CD135 _ FLT3 Control Peptide
- Known as:
- CD135 _ FLT3 Control Peptide
- Catalog number:
- AP14352CP-N
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- CD135 _ FLT3 Control Peptide
Related genes to: CD135 _ FLT3 Control Peptide
- 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 Control Peptide
Related articles to: CD135 _ FLT3 Control Peptide
- 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 - Acute myeloid leukemia (AML) remains difficult to treat because profound molecular heterogeneity enables rapid adaptive resistance to targeted therapy. We developed an AI-driven pharmacogenomic pipeline that integrates genomic, transcriptomic, epigenetic, and clinical features to predict patient-specific response to venetoclax and translate resistance-associated signals into actionable therapeutic hypotheses. Across internal and external cohorts, the deep learning model showed strong discrimination and generalization (AUROC 0.84-0.90), produced calibrated probabilities, and stratified overall survival independent of standard prognostic factors. Explainable modeling (SHAP) identified mechanistically coherent drivers of sensitivity and resistance: high BCL2 and apoptotic priming favored response, whereas MCL1 upregulation, TP53 disruption, and RAS/MAPK activation were dominant resistance programs. Translating these findings into therapy design, network-based modeling and in silico perturbation prioritized rational combinations expected to block escape routes, including venetoclax plus MCL1 inhibition (e.g., AZD5991-class inhibitors), venetoclax plus FLT3 inhibition (e.g., gilteritinib-class agents) in signaling-driven disease, and venetoclax plus p53-axis modulation (e.g., MDM2 inhibition) in TP53-altered contexts. Structural candidate evaluation using ensemble docking provided supportive drug-target interaction evidence for prioritized dependencies. Together, these results establish a clinically interpretable, resistance-aware AI framework for precision optimization of venetoclax-based combination therapy in AML. - Source: PubMed
Publication date: 2026/09/10
Wang ChenYou ZhijieChen SiqiHe YihuiChen XinQu ShuangChen XinJiang Sicong - Fms-like tyrosine kinase 3 (FLT3), a member of the type III receptor tyrosine kinase family, is identified as a promising drug target for treatment of acute myeloid leukemia (AML). Here, we designed and synthesized a series of new FLT3 PROTAC degraders by incorporating rigid linkers between gilteritinib and CRBN ligand. Among them, ZLC6-49 and ZLC10-3 were identified as the most potent degraders with DC values of 0.74 nM and 1.28 nM, and D values of 85% and 88%, respectively. Mechanistic studies demonstrated that ZLC6-49 and ZLC10-3 induce FLT3 degradation in a cereblon- and proteasome-dependent manner. Furthermore, ZLC6-49 and ZLC10-3 potently inhibit FLT3 downstream signaling, suppress cell proliferation, induce apoptosis and G0/G1-phase arrest in MV4-11 cells. - Source: PubMed
Publication date: 2026/09/19
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