) • BCL2 (B-cell CLL/lymphoma 2)
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Venclexta (venetoclax) • dasatinib
26d
Pemigatinib After Chemotherapy for the Treatment of Newly Diagnosed Acute Myeloid Leukemia (clinicaltrials.gov)
P1, N=32, Recruiting, OHSU Knight Cancer Institute | Trial completion date: Aug 2024 --> Feb 2026 | Trial primary completion date: Feb 2024 --> Aug 2025
Trial completion date • Trial primary completion date
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TP53 (Tumor protein P53) • FLT3 (Fms-related tyrosine kinase 3) • ABL1 (ABL proto-oncogene 1) • BCR (BCR Activator Of RhoGEF And GTPase) • EZH2 (Enhancer of zeste 2 polycomb repressive complex 2 subunit) • RUNX1 (RUNX Family Transcription Factor 1) • SF3B1 (Splicing Factor 3b Subunit 1) • ASXL1 (ASXL Transcriptional Regulator 1) • KMT2A (Lysine Methyltransferase 2A) • SRSF2 (Serine and arginine rich splicing factor 2) • BCOR (BCL6 Corepressor) • U2AF1 (U2 Small Nuclear RNA Auxiliary Factor 1) • STAG2 (Stromal Antigen 2) • MECOM (MDS1 And EVI1 Complex Locus) • NUP214 (Nucleoporin 214) • GATA2 (GATA Binding Protein 2) • MLLT3 (MLLT3 Super Elongation Complex Subunit) • CDKN1A (Cyclin-dependent kinase inhibitor 1A) • DEK (DEK Proto-Oncogene) • ZRSR2 (Zinc Finger CCCH-Type, RNA Binding Motif And Serine/Arginine Rich 2)
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TP53 mutation • FLT3 mutation • RUNX1 mutation • ASXL1 mutation • EZH2 mutation • MLL rearrangement • SRSF2 mutation • U2AF1 mutation • BCOR mutation • Chr del(5q) • STAG2 mutation • FLT3 wild-type • Chr t(9;11) • ZRSR2 mutation
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cytarabine • Pemazyre (pemigatinib) • daunorubicin • Starasid (cytarabine ocfosfate)
26d
The molecular signature of BCR::ABLP210 and BCR::ABLT315I in a Drosophila melanogaster chronic myeloid leukemia model. (PubMed, iScience)
We identified six genes that were consistently upregulated in the fly CML model and validated in adult and pediatric CML patients and in a mouse cell line expressing BCR::ABL1T315I. This study provides a comprehensive analysis of gene signatures in BCR::ABL1p210 and BCR::ABL1T315I, laying the groundwork for targeted investigations into the role of these genes in CML pathogenesis.
Journal
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ABL1 (ABL proto-oncogene 1)
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BCR-ABL1 T315I • ABL1 T315I • BCR expression