Acute Myelogenous Leukemia
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  • ||||||||||  sepantronium bromide (PC-002) / Cothera Biosci, ONC212 / Chimerix, hydroquinone / Generic mfg.
    Journal:  ONC212 enhances YM155 cytotoxicity by triggering SLC35F2 expression and NOXA-dependent MCL1 degradation in acute myeloid leukemia cells. (Pubmed Central) -  May 19, 2024   
    The continuous treatment of U937 cells with the benzene metabolite hydroquinone (HQ) generated U937/HQ cells, exhibiting enhanced responsiveness to the cytotoxic effects of ONC212...Collectively, our data suggested that ONC212 upregulated SLC35F2 expression and triggered NOXA-mediated MCL1 degradation in U937, U937/HQ, and HL-60 cells by activating the AKT/NOX4/HuR/ATF4 pathway. The ONC212-induced signaling pathway showed anti-AML activity and enhanced YM155 cytotoxicity.
  • ||||||||||  Journal:  Leukemia Cutis in Relapsed Acute Myeloid Leukemia: A Call for Distinct Classification. (Pubmed Central) -  May 18, 2024   
    Consequently, it can be deduced that patients who simultaneously have relapsed acute myeloid leukemia and leukemia cutis are expected to fare worse in terms of clinical outcomes than those with primary acute myeloid leukemia and leukemia cutis. Relapsed acute myeloid leukemia patients with leukemia cutis should be classified as a distinct group, warranting further research into aggressive therapeutic targets and survival rates, while emphasizing the need for more vigilant follow-up and lower biopsy thresholds for cutaneous lesions in patients with treated hematologic malignancies.
  • ||||||||||  cytarabine / Generic mfg.
    Biomarker, Clinical, Journal:  Pharmacogenomics, Race, and Treatment Outcome in Pediatric Acute Myeloid Leukemia. (Pubmed Central) -  May 16, 2024   
    Patients in AML02 were randomly assigned to receive standard low-dose cytarabine-based induction therapy or augmented high-dose cytarabine-based induction therapy, whereas patients in AML08 received high-dose cytarabine-based therapy...When accounting for ACS10 scores, no outcome disparities were seen between Black and White patients. Our results suggest that using pharmacogenomics parameters to tailor induction regimens for both Black and White patients may narrow the racial disparity gap in patients with AML.
  • ||||||||||  Trial completion, Trial completion date:  A Study of FMT in Patients With AML Allo HSCT in Recipients (clinicaltrials.gov) -  May 16, 2024   
    P2,  N=100, Completed, 
    These findings highlight the FHD-286-based combinations as promising therapy of AML with MLL1r or mtNPM1. Active, not recruiting --> Completed | Trial completion date: Jan 2025 --> Dec 2023
  • ||||||||||  Biomarker, Journal:  circRNAs as prognostic markers in pediatric acute myeloid leukemia. (Pubmed Central) -  May 15, 2024   
    Through the integration of drug sensitivity data, we pinpointed 25 drugs that could target high-risk AMLs characterized by aberrant circRNA transcription. These findings underscore prognostic significance of circRNAs in pediatric AML and offer an alternative perspective for treating high-risk cases in this malignancy.
  • ||||||||||  Journal:  Crenolanib and Intensive Chemotherapy in Adults With Newly Diagnosed FLT3-Mutated AML. (Pubmed Central) -  May 15, 2024   
    Crenolanib plus intensive chemotherapy in adults with newly diagnosed FLT3-mutant AML results in high rate of deep responses and long-term survival with acceptable toxicity. A randomized trial of crenolanib versus midostaurin plus chemotherapy in younger patients is ongoing.
  • ||||||||||  Xospata (gilteritinib) / Astellas, Rydapt (midostaurin) / Novartis, Vanflyta (quizartinib) / Daiichi Sankyo
    Review, Journal, Combination therapy:  The potential of triplet combination therapies for patients with FLT3-ITD -mutated acute myeloid leukemia. (Pubmed Central) -  May 15, 2024   
    In addition, the review discusses the emergence of drug resistance and the need for a nuanced approaches in treating patients who are ineligible for or resistant to intensive chemotherapy. Specifically, it explores the historical context of FLT3 inhibitors (FLT3Is) and their impact on treatment outcomes, emphasizing the pivotal role of midostaurin, as well as gilteritinib and quizartinib, and providing detailed insights into ongoing trials exploring the safety and efficacy of novel triplet combinations involving FLT3Is in different AML settings.
  • ||||||||||  Journal:  BATF promotes extramedullary infiltration through TGF-?1/Smad/MMPs axis in acute myeloid leukemia. (Pubmed Central) -  May 15, 2024   
    Notably, our observations validated that BATF is bound to the promoter region of TGF-?1, which could transcriptionally enhance the expression of TGF-?1 and activate the TGF-?1/Smad/MMPs signaling pathway. In summary, our study established the aberrantly high expression of BATF and its pro-migratory function via the TGF-?1-Smad2/3-MMP2/9 axis in AML, which provides novel insights into extramedullary infiltration of AML.
  • ||||||||||  Biomarker, Journal:  Stellae-123 gene expression signature improved risk stratification in taiwanese acute myeloid leukemia patients. (Pubmed Central) -  May 15, 2024   
    We further show that incorporating age, Stellae-123, and ELN classification remarkably improves risk stratification, revealing c-indices of 0.73 and 0.728 for OS and RFS, respectively. In summary, the Stellae-123 gene expression signature is a valuable prognostic tool for AML patients and model retraining can improve the accuracy and applicability of the model in different populations.
