CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- AP07015PU-N
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3
Related genes to: CD135 _ FLT3
- 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: CD135 _ FLT3
AC220 AC220 is a uniquely potent and selective FLT3 inhibitor with IC50 of 0.56 +_- 0.3 nM and >10 mM for MC4-11 and A375, respectively. For research use only.anti-Flt3 CD135 (1A11)anti-Flt3 CD135 (1A11) type: Primary antibodies host: Mouseanti-Flt3 CD135 (3H1)anti-Flt3 CD135 (3H1) type: Primary antibodies host: Mouseanti-FLT3 CD135 (BV10A4H2)anti-FLT3 CD135 (BV10A4H2) type: Primary antibodies host: Mouseanti-FLT3 CD135 (Internal)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591)anti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host Rabbitanti-FLT3 (Ab-591), Rabbit polyclonal to FLT3, Isotype IgG, Host RabbitAnti-FLT3 (BV10A4H2), Mouse Monoclonal to FLT3, Isotype IgG1, Host Mouseanti-FLT3 (Phospho-Tyr591) Related articles to: CD135 _ FLT3
- -mutated acute myeloid leukemia (AML) represents one of the most frequent and biologically distinct AML entities, characterized by the aberrant cytoplasmic localization of the NPM1 mutant protein. The recent advances in molecular biology and translational research have progressively redefined the clinical management of this disease. This narrative review summarizes the evolution of -mutated AML over the last two decades, focusing on the transition from immunohistochemical observations to modern genetics-based and measurable residual disease (MRD)-driven approaches. We discuss the biological role of mutant NPM1, the prognostic impact of co-occurring genetic alterations, and the integration of molecular monitoring into routine clinical practice. Particular attention is given to the prognostic and therapeutic implications of the co-mutational landscape. We also discuss emerging targeted therapies directed against key pathogenic pathways, including the menin-KMT2A axis and nuclear export machinery. Despite significant advances in risk stratification and treatment, considerable heterogeneity in clinical outcomes persists among patients with -mutated AML, indicating that genomic information obtained at diagnosis alone is insufficient to fully capture prognostic differences. Future advances will likely depend on the integration of genetic, transcriptional, and broader cellular-state information to better define biologically relevant disease states and guide more personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/09/19
Cimino GaetanoCaridi MatteoCelenza RosannaMillucci FrancescoCrocioni MartinaSciabolacci SofiaCardinali ValeriaMartelli Maria Paola - Cytarabine is a cornerstone of acute myeloid leukemia (AML) therapy; however, acquired resistance remains a major clinical challenge. FMS-like tyrosine kinase 3 internal tandem duplication (FLT3-ITD), a common genetic alteration in AML, is associated with high relapse rates and poor outcomes. Here, we investigated the cellular and molecular mechanisms of acquired cytarabine resistance in FLT3-ITD AML. Cytarabine-resistant MV4-11-CR and MOLM-13-CR cells were generated from parental MV4-11 and MOLM-13 cells, respectively, by stepwise drug selection. Both models exhibited markedly elevated cytarabine IC values and enhanced proliferation. FLT3 expression and activation increased in MV4-11-CR cells but decreased in MOLM-13-CR cells. Midostaurin pretreatment failed to restore cytarabine sensitivity, indicating that altered FLT3 signaling is not a shared mechanism of resistance. Cytogenetic analyses and interphase FISH revealed greater numerical and structural chromosomal heterogeneity in the resistant cells than in their parental counterparts, including the presence of polyploid and near-tetraploid subpopulations. RNA sequencing identified common transcriptional alterations, with among the most significantly downregulated genes. Reduced expression was confirmed at the mRNA and protein levels. knockdown in parental MV4-11 cells attenuated cytarabine-induced cytotoxicity, whereas its re-expression