CD135 _ FLT3 pTyr591
- Known as:
- CD135 _ FLT3 pTyr591
- Catalog number:
- AP20941PU-N
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3 pTyr591
Related genes to: CD135 _ FLT3 pTyr591
- 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 pTyr591
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 pTyr591
- Quizartinib is a potent type II inhibitor of FMS-like tyrosine kinase 3 (FLT3) that demonstrated significant survival benefit among patients with newly diagnosed (ND) acute myeloid leukemia (AML) without -internal tandem duplication (-ITD) in the randomized, Phase II QUIWI trial. Here, we present the rationale and design of QuANTUM-Wild, a double-blind, randomized, placebo-controlled, Phase III study to confirm the efficacy and safety of quizartinib plus standard induction and consolidation chemotherapy and as maintenance monotherapy in adult patients with ND -ITD-negative AML. Eligible patients are randomized 2:2:1 to one of three treatment arms. Patients in Arm A (n ≈ 280) receive quizartinib plus chemotherapy during induction and consolidation (with option for transplant without study drug), followed by up to 36 cycles of single-agent maintenance therapy. Patients in Arm B (n ≈ 280) receive placebo in all treatment phases plus chemotherapy, then as maintenance monotherapy. Patients in Arm C (n ≈ 140) receive quizartinib plus chemotherapy in the induction and consolidation phases, then placebo during the maintenance phase, to specifically assess the utility of quizartinib maintenance. The primary endpoint is overall survival. Secondary endpoints include event-free survival, remission rate, and safety. http://www.clinicaltrials.gov identifier is NCT06578247. - Source: PubMed
Publication date: 2026/07/11
Montesinos PauAltman Jessica KBullinger LarsCheong June-WonFathi Amir TLevis Mark JLuger SelinaMiyamoto ToshihiroOliva Esther NataliePerl Alexander ERécher ChristianVeiga Rebeca RodriquezWang JianxiangZeidan Amer MLiu LiDuong YvonneRohrbach Jaime E ConnollyInghirami GiorgioAlexis KarenzaGosberg AndreasNahar AkashBurns KristyDaver NavalErba Harry P - A custom Genexus myeloid assay (CMA) underwent a technical evaluation for detection of variants from both DNA and RNA in a single assay format. The custom assay was initially verified with commercial DNA and RNA controls containing known myeloid variants. Seventy-five patient specimens with various DNA and RNA variants were selected for replicate testing. The CMA generated consistent data on two Genexus sequencers, with occasional samples failing quality metrics randomly. All 22 control DNA variants were detected, with 95% reported as key. Sensitivity and positive predictive value for clinical variants were 95.60% and 97.60%, rising to 98.63% and 99.65% for allele frequencies ≥5%. FLT3 duplications were consistently detected at lower expected frequencies. Low-level, false-positive key variants were mostly recurrent and filterable. Fusion calling sensitivity was 100% for control and clinical RNA samples, with 97.09% of replicates reporting expected fusions. The CMA reliably detects key DNA and RNA variants in myeloid specimens within 24 hours on the Genexus platform. Variants and fusion transcripts were identified with high sensitivity and minimal nucleic acid input, providing a rapid and precise workflow for reporting clinically relevant myeloid disease variants. - Source: PubMed
Publication date: 2026/07/10
Dina Michelle ABlommel Joseph HBalan JagadheshwarSankaranarayanan SaranyaBurke Jennifer ESedova MarinaJianjun JimJerde Calvin RHenry Justin NVoss Jesse SKlee Eric WKipp Benjamin RSherlock JonSadis SethViswanatha David SMurphy Stephen J - TP53 mutations confer poor prognosis in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Inconsistent definitions of TP53 allelic status and limited access to routine testing impede accurate prognostic risk stratification for this high-risk myeloid population. This multicenter retrospective cohort study analyzed 303 patients with TP53-mutated AML/MDS undergoing allo-HSCT to evaluate the prognostic impact of co-occurring somatic genetic alterations. After a median follow-up of 25 months, the 3-year overall survival (OS), progression-free survival (PFS), cumulative incidence of relapse (CIR), and non-relapse mortality (NRM) rates were 55%, 46.9%, 35.9%, and 17.1%, respectively. Multivariate analysis confirmed complex karyotype (CK) as an independent adverse prognostic factor for both OS and PFS. Among 137 patients with available TP53 allelic data (45.2%), no statistically significant survival differences were observed between monoallelic (single-hit) and multiallelic (multi-hit) cases (OS: HR=0.727, 95% CI 0.405-1.307, P=0.287; PFS: HR=0.787, 95% CI 0.466-1.328, P=0.370), though statistical power was limited. In AML, pre-transplant complete remission (CR) improved OS, and specific concurrent genetic alterations (SCGAs: CBF fusions, NPM1, FLT3-ITD, CEBPA mutations) conferred favorable outcomes. Combined CK and SCGA status stratified AML into a three-tier prognostic model. In MDS, co-occurring myeloid mutations improved PFS; absence of co-mutations or presence of CK was associated with poor prognosis, supporting a two-tier risk framework. This Chinese Blood and Marrow Transplantation Registry Group (CBMTG) study presents an exploratory prognostic model integrating co-occurring genetic alterations, enabling feasible risk stratification for TP53-mutated AML/MDS transplant patients without comprehensive TP53 molecular profiling. - Source: PubMed
Publication date: 2026/07/10
Sun YaoLiu JingChen JiaXuan LiLiu JiaFan Meng-LinLu Sheng-YeXu Lan-PingZhang XiLiu Qi-FaWu De-PeiHuang Xiao-JunLiu Dai-Hong - Left-sided colon-cancer (LCC) and right-sided colon cancer (RCC) harbor different clinical entities and different therapy protocols. Our study aimed to demonstrate genomic expression differences and clarify the clinical differences between LCC and RCC by using in-silico methods. - Source: PubMed
Publication date: 2026/07/10
Solak Hatice CilemMert NazliLeblebici AsimIsik ZerrinEllidokuz Ender BeratBasbinar Yasemin - - Source: PubMed
Zwick MelissaKöhler Natalie