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AKT inhibitor Hu7691 induces differentiation of neuroblastoma cells

This study defines the key role of AKT in the progression of neuroblastoma differentiation but also provides potential drugs and key targets for the application of differentiation therapies for Neuroblastoma clinically and confirms the therapeutic effects of Hu7691.
PubMed (opens in a new tab)

Blockade of deubiquitinase YOD1 degrades oncogenic PML/RARα and eradicates acute promyelocytic leukemia cells

This study reveals the DUB-involved regulatory mechanism on PML/RARα stability and validates YOD1 as a potential therapeutic target for APL, but also identifies G5 as a Y OD1 inhibitor and a promising candidate for APl, particularly drug-resistant APL treatment.
PubMed (opens in a new tab)

Discovery of Novel Oxazepine Derivatives as Akt/ROCK Inhibitors for Growth Arrest and Differentiation Induction in Neuroblastoma Treatment.

The synergistic effect of inhibiting Akt and ROCK in antineuroblastoma is demonstrated and the design and discovery of a new Akt/ROCK inhibitor, B12 is presented, which displays strong antiproliferative effects and excellent differentiation inducing activity against Neuro2a cells.
PubMed (opens in a new tab)

Succinate dehydrogenase deficiency-driven succinate accumulation induces drug resistance in acute myeloid leukemia via ubiquitin-cullin regulation

It is shown that succinate accumulation, associated with succinate dehydrogenase deficiency, impairs the activity of the ubiquitin-conjugating enzyme UBC12 leading to tumor-promoting protein accumulation and drug resistance in AML.
Springer Nature (opens in a new tab)

Targeting Cul3-scaffold E3 ligase complex via KLHL substrate adaptors for cancer therapy.

These findings reveal multiple potential therapeutical targets and provide evidence for targeting CRL3 via KLHL substrate adaptors for cancer therapy and clarify the novel biological function of KLHL13 as a vital factor that contributes to malignant progression in lung cancer.
PubMed (opens in a new tab)

Disruption of the KLHL37–N-Myc complex restores N-Myc degradation and arrests neuroblastoma growth in mouse models

It is discovered that Kelch-like protein 37 (KLHL37) played a crucial role in enhancing the protein stability of N-Myc in neuroblastoma and indicates that KLHL37 inhibition is a promising therapeutic regimen for neuroblastoma, especially in patients with MYCN-amplified tumors.
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A novel gene fusion RUNX1/ZNF423 promotes leukemic relapse of NUP98-rearranged AML

Although the molecular process involving in NUP98 -fusion-driven leukemogenesis has been uncovered, the lack of molecular biomarkers predicting further disease progression and outcome impeded the development of precise diagnosis and therapeutic for NUP 98 - rearranged AML subgroup.
Springer Nature (opens in a new tab)

Chromosomal rearrangement-enhanced mRNA stability drives the oncogenic potential of fusion genes in pediatric leukemia.

It is demonstrated that enhanced mRNA stability represents an important tumorigenic mechanism for oncogenic fusions, including classical PAX5 fusions, and proposed venetoclax as an innovative and clinically available therapy for ALL driven by these oncogenic fusions characterized by high mRNA stability.
PubMed (opens in a new tab)
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