ABL1 (phospho-Tyr412) Antibody
- Known as:
- ABL1 (phosphorilated-Tyr412) Antibody
- Catalog number:
- abx000351
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Abbexa
- Gene target:
- ABL1 (phospho-Tyr412) Antibody
Related genes to: ABL1 (phospho-Tyr412) 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-Tyr412) Antibody
Related articles to: ABL1 (phospho-Tyr412) Antibody
- Mutations in calreticulin have been identified as driver mutations in BCR-ABL1-negative myeloproliferative neoplasms (MPNs) and are especially important for diagnostics and prognosis in primary myelofibrosis and essential thrombocythemia. The vast majority of pathogenic variants are insertions or deletions in exon 9 that result in a mutant C-terminal sequence that activates the signaling of the thrombopoietin receptor, which in turn promotes megakaryocytic proliferation. This review examines the potential clinical utility of calreticulin mutations as laboratory biomarkers in essential thrombocythemia (ET) and primary myelofibrosis (PMF). It emphasizes their role in confirming clonality in JAK2/MPL-unmutated cases, distinguishing a clonal myeloproliferative disease from reactive thrombocytosis, clarifying the molecular interpretation, and guiding molecular diagnostic workflows. Special focus is placed on practical laboratory challenges, such as choosing assays, detecting rare and non-canonical variants in exon 9, analytical sensitivity, molecular reporting, and the integration of bone marrow morphology, cytogenetics, co-mutations, and next-generation sequencing. Overall, clinical information gained from calreticulin testing is greatest when it is used in an integrated clinicopathologic and molecular testing context rather than as a standalone test. To make calreticulin mutations more effectively used for diagnosis or prognosis in routine hematology practice, we need standardization of testing, harmonization of reporting, and prospective validation of risk-models based on both the subtypes and the burden of the mutation. - Source: PubMed
Publication date: 2026/06/01
Bhat Asif AhmadFuloria ShivkanyaThapa RiyaAgnihotri SupriyaAnsari Mohammed TahirNarain KamalBiswas AnupamBiswas SangitaBhatia SumitaFuloria Neeraj Kumar - Several approved and investigational BCR::ABL1 tyrosine kinase inhibitors (TKIs) and STAMP inhibitors are used for the treatment of chronic myeloid leukemia in chronic phase (CML-CP). In the frontline setting, multiple factors affect selection of therapy including the goal of treatment, cost of TKIs, CML risk, and patient's comorbidities. Achieving a complete cytogenetic response (BCR::ABL1 transcripts on the International Scale [IS] <1%) with TKI therapy within the first year is associated with normalization of survival, whereas achieving a deeper molecular response (BCR::ABL1 transcripts < 0.01% [IS]) may allow for treatment discontinuation with the possibility of treatment-free remission. Although standard doses are approved for each TKI, post approval studies have demonstrated that an optimal biologic dose is safer than and as effective as the approved dose. In cases of TKI toxicities, reducing the dose rather than switching TKIs is recommended unless the patient experiences a prohibitive toxicity, in which case the treatment should be changed. In patients experiencing failure of frontline therapy due to resistance or intolerance, multiple second- and third-line options are available, including second-generation TKIs, ponatinib, and asciminib, as well as novel investigational agents, including the ABL1 kinase domain inhibitors olverembatinib and ELVN-001 and the STAMP inhibitors TGRX-678 and TERN-701. In this review, we discuss the recent advances in the treatment of CML-CP and challenge some established management practices. - Source: PubMed
Publication date: 2026/05/28
Haddad Fadi GKantarjian Hagop - Imatinib has transformed chronic myeloid leukemia treatment, yet early molecular events linking BCR-ABL1 inhibition to leukemic cell fate remain incompletely understood. We investigated whether imatinib induces time-dependent Hippo-YAP transcript changes and delayed microRNA alterations in K562 cells. - Source: PubMed
Publication date: 2026/05/27
Akbari-Ardabili SoroushAghazadeh SafiyehImani Mehdi - Accurate quantification is essential for monitoring chronic myeloid leukemia (CML), particularly at the major molecular response (MMR; ≤0.1% IS) and deep molecular response (DMR) levels: MR4 (≤0.01% IS) and MR4.5 (≤0.0032% IS). We evaluated the analytical performance of the 1copy BCR::ABL1 qPCR Kit (1drop, Republic of Korea), a one-step real-time quantitative PCR (qPCR) Kit and compared it with two established assays. - Source: PubMed
Publication date: 2026/05/11
Kim HyerinKim Do YoungKim Hyerim - Molecular analysis of BCR-ABL1-negative myeloproliferative neoplasms has shown a shared codon 617 substitution of JAK2 that leads to a constitutively active tyrosine kinase and a pathogenic lesion that unites all three polycythemia vera, essential thrombocythemia, and primary myelofibrosis. This mutation interferes with the autoinhibitory regulation and results in persistent downstream JAK-STAT signaling, and thereafter, myeloid, megakaryocytic, and inappropriate erythroid proliferation. JAK2 V617F has emerged as a major molecular biomarker in the diagnostic workup and classification of myeloproliferative neoplasms in laboratory medicine when used together with blood counts, bone marrow morphology, serum erythropoietin, and other molecular markers, such as CALR and MPL. Outside its diagnostic application, variant allele burden has also been linked to thrombosis, disease phenotype, clonal growth, fibrotic development, and survival but not uniformly across disease subtypes and clinical contexts. JAK2 V617F detection in laboratories has moved beyond traditional approaches based on PCR to sensitive quantitative technologies, such as digital PCR and next-generation sequencing-based technologies, making the standardization of assays, assurance of quality and more clinically integrated interpretation more important. In general, JAK2 V617F is an effective prognostic and diagnostic biomarker in myeloproliferative neoplasms. It can be further enhanced in diagnostic laboratory hematology with further optimization of the strategies of molecular testing, reporting systems, and multi-marker diagnostic algorithms. - Source: PubMed
Publication date: 2026/05/22
Bhat Asif AhmadFuloria ShivkanyaThapa RiyaNarain KamalBiswas AnupamGnanam PadmashiniDhandapani Satish VasanthBiswas SangitaBhatia SumitaFuloria Neeraj Kumar