FLT3 Ligand
- Known as:
- FLT3 Ligand
- Catalog number:
- PR-419
- Product Quantity:
- 10
- Category:
- -
- Supplier:
- Jena Bio
- Gene target:
- FLT3 Ligand
Related genes to: FLT3 Ligand
- 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: FLT3 Ligand
&_945;2&_946;1 Integrin Ligand Peptide(1R,2R)_(+)_1,2_Diaminocyclohexane_N, min. 94%rost ligand (na(1S,2S)_(+)_1,2_Cyclohexanediamino_N, (S,S)_Jacobsen ligand(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N min. 94% rost ligand (n(1S,2S)_(_)_1,2_Diaminocyclohexane_N,N Rost ligand24(S)-Hydroxycholesterol Ligand24(S)-Hydroxycholesterol Ligand24(S)-Hydroxycholesterol, LXR ligand, (3β,24S)-Cholest-5-ene-3,24-diol, CAS: 474-73-724(S)-Hydroxycholesterol, LXR ligand, (3β,24S)-Cholest-5-ene-3,24-diol, CAS: 474-73-72B4,CD244,h2B4,Homo sapiens,Human,NAIL,Natural killer cell receptor 2B4,NK cell activation-inducing ligand,NK cell type I receptor protein 2B4,NKR2B42C101 Fas Ligand4-1BB ligand , 71-254aa, Human, His tag, E.coli4-1BB ligand , 71-254aa, Human, His tag, E.coli4-1BB ligand , 71-254aa, Human, His tag, E.coli4-1BB ligand , 71-254aa, Human, His-tag, Recombinant, E.coli Related articles to: FLT3 Ligand
- We report a large cohort of 95 adult patients with acute myeloid leukemia (AML) harboring NUP98 rearrangements (NUP98r). Patient characteristics included a young age (median 50 years [IQR 38-64]), 20% of therapy-related AML, a high WBC count (median 52×10/L), normal karyotype in 32%, FLT3-ITD in 48% and WT1 mutations in 34%. NUP98::NSD1 fusion was the most common (54%), and these patients were significantly younger (41 y vs. 61 y), had more de novo AML (94% vs. 64%), higher rates of normal karyotypes (56% vs. 4.5%), FLT3-ITD (76% vs. 18%) and WT1 mutations (50% vs. 16%) than other NUP98r AML. The median overall survival (OS) for the entire cohort was 15.2 months (95% CI, 11.9-20.8) and event-free survival was 5.8 months (2-7.5). Among patients treated intensively (n = 73), age (HR = 2.7), FLT3 inhibitor therapy (HR = 0.45) and hematopoietic stem cell transplant (HR = 0.5) influenced OS in univariate analysis. Compared with NUP98 wild-type (WT) AML, NUP98r patients had a prognosis more similar to that of NUP98 WT ELN adverse patients whether initially classified as intermediate (20.3 months [11.7-30.2]) or adverse (15.7 months [13.5-42.9]). However, treatment with FLT3 inhibitors improved prognosis, with median OS not reached and 5-year OS of 53.3%, approaching that of intermediate-risk patients. - Source: PubMed
Publication date: 2026/05/12
Ducourneau BenoitPages ArnaudStruski StéphanieDecamp MatthieuRaffoux EmmanuelBerthon CélineFenwarth LaurèneMarmouset VincentPautas CécileCluzeau ThomasLebon DelphineUzunov MadalinaPereyra PatricioHeiblig MaëlMalfuson Jean-ValèreFarnault LaureDumas Pierre-YvesHieulle JuliaBertoli SarahChantepie SylvainAuger NathalieBidet AudreyMozziconacci Marie-JoelleBoudry AugustinLuquet IsabelleChat LaureenLoyaux RomainEl-Mur LinaClappier EmmanuelleGardin ClaudeHunault MathildeDe Botton StéphanePigneux ArnaudPenther DominiqueDelabesse EricItzykson RaphaelPreudhomme ClaudeDombret HervéRecher ChristianDuployez NicolasMicol Jean-Baptiste - To determine midostaurin and posaconazole plasma concentrations and investigate adverse events (AEs) resembling drug-drug interactions (DDI) when both drugs were administered concomitantly during induction chemotherapy for acute myeloid leukemia (AML). Patients with FLT3-mutated AML who received midostaurin and posaconazole concomitantly between May 2019 and December 2022 were included and followed up to March 2023. Twice-weekly trough levels for midostaurin and posaconazole were measured with validated liquid chromatography-tandem mass spectrometry methods. Potential DDIs were independently reviewed by two physicians and attributed using the Drug Interaction Probability Scale (DIPS). Population pharmacokinetics analysis was done via nonlinear mixed-effect modeling. In 29 patients, concentrations ranged from 0.6 to 24.5 mg/L for midostaurin and from <30 to 2,572 µg/L for posaconazole. A total of 375 AEs in 66 midostaurin cycles, with 280 AEs classified as grade ≥3, were recorded. Probable DDI with a DIPS score of ≥5 was attributed in 14/375 AEs; no highly probable AEs were registered. Eight AEs led to dose modification or discontinuation of midostaurin in seven patients. Clearance for midostaurin during co-administration with posaconazole was 0.52 L/h (95% CI, 0.42-0.62 L/h). A breakthrough fungal infection was recorded in eight patients (27.5%). DDI of midostaurin and posaconazole is clinically meaningful but infrequent. High inter- and intra-individual variabilities of midostaurin and posaconazole plasma exposure were observed. Midostaurin clearance was delayed during co-administration. Midostaurin therapeutic drug monitoring may serve for decision-making when DDI with CYP3A4 inhibitors is suspected. - Source: PubMed
