Recombinant Human FLT3 Ligand
- Known as:
- Recombinant Human FLT3 Ligand
- Catalog number:
- CRF110C
- Product Quantity:
- 1.0 mg
- Category:
- -
- Supplier:
- Cell Sciences
- Gene target:
- Recombinant Human FLT3 Ligand
Related genes to: Recombinant Human 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: Recombinant Human FLT3 Ligand
Related articles to: Recombinant Human FLT3 Ligand
- Conventional type-1 dendritic cells (cDC1) are the main mediators of crosspresentation of tumor antigens to CD8+ T cells and provide a context of costimulatory molecules and cytokines that lead to cytotoxic T lymphocyte (CTL) responses. We analyzed bulk RNA sequences from 7 key clinical trials testing checkpoint inhibitors across multiple cancer types. cDC1- and CD8-associated gene signatures were analyzed. Multiplex tissue immunofluorescence was used to quantify cDC1 in melanoma, urothelial cancer, and non-small-cell lung cancer (NSCLC) samples and assess cDC1 tissue neighborhoods. Melanoma samples were studied with Xenium spatial transcriptomics (ST) and one series of NSCLC was analyzed using GeoMX-DSP. Strong associations across tumor types were found between cDC1 and CD8+ T cell transcripts with clinical outcomes. As mechanistically expected, transcripts for the CCL4 and CCL5 chemokines and the growth factor FLT3-L showed associations with cDC1 abundance. Tissue immunofluorescence showed a strong correlation of cDC1 and CD8+ T cell infiltration with clinical benefit upon treatment with checkpoint inhibitors (CPIs). Moreover, short distance between cDC1 and CD8+ T cells was found to define tissue niches associated with favorable outcomes. ST revealed recent T cell activation within immune cDC1-rich niches. cDC1 abundance, which determines CD8+ T lymphocyte density and activation in tumor tissues across cancer types, is strongly associated with clinical response to CPI-based immunotherapies. - Source: PubMed
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Lopez-Janeiro AlvaroGonzález-Gomariz JoséIssa FadiHester JoannaPorciuncula AngeloTeijeira AlvaroLuri-Rey CarlosRuiz-Guillamon DavidPerez-Gracia Jose LuisPerez-Ruiz ElisabethBarragan IsabelMartín-Algarra SalvadorSanmamed Miguel FOrtego IgnacioRodriguez-Ruiz Maria EAlexandru RalucaRodriguez InmaculadaArrieta-Aranzueque SaioaRimm DavidAung ThazinSchalper Kurt Ade Andrea Carlos EMelero Ignacio - Second generation tyrosine kinase inhibitors (TKIs) such as gilteritinib, characterized by minimal EGFR and absent VEGFR inhibition, are in theory associated with low dermatologic toxicity. This case report brings to the awareness that the opposite may occur and emphasize the need for attentive pharmacovigilance. - Source: PubMed
Publication date: 2026/04/12
Seki Jack TSibai JadPerusini Maria AgustinaSibai Hassan - Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia defined by the t(15;17)(q24;q21)-derived fusion. However, a small subset of patients harbor cryptic or atypical rearrangements that escape detection by routine real-time quantitative RT-PCR (qRT-PCR). We report a 34-year-old man presenting typical APL in whom repeated testing for the canonical long, short, and variant transcripts yielded negative results. RNA sequencing subsequently identified a previously unreported in-frame fusion linking exon 8 to a 58-base pair-deleted exon 3. The resulting chimeric transcript retained the coiled-coil domain as well as the DNA- and ligand-binding domains of , suggesting preserved sensitivity to retinoid-based therapy. Consistent with this prediction, induction therapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) resulted in achievement of complete molecular remission. Molecular relapse occurred three months after premature discontinuation of maintenance therapy, underscoring the leukemogenic potential of this novel fusion. This observation expands the molecular spectrum of APL and highlights the potential value of incorporating RNA sequencing into the diagnostic workflow for morphologically suspected but PCR-negative APL. - Source: PubMed
Publication date: 2026/04/14
Chen Jia-PingHou Jun-JieChen Xiao-YongCao Yi-XuanKe PengZhou Ji-HaoHu Li-Na - Minimally differentiated acute myeloid leukemia (AML-M0) is a rare and therapeutically challenging subgroup of AML characterized by immature hematopoietic stem cell-like features. To uncover the molecular basis, we conducted a comprehensive multi-omics analysis of 23 pediatric AML-M0 cases and compared them with 1483 leukemia samples. AML-M0 formed a characteristic group that exhibited global DNA hypermethylation and transcriptional suppression, particularly downregulation of genes related to oxidative phosphorylation and ribosome assembly compared to non-M0 AML. Genomic profiling revealed frequent loss-of-function alterations in RUNX1 (26%) and ETV6 (22%), along with activating mutations in signaling pathways (83%), such as RAS, FLT3, and JAK. Notably, RUNX1 alterations were significantly associated with a poor prognosis. Functional analyses using a CRISPR/Cas9-mediated RUNX1 knockout in a pediatric AML-M0 cell line showed stem cell-like transcriptional features and reduced expression of genes related to oxidative phosphorylation and ribosomal pathways. RUNX1 disruption was also associated with reduced in vitro sensitivity to multiple drugs, including cytarabine and anthracyclines. Our study provides the most comprehensive molecular characterization of pediatric AML-M0 to date and identifies RUNX1 alterations as important biological and clinical determinants. These insights highlight the potential strategies for precision therapy, including hypomethylating agents, signaling inhibitors, and metabolic targeting, to improve outcomes. - Source: PubMed
Publication date: 2026/04/29
Kamitori TatsuyaSaida SatoshiMitani KazukiTsujimoto ShinichiGoto HiroakiShibata HirofumiAkazawa RyoIsobe KiyotakaUeno HirooKakiuchi NobuyukiSaito Akiko MHiwatari MitsuteruKudo KoHirabayashi ShinsukeFukuoka KoheiKoh KatsuyoshiTaga TakashiKubota HirohitoKato ItaruUmeda KatsutsuguAdachi SouichiKawai TomokoTomizawa DaisukeIkeda JunjiShiba NorioHayashi YasuhideOgawa SeishiTakita Junko - The geographic diversity of molecular genetic abnormalities in AML can help understand the genetic and environmental factors involved in the development of leukemia. In addition, high-risk groups can be recognized by identifying common mutations in AML patients, and appropriate treatment based on the type of mutation can be adopted. This systematic study and meta-analysis analyzed the common mutations in AML patients in Iran. - Source: PubMed
Publication date: 2026/01/11
Khaksari Mohammad NavidMeghdadi MohammadrezaRostami MehrdadKhoshnegah ZahraBoroumand-Noughabi SamanehBazi AliKhiabani AlirezaKeramati Mohammad Reza