ABL1 (phospho-Tyr204) Antibody
- Known as:
- ABL1 (phosphorilated-Tyr204) Antibody
- Catalog number:
- abx000093
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- ABL1 (phospho-Tyr204) Antibody
Ask about this productRelated genes to: ABL1 (phospho-Tyr204) Antibody
- 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 (phospho-Tyr204) Antibody
Related articles to: ABL1 (phospho-Tyr204) Antibody
- Philadelphia chromosome (Ph)-positive acute lymphoblastic leukemia (ALL), the most common subtype of adult ALL, has undergone dramatic transformation in prognosis over the past two decades. Introduction of tyrosine kinase inhibitors (TKIs) targeting BCR::ABL1 fusion protein has revolutionized frontline therapy, with successive generations of TKIs-from imatinib to dasatinib and most recently ponatinib-achieving progressively deeper and more durable molecular responses. Concurrently, the integration of immunotherapy, particularly blinatumomab, has enabled chemotherapy-sparing approaches further improving tolerability and efficacy. These advances have fundamentally challenged the historical paradigm that allogeneic hematopoietic cell transplantation (HCT) is indispensable for all Ph+ ALL patients in first complete remission. The role of allogeneic HCT is often debated and increasingly individualized, guided by measurable residual disease (MRD) assessment, TKI generation, depth and duration of molecular response, and patient-specific factors. Emerging data suggest that a subset of patients achieving early, deep MRD negativity with TKIs and immunotherapy may achieve durable remissions without transplant, though long-term follow-up remains limited. For patients proceeding to allogeneic HCT, optimization of transplant strategy-including donor selection, conditioning intensity, graft-versus-host disease prophylaxis, and posttransplant TKI maintenance-is critical to maximize graft-versus-leukemia effects while minimizing toxicity. Treatment-free remission strategies following prolonged TKI maintenance in non-transplant patients, and the integration of chimeric antigen receptor (CAR) T-cell therapy as bridge, consolidation, or salvage, represent emerging frontiers. This review critically examines the contemporary role of allogeneic HCT in Ph+ ALL and provides a framework for transplant decision-making in the contemporary era of targeted and cellular immunotherapy. - Source: PubMed
Publication date: 2026/04/15
Pasic IvanLipton Jeffrey H - Chronic myeloid leukemia (CML) often presents with hematologic findings that overlap with reactive leukocytosis and other myeloproliferative neoplasms (MPNs), creating diagnostic uncertainty that may delay targeted therapy or prompt unnecessary molecular testing. Harlequin cells-abnormal eosinophils containing basophilic granules-are well described in acute myeloid leukemia (AML) with fusion, but their diagnostic relevance in CML has not been systematically assessed. - Source: PubMed
Publication date: 2026/04/06
Cai JenniferYue ChangjunTomassetti Sarah - We report a 65-year-old man with D835V-mutated acute myeloid leukemia (AML) and -positive chronic myeloid leukemia (CML) that coexisted as genetically independent clones. Cytogenetic and targeted sequencing analyses demonstrated that the AML and CML clones coexisted as distinct entities. During treatment with gilteritinib, the AML blasts regressed, and then the CML clone expanded. Subsequently, the CML burden declined as the AML clone regrew. This case highlights the importance of accurately assessing clonal changes using genetic analysis when implementing molecular targeted therapy for hematologic malignancies. - Source: PubMed
Publication date: 2026/04/13
Osone KaiKatagiri SeiichiroChi SungGiMinami YosukeGotoh AkihikoAkahane Daigo - While epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) are a cornerstone of therapy for advanced -mutant non-small cell lung cancer (NSCLC), resistance remains a major clinical challenge. The genomic landscape of early-stage (ES) -mutant NSCLC and its evolution to advanced-stage (AS) disease is not fully understood. This study aimed to characterize the molecular disparities between ES and AS -mutant NSCLC and to identify genomic alterations associated with EGFR-TKI treatment outcomes. - Source: PubMed
Publication date: 2026/02/26
Yoon DayoungLee Ji WonCho Byoung ChulKang Eun JooKim Jung SunLim TaekyuYi Seong YoonKim Yu JungAhn Mi SunKim Young SaingPark Ji HyunLim SeungtaekPark Hyung SoonCho Jang HoJang ByunghyunLee Ji YoonKim JiwonHong JisooKoo HarimChung SeokShin Sang WonKim Yeul HongSa Jason KChoi Yoon Ji - Cell-specific detection of aberrant mRNA in blood is essential for diagnosing and treating hematological malignancies. However, current sensors are unable to function in unprocessed whole blood due to limitations in chemical stability and cell-targeting capability. Here, we engineer a cell-resolved ultrastable sensor for hematology (CRUSH) via spherical-nucleic-acid (SNA) technology, which enables live-cell detection of leukemia fusion transcripts in unprocessed whole blood. CRUSH employs stoichiometrically controlled thiol protector to achieve a defect-free thiol monolayer on AuNPs. This design feature endows CRUSH with a record-breaking stability, withstanding 0.1 M dithiothreitol, a 10,000-fold improvement over conventional SNAs. We also demonstrate that the phagocytic bias of myeloid cells over lymphoid cells drives selective internalization of CRUSH in myeloid lineages in whole blood. Leveraging cellular selectivity and engineered stability, CRUSH offers a mixed-and-read diagnostic test, where lyophilized sensors are directly mixed with whole blood samples, followed by standard flow cytometry analysis. This one-step test detects BCR-ABL1 fusions in living myeloid cells with high specificity and robustness, enabling accurate discrimination of multilineage acute lymphoblastic leukemia within 1 h. Our study bridges biosensing innovation with urgent diagnostic needs, offering a rapid, specific, and robust tool for accurate diagnosis and treatment of hematologic malignancies. - Source: PubMed
Publication date: 2026/04/14
Kong ChuipengZhang XinChen YuanyuanPeng CuizhengYao GuoyingJiang NenggangHuang DanDu LijieChen JunboZeng TaoWang JieSong TurunXing HangLiao HongyanLi Feng