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1d
BCOR mutations define a therapeutic vulnerability to DHODH Inhibition in acute myeloid leukemia. (PubMed, Ann Hematol)
We demonstrate that BCOR-deficient cells have a heightened sensitivity to DHODH inhibitors such as brequinar and leflunomide, that are already in clinical use. Rather, DHODH's role in the electron transport chain, essential for mitigating reactive oxygen species, may be the physiological vulnerability that pushes BCOR-mutant cells toward cell death when DHODH is inhibited. DHODH inhibitors could be repurposed as targeted therapies for BCOR-mutant tumors, offering a promising strategy for precision medicine in AML and other cancers.
Journal
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BCL6 (B-cell CLL/lymphoma 6) • BCOR (BCL6 Corepressor)
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brequinar (DUP 785) • leflunomide
3d
New trial
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Orca-T
3d
The contribution of the membrane-bound complement regulatory proteins CD46 and CD55 in phases of acute lymphocytic leukemia and acute myelogenous leukemia. (PubMed, Sci Rep)
Flow cytometric analysis conducted for proteomic expression of CD46 and CD55 on cell surfaces of leukemia patients showed a reduction in expression by 1.2-fold and 2.8-fold in AML patients, respectively. Post transcriptional knockdown of both genes in leukemic cell model using customized shRNA, followed by cell viability assays showed a significant reduction in the viability of cells by 3-fold, suggesting that although the expression of both proteins could be compromised by cancerous cells to evade complement attack mechanisms, they could also be vital to the viability of cancerous cells suggesting a dual role of complement in the tumor microenvironment.
Journal
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CD55 (CD55 Molecule) • CD46 (CD46 Molecule)
3d
A Study of JNJ-89853413 for Relapsed or Refractory Acute Myeloid Leukemia or Myelodysplastic Neoplasms (clinicaltrials.gov)
P1, N=100, Recruiting, Janssen Research & Development, LLC | Trial completion date: Aug 2028 --> Jan 2028
Trial completion date • First-in-human
3d
New P1 trial
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CD8 (cluster of differentiation 8) • CD4 (CD4 Molecule)
3d
DR-18 for the Treatment of Relapsed or Persistent Acute Myeloid Leukemia or Myelodysplastic Syndrome After Hematopoietic Cell Transplantation, the DR. DREAM Trial (clinicaltrials.gov)
P1, N=20, Recruiting, Fred Hutchinson Cancer Center | Trial completion date: Oct 2027 --> Oct 2028 | Trial primary completion date: Oct 2026 --> Oct 2027
Trial completion date • Trial primary completion date
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HLA-B (Major Histocompatibility Complex, Class I, B) • HLA-C (Major Histocompatibility Complex, Class I, C)
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vevoctadekin (ST-067)
3d
Venetoclax in Combination With Intensive Induction and Consolidation Chemotherapy in Treatment Naïve AML (clinicaltrials.gov)
P1, N=50, Active, not recruiting, Dana-Farber Cancer Institute | Recruiting --> Active, not recruiting | Trial primary completion date: Dec 2025 --> Feb 2025
Enrollment closed • Trial primary completion date
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Venclexta (venetoclax) • cytarabine • daunorubicin
3d
Comparison of Three Procedures for Cytochemical Detection of Leukocyte Alkaline Phosphatase Activity in Dogs With Leukemia. (PubMed, Vet Clin Pathol)
Our results indicate that the three procedures can be used interchangeably for determining ALP activity in blasts of dogs with leukemia.
Clinical • Journal
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MPO (Myeloperoxidase)
3d
CSF1R marks a subset of foetal haematopoietic multipotent progenitor cells with acute myeloid leukaemia propagation properties. (PubMed, Leukemia)
Finally, CSF1R inhibition on a KMT2A::MLLT3+ paediatric leukaemia cell line resulted in significant cell death, suggesting that CSF1R could be therapeutically targeted in these patients. Our findings suggest that KMT2A::MLLT3+ infant AML may originate from foetal liver CSF1R+ LMPPs, and that these patients may benefit from anti-CSF1R-CAR-T cell therapy.
Journal • IO biomarker
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KMT2A (Lysine Methyltransferase 2A) • CSF1R (Colony stimulating factor 1 receptor) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
3d
Lycorine inhibits the proliferation of acute myeloid leukemia cells by upregulating the expression of THBS1. (PubMed, Ann Hematol)
Therefore, it has antileukemic actions. One of the main targets for anti-AML treatment is THBS1.
Journal
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THBS1 (Thrombospondin 1)