Human FLT3 Ligand ELISA Kit
- Known as:
- Human FLT3 Ligand Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- CKH138
- Product Quantity:
- 1 x 96 tests
- Category:
- Peptides
- Supplier:
- Cell Sciences
- Gene target:
- Human FLT3 Ligand ELISA Kit
Related genes to: Human FLT3 Ligand ELISA Kit
- 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: Human FLT3 Ligand ELISA Kit
Related articles to: Human FLT3 Ligand ELISA Kit
- 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 - This case report examines three patients with relapsed/refractory + acute myeloid leukemia (AML) treated with FLT3 inhibitors (FLT3i) and venetoclax (VEN). While the combination therapy showed promising antileukemic activity, all patients experienced severe myelosuppression, leading to treatment interruptions. Two patients died following disease progression after therapy discontinuation, while one maintained remission with an alternating treatment schedule. These cases highlight the importance of minimizing treatment interruptions while balancing infection risks and suggest that combination or sequential therapy with VEN and FLT3i may be effective for relapsed/refractory (R/R) + AML when treatment duration and dosing are properly managed. - Source: PubMed
Publication date: 2026/04/22
Ikeda DaisukeUchiyama SatoshiGuo Yong-MeiSato NobueNakamura HirotakaNagata AkihitoSong-Gi ChiMinami YosukeYuda Junichiro