Anti-Human FLt3 (IgG), polyclonal antibody
- Known as:
- Antibody toHuman FLt3 (Immunoglobulin G), pab (anti-)
- Catalog number:
- RF0058
- Product Quantity:
- 100 μg
- Category:
- -
- Supplier:
- Agren
- Gene target:
- Anti-Human FLt3 (IgG) polyclonal antibody
Ask about this productRelated genes to: Anti-Human FLt3 (IgG), polyclonal antibody
- Gene:
- FLT3 NIH gene
- Name:
- fms related tyrosine kinase 3
- Previous symbol:
- -
- Synonyms:
- STK1, FLK2, CD135
- Chromosome:
- 13q12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1990-07-30
- Date modifiied:
- 2019-04-23
Related products to: Anti-Human FLt3 (IgG), polyclonal antibody
Related articles to: Anti-Human FLt3 (IgG), polyclonal antibody
- We retrospectively analyzed the impact of conditioning intensity on transplant outcomes according to their cytogenetic/molecular risk in a cohort of 1823 patients with acute myeloid leukemia (AML) and intermediate- or adverse-risk cytogenetics in first complete remission (CR1). These patients received their first hematopoietic stem cell transplantation (HSCT) using post-transplant cyclophosphamide (PTCy). The intermediate-risk cytogenetic group included 1386 (76%) patients, and 608 (34%) had mutated FLT3-ITD. Myeloablative conditioning was used in 930 patients (51%), while 1130 (62%) received an intensified conditioning (score ≥2.5) based on the transplant conditioning intensity (TCI) score. Conditioning intensity using the myeloablative/reduced intensity stratification did not impact transplant outcomes across the entire cohort. However, a higher TCI score was associated with a lower risk of relapse, with no effect on survival. In specific cytogenetic risk groups, a higher TCI score did not influence outcomes in the adverse-risk group. In the intermediate-risk group, the impact varied with FLT3-ITD status. Patients with FLT3-ITD mutation who received a higher TCI showed a beneficial effect on relapse, leukemia-free survival (LFS), and overall survival. Conversely, in FLT3-ITD wild-type patients, more intense conditioning had a detrimental effect on graft-versus-host disease-free, and relapse-free survival with no effect on other outcomes. In conclusion, for AML patients in CR1 undergoing HSCT with PTCy, it is crucial to consider cytogenetic risk and molecular status when selecting the conditioning regimen. Intensive conditioning should be considered for patients with intermediate-risk cytogenetics and mutated FLT3-ITD but should probably be avoided for those with wild-type FLT3-ITD. - Source: PubMed
Publication date: 2025/02/12
Sanz JaimeLabopin MyriamVersluis JurjenBlaise DidierLazzari LorenzoMontoro JuanVan Gorkom Gwendolynvon dem Borne PeterSandrine LoronRovira MontserratReményi PéterChevallier PatriceKwon MiEder MatthiasVydra JanBrissot EoliaSpyridonidis AlexandrosPiemontese SimonaMohty MohamadCiceri Fabio - Mutations found in AML such as DNMT3A, TET2 and ASXL1 can be found in the peripheral blood of healthy adults - a phenomenon termed clonal hematopoiesis (CH). These mutations are thought to represent the earliest genetic events in the evolution of AML. Genomic studies on samples acquired at diagnosis, remission, and at relapse have demonstrated significant stability of CH mutations following induction chemotherapy. Meanwhile, later mutations in genes such as NPM1 and FLT3, have been shown to contract at remission and in the case of FLT3 often are absent at relapse. We sought to understand how early CH mutations influence subsequent evolutionary trajectories throughout remission and relapse in response to induction chemotherapy. We assembled a retrospective cohort of patients diagnosed with de novo AML at our institution that underwent genomic sequencing at diagnosis, remission and/or relapse (total n=182 patients). FLT3 and NPM1 mutations were generally eliminated at complete remission but subsequently reemerged upon relapse, whereas DNMT3A, TET2 and ASXL1 mutations often persisted through remission. CH-related mutations exhibited distinct constellations of co-occurring genetic alterations, with NPM1 and FLT3 mutations enriched in DNMT3Amut AML, while CBL and SRSF2 mutations were enriched in TET2mut and ASXL1mut AML, respectively. In the case of NPM1 and FLT3 mutations, these differences vanished at the time of complete remission yet readily reemerged upon relapse, indicating the reproducible nature of these genetic interactions. Thus, CH-associated mutations that likely precede malignant transformation subsequently shape the evolutionary trajectories of AML through diagnosis, therapy, and relapse. - Source: PubMed
