CD135 _ FLT3
- Known as:
- CD135 _ FLT3
- Catalog number:
- AP21030PU-N
- Product Quantity:
- 100 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
- Acute myeloid leukemia (AML) is a fatal blood cancer with cytotoxic chemotherapy offering at best 25% 5-year survival. While targeted BCL2 and FLT3 inhibitors venetoclax and gilteritinib are used upfront in the treatment of a subset of adult patients with AML and help to extend the survival of some patients, a curative treatment combination with minimal side effects has yet to be discovered. We find that use of the dual histone acetyltransferase p300/CBP bromodomain inhibitor CCS1477 (inobrodib), together with venetoclax and gilteritinib, virtually eliminates leukemia stem cells in an aggressive preclinical model of -mutant AML by impairing pro-oncogenic survival and proliferation factors to effectively block leukemogenesis. This work identifies potential clinical utility of a targeted, triplet combination therapy for treatment of AML. - Source: PubMed
Publication date: 2026/05/15
Goetz Melanie LRomer-Seibert Jennifer SVersace Amanda MKogan ScottJeurkar ChetanBowman Robert LBrooks NigelFrese KrisMeyer Sara E - Anthracyclines are key components of induction therapy for acute myelogenous leukemia with well-understood cardiotoxicity. Quizartinib inhibits FLT3 and has been shown to potentiate apoptosis and promote maladaptive remodeling after myocardial infarction in mice; however, the impact of FLT3 inhibition on a heart already exposed to anthracyclines is poorly understood. - Source: PubMed
Publication date: 2026/05/14
Spahr Zachary RVasquez Moises ATangella AdarshvardhanHusain Mohammad SaadTaylor Allen J - Despite advances, over half of AML patients relapse or become refractory to chemotherapy. TREM1 (CD354), a regulator of tumor inflammation and immune evasion in solid cancers, remains poorly characterized in AML, especially in underrepresented populations like Egyptians. We aimed to evaluate TREM1 expression in de novo AML, its association with high-risk features (FLT3-ITD, CD123), and its prognostic impact on treatment response and survival. - Source: PubMed
Publication date: 2026/05/14
Mansor Shima GafarElgamal RashaSaleh Mostafa F MohammedOthman Amira A ANawar Sarah M - Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia characterized by PML::RARA fusion, typical morphology, and a characteristic flow cytometric immunophenotype that enables rapid diagnosis. However, immunophenotypic aberrancies may occur and can mimic mixed phenotype acute leukemia (MPAL), leading to diagnostic and therapeutic dilemmas. We report two adult male patients with APL confirmed by fluorescence in situ hybridization (FISH) demonstrating PML::RARA fusion. Both cases exhibited unusual immunophenotype. In the first case, peripheral blood flow cytometry revealed blasts with bright cMPO, CD34, dim HLA-DR, along with aberrant expression of CD19 (moderate), cCD79a (dim), cCD3 (heterogeneous), and CD7, raising a suspicion for MPAL. However, lineage defining criteria for T- and B-lineages were not fulfilled. Marrow showed abnormal promyelocytes with bundles of Auer rods, and molecular studies confirmed APL. In the second case, morphology suggested microgranular variant APL. Flow cytometry demonstrated aberrant expression of lymphoid and monocytic markers, including CD19 (dim), sCD3 (moderate), CD7, and CD14 (moderate), in addition to cMPO. Cytogenetics and molecular studies confirmed t(15;17)/PML::RARA in both cases, along with FLT3-ITD mutations. One patient developed differentiation syndrome and responded to all-trans-retinoic acid, while the follow-up of the second patient is unavailable. APL may exhibit immunophenotypic aberrancies mimicking MPAL. Molecular confirmation of PML::RARA and an integrated diagnostic approach are essential to avoid misclassification and ensure timely therapy. - Source: PubMed
Publication date: 2026/05/14
Prattipati Lumen AgarkarKar RakheeGupta Arvind KumarRonanki KavyaThangavel Prem Venkatt - Approximately half of newly diagnosed acute myeloid leukemia (AML) cases are cytogenetically normal (CN) when analyzed with conventional karyotyping. However, CN-AML exhibits a wide range of clinical heterogeneity, which may partly be explained by structural variants (SVs) that are not detected with current standard cytogenetic techniques. Here, 48 CN-AML cases were analyzed using optical genome mapping (OGM) for comprehensive SV assessment and to identify novel candidate gene alterations. Abnormalities were detected in 22 of 48 cases (46%). Large SVs, or those affecting leukemia-associated genes, were identified in 16 cases (33%), encompassing 18 abnormalities. Copy-neutral loss-of-heterozygosity regions were detected in seven cases (15%), and they were mutually exclusive with the presence of SVs in all but one case. SVs included eight deletions, six partial tandem duplications, two balanced translocations, and two complex rearrangements. The most frequently altered genes were KMT2A (5 cases) and RUNX1 (3 cases), followed by deletions of NF1 and the 13q14 (DLEU) region (2 cases each). Single alterations included NUP98::NSD1 and deletions of TET2, PRPF8, and FLT3. In addition, as a novel finding, we identified a balanced translocation t(3;20)(p13;q13.12) leading to a putative FOXP1::EYA2 fusion. Notably, the presence of OGM-detected abnormalities was associated with worse disease-specific survival (Mantel-Cox test, p = 0.007). Overall, this study demonstrates that a significant proportion of CN-AML cases harbor clinically relevant SVs, especially those associated with adverse prognosis, that escape detection by standard techniques. Our results support the use of OGM as a streamlined, genome-wide tool for both research and diagnostic applications in AML. - Source: PubMed
Publication date: 2026/05/14
Turtinen TuuniValkama AndrianaWray ChristopherVorimo SandraRäsänen HanneleSavolainen Eeva-RiittaPylkäs KatriMantere Tuomo