Publication date: 2026/05/12
Joisten Carolin SMellinghoff Sibylle CSeidel DanilaMüller CarstenMüller-Ohrem CharlotteKreuzer Karl-AntonFrenzel Lukas PSimon FlorianHallek MichaelKoehler PhilippCornely Oliver AStemler Jannik - Chimeric antigen receptor T cell (CAR-T cell) therapy is an immunotherapy for acute leukemias utilizing recombinant receptors specific to antigens involved in T-cell function to direct tumor cell recognition and elimination. However, major limitations include relapse due to antigen escape and tumor heterogeneity, as well as on-target off-tumor effects. Bispecific CAR-T cells are developed to overcome these issues. - Source: PubMed
Publication date: 2026/04/23
Husodho Gabriela Valencia PutriKumalasari Anatalya Diah AyuFaiza Agyta HanifaLimijadi Edward Kurnia SetiawanHendrianingtyas Meita - The serine/threonine phosphatase-2 (PP2A) controls mitogen-associated signaling and DNA replication. The WEE1 protein tyrosine kinase controls S phase progression and G2/M phase transition. Databases disclose that the levels of PP2A and WEE1 are associated with poor prognosis of leukemic patients (p = 0,0017/0,025; n = 54-163). We applied advanced, clinically used drugs that block PP2A and WEE1 to human cultured leukemia cells, primary pre-leukemic and chronic myeloid leukemia cells, and pancreatic ductal adenocarcinoma cells. Combined application of the drugs depleted cells in all cell cycle phases, synergistically triggered apoptosis, and evoked the induction of DNA stress foci and mitotic catastrophe. In 93 lymphoid, 40 myeloid, and 47 pancreatic cancer cells, genetic depletion of PP2A-Cα and WEE1 stalls the proliferation of most cells. Unlike cancer cells, normal human immune cells are not killed upon inhibition of PP2A and WEE1. This is linked to higher expression of PP2A and WEE1 in chronic myeloid (n = 274), acute myeloid (n = 1858) and acute lymphoblastic leukemia cells (n = 1817) than in normal blood cells. These data suggest that pharmacological modulators of serine/threonine and tyrosine signaling allow targeted chemotherapy. - Source: PubMed
Publication date: 2026/05/08
Mustafa Al-Hassan MNguyen AlexandraKreissig SophieZeyn YaniraGürbüzoglu Yesim MelisaStoldt StefanBros MatthiasRadsak Markus PBrenner WalburgisChen-Wichmann LinpingWichmann ChristianKrämer Oliver H - DNA topoisomerase II-binding protein 1 (TopBP1) plays a critical role in V(D)J recombination and DNA damage repair during B and T cell development. However, its role in the development of conventional dendritic cells (cDCs) remains unexplored. Mice with DC-specific depletion of TopBP1 (TopBP1) exhibited accelerated tumor progression due to impaired anti-tumor immunity, which was characterized by cDC deficiency and pre-DC accumulation. The cDC deficiency observed in TopBP1 mice was not attributable to cell death resulting from accumulated DNA damage during DC development. Notably, Flt3 ligand (Flt3L)-mediated tumor immunotherapy was ineffective in TopBP1 tumor-bearing mice. Here we demonstrate that TopBP1 is required not only for the steady-state differentiation of total cDCs, including both cDC1 and cDC2, but also for the terminal differentiation of XCR1CD24⁺ emergency progenitors (CD11c⁺cKit⁺) into XCR1⁺CD24⁺ cDC1s in response to Flt3L. Furthermore, TopBP1 was found to be essential for the function of the PU.1-IRF8 heterodimeric transcription factor complex, which is critical for cDC lineage specification. TopBP1 directly binds to this complex and facilitates the transcription of downstream target genes required for cDC development. These findings establish TopBP1 as a pivotal regulator of both steady-state and Flt3L-driven emergency cDC differentiation, particularly in guiding emergency progenitors into functional cDC1s. Our study highlights the previously unrecognized role of TopBP1 as a co-regulator of lineage-defining transcription factors and as a determinant of Flt3L-mediated anti-tumor efficacy. - Source: PubMed
Publication date: 2026/05/08
Cha Min-SukKang Myeong-HoLee JinjooHong JungHyubJeong Yu SunBae Yoe-SikLee HoPark Seok-HeeBae Yong-Soo