Publication date: 2025/02/12
Chow Ryan DVelu PriyaDeihimi SafooraBelman Jonathan PYoun AngelaShah NisargbhaiLuger Selina MCarroll Martin PMorrissette Jennifer JdBowman Robert L - We aim to analyze the efficacy and safety of Venetoclax (Ven) added to cladribine + cytarabine + granulocyte colony-stimulating factor (G-CSF) ± idarubicin or mitoxantrone (CLAG ± Ida/Mito) regimen as a salvage treatment of relapsed/refractory acute myeloid leukemia (RR-AML). - Source: PubMed
Publication date: 2025/02/10
Zhang YuYin ZhaoYao ZurongXu DanJiang XuejieNie XiaqiChen DandanZhou HongshengShi PengchengLiu HuiLiu QifaYu Guopan - In acute myeloid leukemia (AML), malignant cells surviving chemotherapy rely on high mRNA translation and their microenvironmental metabolic support to drive relapse. However, the role of translational reprogramming in the niche is unclear. Here, we found that relapsing AML cells increase translation in their bone marrow (BM) niches, where BM mesenchymal stromal cells (BMSCs) become a source of eIF4A-cap-dependent translation machinery that is transferred to AML cells via extracellular vesicles (EVs) to meet their translational demands. In two independent models of highly chemo-resistant AML driven by MLL-AF9 or FLT3-ITD (internal tandem duplication) and nucleophosmin (NPMc) mutations, protein synthesis levels increase in refractory AML dependent on nestin+ BMSCs. Inhibiting cap-dependent translation in BMSCs abolishes their chemoprotective ability, while EVs from BMSCs carrying eIF4A boost AML cell translation and survival. Consequently, eIF4A inhibition synergizes with conventional chemotherapy. Together, these results suggest that AML cells rely on BMSCs to maintain an oncogenic translational program required for relapse. - Source: PubMed
Publication date: 2024/12/28
Lisi-Vega Livia EPievani AliceGarcía-Fernández MaríaForte DorianWilliams Tim LSerafini MartaMéndez-Ferrer Simón - AXL, a member of the TAM receptor family, has emerged as a potential target for advanced-stage human malignancies. It is frequently overexpressed in different cancers and plays a significant role in various tumor-promoting pathways, including cancer cell proliferation, invasion, metastasis, epithelial-mesenchymal transition (EMT), angiogenesis, stemness, DNA damage response, acquired therapeutic resistance, immunosuppression, and inflammatory responses. Beyond oncology, AXL also facilitates viral infections, including SARS-CoV-2 and Zika highlighting its importance in both cancer and virology. In preclinical models, small-molecule kinase inhibitors targeting AXL have shown promising anti-tumorigenic potential. This review primarily focuses on the induction, regulation and biological functions of AXL in mediating these tumor-promoting pathways. We discuss a range of therapeutic strategies, including recently developed small-molecule tyrosine kinase inhibitors (TKIs), monoclonal antibodies, and antibody-drug conjugates (ADCs), anti-AXL-CAR, and combination therapies. These interventions are being examined in both preclinical and clinical studies, offering the potential for improved drug sensitivity and therapeutic efficacy. We further discuss the mechanisms of acquired therapeutic resistance, particularly the crosstalk between AXL and other critical receptor tyrosine kinases (RTKs) such as c-MET, EGFR, HER2/HER3, VEGFR, PDGFR, and FLT3. Finally, we highlight key research areas that require further exploration to enhance AXL-mediated therapeutic approaches for improved clinical outcomes. - Source: PubMed
Publication date: 2025/02/10
Yadav MonikaSharma AkanshaPatne KetkiTabasum SabaSuryavanshi JyotiRawat LaxminarayanMachaalani MarcEid MarcSingh Rana PChoueiri Toni KPal SoumitroSabarwal Akash