ABL1
- Known as:
- ABL1
- Catalog number:
- 000958A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ABL1
Ask about this productRelated genes to: ABL1
- Gene:
- ABL1 NIH gene
- Name:
- ABL proto-oncogene 1, non-receptor tyrosine kinase
- Previous symbol:
- ABL
- Synonyms:
- JTK7, c-ABL, p150
- Chromosome:
- 9q34.12
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: ABL1
Related articles to: ABL1
- Non-receptor Tyrosine kinase inhibitors (TKIs), such as ABL1 and JAK inhibitors, are central to the management of classical myeloproliferative neoplasms (MPNs), yet non-adherence remains frequent and is associated with poorer clinical outcomes. Although adherence-related factors have been explored, the evidence has not been systematically synthesised within a behavioural theory framework to guide the development of effective interventions. This review aims to synthesise evidence on modifiable determinants (barriers and facilitators) influencing adherence to TKI therapy in adults with classical MPNs, and to classify these determinants using the Theoretical Domains Framework (TDF) and Capability, Opportunity, Motivation-Behaviour (COM-B) model. - Source: PubMed
Publication date: 2026/09/18
Inouye Fabiana CoelhoTeo VivienClarke JessieGeorgopoulou SofiaFreato Gonçalves Ana Maria Rosade Figueiredo-Pontes Lorena LôboRégis Leira Pereira LeonardoChapman Sarah - To describe the impact of adding a tyrosine kinase inhibitor (TKI) to intensive chemotherapy (IC) on the outcome of de novo BCR::ABL1+ acute myeloid leukemia (AML), we retrospectively analyzed the data of 212 adult AML with ≥20% bone marrow blasts, BCR::ABL1+ or t(9;22)(q34.1;q11.2), no history of previous chronic myeloid leukemia and no prior exposure to BCR-ABL1 TKI. Eighty-nine patients were treated with IC alone and 123 with IC+TKI between 1999 and 2024. Complete remission (CR) or CR with incomplete hematologic recovery (CRi) was achieved in 52/77 patients (68%) with IC and 110/123 patients (89%) with IC+TKI (P<0.0001). With a median follow-up of 66.7 months, the median overall survival (OS) was 20.5 months with IC and not reached with IC+TKI. The 3-year and 5-year OS rates were 42.1% and 38.5% with IC and 70.9% and 62.9% with IC+TKI (P<0.0001) respectively. In multivariate analyses, the addition of TKI to IC was significantly and independently associated with an improved CR/CRi rate (odds ratio: 4.74 [95% confidence interval: 2.17-10.35]; P<0.001) and OS (hazard ratio: 0.40 [0.27-0.62]; P<0.001). Also, adding TKI to IC and alloHSCT in CR1 were independent prognostic factors for relapse-free survival (HR: 0.42; 95% CI: 0.23-0.75; P=0.004 and HR: 0.31; 95% CI: 0.17-0.55; P<0.0001). The outcome of de novo BCR::ABL1+ AML is strongly improved by the addition of a TKI to IC and should become the standard of care. The classification as adverse-risk should be reconsidered in the future ELN classification. - Source: PubMed
Publication date: 2026/09/18
Bertoli SarahLandberg NiklasBérard EmilieGondran CamilleLargeaud LaetitiaMansat-De Mas VéroniqueDumas Pierre-YvesPigneux ArnaudBidet AudreyGarciaz SylvainGabellier LudovicRoth Guepin GabrielleOrvain CorentinPeterlin PierreBirsen RudyAlexis MagdaCarré MartinTavernier EmmanuelleBoissard Simonet MarionHimberlin ChantalMaynadié MarcLaribi KamelMoluçon Chabrot CécileBelhabri AmineChraibi SamyCabrera QuentinLebon DelphineRaffoux EmmanuelCluzeau ThomasMicol Jean-BaptisteLeclerc MathieuBerthon CélineDombret HervéJuliusson GunnarRobelius AnnaLehmann SorenJädersten MartinVennström LovisaMontesinos PauBotella CarmenBergua Burgues Juan MiguelGarcia RaimundoSerrano JosefinaAmigo Maria LuzGarcía Ramirez PatriciaSossa-Melo Claudia LucíaAlonso-Domínguez Juan ManuelDöhner HartmutDöhner KonstanzeSpäth DanielaKühn Michael WmLengerke ClaudiaTischler Hans-JörgRöllig ChristophRuhnke LeoThiede ChristianBurchert AndreasServe HubertMüller-Tidow CarstenBaldus Claudia DVersluis JurjenValk Peter JmKristensen Daniel TuyetStidsholt Roug AnneMayer JiriKontro MikaEttala PiaLazarevic Vladimir LjRécher Christian - Therapeutic goals in BCR::ABL1-negative myeloproliferative neoplasms (MPNs) are evolving to include biologically anchored measures of disease modification with control of blood counts, splenomegaly, and symptoms. Disease modification endpoints and their linkage to survival in MPNs were central to the framework of MPN Asia 2026, which took place in Seoul. This review summarizes key themes from MPN Asia 2026 and relevant recent literature, examining the evolving roles of molecular response and long-term clinical benefits within a broader disease-modification framework across polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF). - Source: PubMed
