rHuman FLt3 Active, Human cytokinesand growth factors
- Known as:
- rHuman FLt3 Active, Human cytokinesand growth factors
- Catalog number:
- RF0041-10
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- Agren
- Gene target:
- rHuman FLt3 Active Human cytokinesand growth factors
Related genes to: rHuman FLt3 Active, Human cytokinesand growth factors
- 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: rHuman FLt3 Active, Human cytokinesand growth factors
Related articles to: rHuman FLt3 Active, Human cytokinesand growth factors
- Acute myeloid leukemia (AML) with FMS-like tyrosine kinase 3 () mutations represent a clinically aggressive subtype of AML characterized by a poor prognosis and high frequency of relapse. Although several inhibitors exist, they differ in their side effects, potency and clinical use. Quizartinib is a potent next generation FLT3 inhibitor with a risk of QTc-prolongation necessitating a Risk Evaluation and Mitigation Strategies (REMS) program as well as potential drug-drug interactions with strong CYP3A4 inhibitors. Here we detail two patient cases illustrating the real-world use of quizartinib in combination with anthracycline and cytarabine-based chemotherapy and maintenance monotherapy for the management of -ITD+ AML. These cases highlight the practical recommendations on management of quizartinib-based chemotherapy in accordance with the Food and Drug Administration (FDA)-mandated REMS requirements. Adopting these strategies to optimize the safe treatment of -ITD+ AML with quizartinib may ultimately improve patient outcomes in this highly challenging malignancy. - Source: PubMed
Publication date: 2026/05/30
Horsch LaurieBaron JeffreySung Pamela JWang Eunice S - Chronic inflammation and aging skew hematopoiesis toward myelopoiesis at the expense of lymphoid output. We screened type 2 and anti-inflammatory cytokines to identify extrinsic signals capable of restoring lymphoid lineage commitment in hematopoietic stem and progenitor cells (HSPCs). Interleukin 4 (IL-4) specifically inhibited inflammation-induced myelopoiesis and shifted multipotent progenitor (MPP) differentiation toward the lymphoid lineage. IL-4 activated a signal transducer and activator of transcription 6 (STAT6)-dependent transcriptional program in MPPs, increasing the expression of lymphoid-specific genes. Mechanistically, the receptor tyrosine kinase FMS-like tyrosine kinase 3 (FLT3), which is highly expressed in MPPs, interacted with IL-4Rα to facilitate STAT6 activation. In vivo, IL-4 reversed inflammation-induced hematopoietic imbalance and accelerated lymphoid recovery. In aged mice, IL-4 administration shifted the MPP composition toward a lymphoid bias and restored B and T lymphocyte output. Long-term IL-4 treatment in aged mice improved immune, metabolic, physical, and cognitive functions; these rejuvenating effects were recapitulated by transplantation of IL-4-treated HSPCs. Promoting IL-4 signaling in MPPs may enable correction of hematopoietic dysregulation in inflammatory and aging-related conditions. - Source: PubMed
Publication date: 2026/05/29
Yao JingfeiWang YutingZhang Yi - In a mouse model of FGFR1-driven leukemia, we demonstrated a role for circulating non-conventional monocyte-derived macrophages in the peripheral blood, which suppressed T-cell function and promoted leukemogenesis. A single cell RNA sequencing (scRNA-Seq) analysis of these leukemia-associated macrophages (LAMs) identified LAM-specific dysregulation of gene expression associated with leukemogenesis. Based on the top markers identified in these LAMs, we generated a LAM score based on the expression levels of a 32 gene signature. This scoring system was then applied to the transcriptomic data from a cohort of 838 newly diagnosed patients treated on Alliance/CALGB protocols, who were similarly treated with intensive cytarabine/daunorubicin-based chemotherapy on the CALGB/Alliance for the Clinical Trials in Oncology protocol. Patients were subclassified as those with high and low LAM scores. Patients with a high LAM score had shorter overall survival, disease-free survival and event-free survival compared to those with a low LAM score. We also noted a strong association of FLT3-ITD, RUNX1 and TP53 mutations with high LAM scores. Applying the LAM score to the current European Leukemia Network risk group criteria, independent prognostic implications and a refined prognostic significance of each subgroup were provided, indicating the value of including immune microenvironment data into AML risk stratification. - Source: PubMed
Publication date: 2026/05/29
Nicolet DeedraZhang TingWalker Christopher JAmeyi JusticeMori Stephanie FFang XuexiuZhang LitaoCortes JorgeHedrick Catherine CCowell John KEisfeld Ann-KathrinHu Tianxiang - B-cell Non-Hodgkin Lymphoma (B-NHL) is a group of lymphoid malignancies characterized by dysregulation of lymphocytes and monocytes. CD135/FLT3 (FMS-like tyrosine kinase 3) and its ligand (FLT3LG) play crucial roles in white blood cell (WBC) proliferation, and their ratios are meaningful indicators of treatment response. - Source: PubMed
Publication date: 2026/05/26
Nandasena C KJayathilake P W D C CDharmarathne H A S GKaluarachchi PSuresh SDe Silva A DPerera I CKottahachchi D U - Not available. - Source: PubMed
Publication date: 2026/05/28
Dobrevski BobanMüller Jörg P