  • ||||||||||  triciribine phosphate (PTX-200) / VioQuest, Prescient Therap
    Journal:  Identification of triciribine as a novel myeloid cell differentiation inducer. (Pubmed Central) -  May 15, 2024   
    Real-time PCR analysis demonstrated that components of these pathways including IL1?, CD3D, IL5RA, ITGA6, CD44, ITGA2B, CD37, CD9, CSF2RA, and IL3RA, were upregulated by TCN-induced differentiation. Collectively, we identified TCN as a novel myeloid cell differentiation inducer, and trials of TCN for APL and non-APL leukemia are worthy of exploration in the future.
  • ||||||||||  pulrodemstat (CC-90011) / BMS, iadademstat (ORY-1001) / Oryzon, seclidemstat (SP2577) / Salarius
    Journal, Epigenetic controller:  Anticancer Drugs of Lysine Specific Histone Demethylase-1 (LSD1) Display Variable Inhibition on Nucleosome Substrates. (Pubmed Central) -  May 15, 2024   
    These data show that SP-2577 is not an LSD1 enzyme inhibitor, although the drug may function independent of demethylation due to its cytotoxic selectivity in TC-32 cells. Taken together, this work highlights the pitfalls of using coupled assays to ascribe a drug's mode of action, emphasizes the use of physiologically relevant substrates in epigenetic drug targeting strategies, and provides insight into the development of substrate-selective inhibitors of LSD1.
  • ||||||||||  Journal, IO biomarker:  Putting the STING back into BH3-mimetic drugs for TP53-mutant blood cancers. (Pubmed Central) -  May 15, 2024   
    Combining clinically relevant STING agonists with BH3-mimetic drugs efficiently kills TRP53/TP53-mutant mouse B lymphoma, human NK/T lymphoma, and acute myeloid leukemia cells. This represents a promising therapy regime that can be fast-tracked to tackle TP53-mutant blood cancers in the clinic.
  • ||||||||||  Preclinical, Journal:  Bahcc1 is critical for the aberrant epigenetic program in a mouse model of MLL-ENL-mediated leukemia. (Pubmed Central) -  May 15, 2024   
    In a public database, high BAHCC1 expression was associated with a poor prognosis in pediatric AML, in which BAHCC1 expression was significantly lower in MLL-AF9-AML than in other MLL-fusion-AML. These findings shed light on the distinct immortalization potential of HSPCs and suggest a novel MLL-fusion-Bahcc1 axis, which may lead to development of molecular targeted therapy against MLL-fusion-mediated leukemia.
  • ||||||||||  Mekinist (trametinib) / Novartis, BeiGene
    Journal:  Targeting CCL2/CCR2 signaling overcomes MEK inhibitor resistance in Acute Myeloid Leukemia. (Pubmed Central) -  May 15, 2024   
    Our study demonstrates a compelling rationale for translating CCL2/CCR2 axis inhibitors in combination with MEK pathway-targeting therapies, as a potent strategy for combating drug resistance in AML. This approach has the potential to enhance the efficacy of treatments to improve AML patient outcomes.
  • ||||||||||  Journal:  Dual-targeting CD33/CD123 NANOBODY (Pubmed Central) -  May 15, 2024   
    Depletion of CD123 and CD33 expressing cells was observed, without signs of cytokine release syndrome nor clinical signs of toxicity. Taken together, the CD33/CD123 dual-targeting NANOBODY
  • ||||||||||  Venclexta (venetoclax) / Roche, AbbVie
    Journal, IO biomarker:  The RTK-RAS signaling pathway is enriched in patients with rare acute myeloid leukemia harboring t(16;21)(p11;q22)/FUS::ERG. (Pubmed Central) -  May 14, 2024   
    Transcriptome analysis revealed enrichment of the phosphatidylinositol-3-kinase-Akt (PI3K-Akt), mitogen-activated protein kinase (MAPK), and RAS signaling pathways and upregulation of BCL2, the target of venetoclax, in FUS::ERG AML compared to RUNX1::RUNX1T1 AML, a more common AML subtype with good prognosis...Allogeneic hematopoietic stem cell transplantation failed to improve outcomes. Overall, the high incidence of RTK-RAS pathway mutations and high expression of BCL2 may indicate promising therapeutic targets in this high-risk AML subset.
  • ||||||||||  Onureg (azacitidine oral) / BMS
    Enrollment closed, Trial primary completion date:  AMADEUS: Randomised Study of Oral Azacitidine vs Placebo Maintenance in AML or MDS Patients After Allo-SCT (clinicaltrials.gov) -  May 14, 2024   
    P3,  N=326, Active, not recruiting, 
    Overall, the high incidence of RTK-RAS pathway mutations and high expression of BCL2 may indicate promising therapeutic targets in this high-risk AML subset. Recruiting --> Active, not recruiting | Trial primary completion date: Apr 2024 --> Apr 2025
  • ||||||||||  HYML-122 / Tarapeutics Science, Youyuan Pharma
    Trial completion date, Trial primary completion date:  A Study of HYML-122 in Patients With FLT3 Positive Relapsed or Refractory Acute Myeloid Leukemia (AML) (clinicaltrials.gov) -  May 14, 2024   
    P2,  N=15, Recruiting, 
    Recruiting --> Active, not recruiting | Trial primary completion date: Apr 2024 --> Apr 2025 Trial completion date: Jun 2024 --> Jun 2026 | Trial primary completion date: Mar 2024 --> Dec 2025