in MV4-11-CR cells partially restored cytarabine sensitivity, supporting the functional contribution of downregulation to acquired resistance. Gene set enrichment analysis demonstrated shared enrichment of G2/M checkpoint and mitotic spindle pathways. Notably, combined TTK/Mps1 and FLT3 inhibition with luvixasertib and midostaurin synergistically suppressed cell viability in both resistant cell lines. These findings identify divergent FLT3 regulation, downregulation, increased chromosomal heterogeneity, and enrichment of mitotic regulatory programs as key features associated with acquired cytarabine resistance. They also support the combined inhibition of TTK/Mps1 and FLT3 as a potential therapeutic strategy for cytarabine-resistant FLT3-ITD AML. - Source: PubMed
Publication date: 2026/09/21
Yen Jui-HungChen Zi-AnLin Yu-XuanJiang Hui-YuLin Liang-InLi Chi-ChengChen Pei-Yi - Sweet syndrome (acute febrile neutrophilic dermatosis) is characterized by fever, leukocytosis, and tender erythematous skin lesions with neutrophilic infiltrate. Although associated with granulocyte colony-stimulating factor (G-CSF) use, its occurrence with pegfilgrastim-the pegylated form-is rare, with fewer than five reported cases. Sweet syndrome has also been rarely linked to FLT3 inhibitors such as quizartinib. We report a 71-year-old male with acute myeloid leukemia who developed bullous Sweet syndrome following concurrent exposure to pegfilgrastim and quizartinib. - Source: PubMed
Publication date: 2026/10/01
London JonathanPatresan JohnBelkin AlexanderElnair Radowan - Juvenile myelomonocytic leukemia (JMML) is a rare and very aggressive pediatric myelodysplastic/myeloproliferative neoplasm with molecular heterogeneity and constitutive activation of the RAS signaling pathway. The aim of this study was to identify the mutational landscape, driver genes, mutational signatures, functional pathways, and therapeutic targets of mutations that affect receptor tyrosine kinases (RTKs) and RAS pathways in JMML. - Source: PubMed
Publication date: 2026/09/18
Goel HarshMajhi Ravi KumarMeena Jagdish PrasadChopra AnitaBakhshi SameerSingh LataSeth RachnaKar BibekanandaTanwar PranayGupta Aditya Kumar - Clinical decision making in Acute Myeloid Leukemia (AML) critically relies on rapid genomic characterization. To better understand the AML diagnostic landscape in Canada, the Canadian Leukemia Study Group (CLSG) conducted a survey of laboratory hematology leadership (n = 18) at 16 laboratories across 10 provinces, administered using Google Forms in September 2024. Nearly all surveyed sites were equipped to deliver a full suite of testing platforms through existing on-site infrastructure or laboratory partnerships. Reporting practices varied in terms of genomic integration into bone marrow results and the use of AML classification systems. Turn-around-time (TAT) targets were predominantly determined through internal institutional consensus (62%) or recommendations by provincial cancer agencies/international groups (44%). TAT reduction was a top priority for 56% of laboratories, suggesting timely biomarker results to be an active area for improvement. Various treatment-determining biomarkers were frequently assessed as rapid-tests (defined as a 5-day TAT), including -ITD (69%), -TKD (56%), and (56%), while others such as and were rapid at a limited number of laboratories. Respondents demonstrated a strong shared interest in joint projects such as the validation of AML measurable residual disease (MRD) assays (56%). There was also unanimous support for establishing CLSG AML laboratory consensus guidelines. This survey documents the current state of Canadian AML laboratories and provides a foundation for future shared development projects. - Source: PubMed
Publication date: 2026/08/25
Luo Tina Yu XuanUsta SilaMcGinnis EricMather Cheryl ABergeron JulieGillan TanyaMahe EtienneCapo-Chichi José-MarioBerardi PhilipPark Paul CItani DohaRajput AshishChin-Yee BenjaminHan Fei-YuButcher Darci TFesser JenniferDeCoteau JohnQuest GraemeMcCready ElizabethTsui Hubert