Publication date: 2026/09/18
Abu-Zeinah GhaithHobbs Gabriela SRampal Raajit KLee Sung-EunGill HarinderKomrokji RamiTashi TsewangBose PrithvirajMascarenhas JohnYacoub AbdulraheemOh Stephen TShimoda KazuyaReeves Brandi NDuan MinghuiYu Lennex Hsueh-LinQin AlbertPrchal Josef TKaushansky KennethMesa Ruben A - A series of novel pyrimidine-based acetamide derivatives (5a-5j) containing various cyclic amine substituents were designed, synthesized, and structurally characterized to identify new lead compounds with dual antiproliferative and antimicrobial activities. The synthesized compounds were evaluated for antiproliferative activity against K562 human chronic myeloid leukemia, MCF-7 human breast adenocarcinoma, and HeLa human cervical carcinoma cell lines, while selectivity toward BJ fibroblasts was assessed. Antimicrobial activity was investigated against representative Gram-positive, Gram-negative, and fungal pathogens. Among the synthesized derivatives, compound 5h exhibited the highest antiproliferative activity with IC values of 6.39 ± 0.61, 10.34 ± 0.83, and 8.90 ± 0.71 μM against K562, MCF-7, and HeLa cells, respectively, while demonstrating comparatively lower cytotoxicity toward BJ cells. Compound 5h also displayed the most potent antibacterial activity against Escherichia coli (MBC = 25 μg/mL) and Pseudomonas aeruginosa (MBC = 50 μg/mL), together with promising antifungal activity. Structure-activity relationship analysis revealed that appropriately substituted aromatic cyclic amines significantly improved biological activity. Molecular docking against ABL1 kinase (PDB ID: 3PYY), together with DFT and ADME studies, supported the experimental findings. These results identify pyrimidine-based acetamide derivatives as promising multifunctional scaffolds for developing novel anticancer and antimicrobial agents. - Source: PubMed
Thakor VishwaPatel PratikPatel MeghaPatel BhavinPatel TarunPatel Paresh - Single-cell RNA-sequencing-based characterization of cells that belong to the neoplastic clone is a major challenge in hematologic neoplasms, where malignant and normal cells coexist. Confident molecular profiling requires simultaneous analysis of gene expression and genetic mutations in individual cells, an ability that is not supported by the standard 10X Genomics workflow. Here, we systematically evaluated the potential and limitations of repurposing amplified cDNA generated during the 10X Genomics 3' workflow for post hoc genotyping of individual cells. We first established a mixed leukemic cell line system comprising one cell line with KIT point mutations and another with the BCR::ABL1 fusion gene. Targeted long-read PacBio sequencing enabled post hoc assignment of mutation data to transcriptionally profiled cells, but recovery differed between targets. Consistent with ambient RNA in microfluidics-based single-cell workflows, mutation-associated transcripts were detected in cells not expected to carry the corresponding mutations, illustrating how transcript recovery complicates cell-level genotype assignment. Target-specific thresholds mitigated this source of misclassification. In primary chronic myeloid leukemia samples, the post hoc approach detected BCR::ABL1-positive cells at diagnosis, but not during imatinib treatment. Together, we present a framework for adding mutation status to cells already profiled using the 10X Genomics workflow and highlight broader considerations for transcript-based single-cell genotyping. - Source: PubMed
Publication date: 2026/09/17
Papavasileiou SofiaWu ChenyanBoey DarylMargerie LucilleMo JiezhenOlsson-Strömberg UllaSöderlund StinaNilsson GunnarDahlin Joakim S