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1d
Gentulizumab in Relapsed/Refractory Acute Myelogenous Leukemia or Myelodysplastic Syndrome (clinicaltrials.gov)
P1, N=58, Terminated, Changchun GeneScience Pharmaceutical Co., Ltd. | Recruiting --> Terminated; Adjusted the product development strategy.
Trial termination
1d
A Collaborative Palliative and Leukemia Care Model for Patients With AML and MDS Receiving Non-Intensive Therapy (clinicaltrials.gov)
P=N/A, N=320, Active, not recruiting, Massachusetts General Hospital | Trial completion date: Dec 2025 --> Dec 2026
Trial completion date
1d
Geriatric Optimization Plan to Improve Survival in Older Adult Allogeneic Hematopoietic Cell Transplant Candidates, OTIS Study (clinicaltrials.gov)
P=N/A, N=30, Completed, Ohio State University Comprehensive Cancer Center | Active, not recruiting --> Completed
Trial completion
2d
New P1 trial
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TP53 (Tumor protein P53)
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TP53 mutation • TP53 deletion
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Venclexta (venetoclax) • decitabine • Niktimvo (axatilimab-csfr)
2d
New P2 trial
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Venclexta (venetoclax) • cytarabine • azacitidine
2d
The ASH HematOmics Program supports integrative analysis of genomic and clinical data in hematologic diseases. (PubMed, Blood)
We illustrate four use cases of ASHOP: (1) stratification of DUX4-rearranged B-cell leukemias into Early/Multipotent and Committed subgroups with distinct outcomes, (2) characterization of HOXA/HOXB expression patterns in acute myeloid leukemias, (3) correlating mutational burden with mismatch repair deficiency and mutational signatures, (4) investigation of TP53 alteration landscape. ASHOP is an open-access resource to inform genomic and transcriptomic data interpretation for hematologic malignancies, and will expand to support additional diseases and data modalities from the ASH community.
Clinical data • Journal • Tumor mutational burden
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TP53 (Tumor protein P53) • TMB (Tumor Mutational Burden) • DUX4 (Double Homeobox 4)
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TP53 mutation
2d
Amlodipine Targeting SPINK1 Attenuates Lung Cancer Cell Growth and Proliferation Through Glycolytic Metabolism. (PubMed, Anticancer Agents Med Chem)
The present study suggests that SPINK1 may modulate glycolytic metabolism in lung cancer cells, inhibiting their growth and proliferation, and potentially providing therapeutic insights.
Journal • IO biomarker
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BCL2 (B-cell CLL/lymphoma 2) • CCND1 (Cyclin D1) • CCNE1 (Cyclin E1) • CDK1 (Cyclin-dependent kinase 1) • SPINK1 (Serine peptidase inhibitor, kazal type 1)
2d
Unraveling the role of TP53 mutations in myeloproliferative neoplasms: Molecular mechanisms of leukemic transformation. (PubMed, Hemasphere)
Additionally, we explore the mechanisms underlying TP53 mutations in the leukemic transformation of MPNs, including clonal evolution to multihit status and the role of inflammation and therapy. Finally, recent findings on the clinical impact of multihit TP53 mutations and potential strategies for targeting the p53 pathway in MPNs and sAML are presented.
Review • Journal
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TP53 (Tumor protein P53)
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TP53 mutation
2d
Reduced STAG2 expression in myelodysplastic neoplasms and acute myeloid leukemia myelodysplasia-related: a potential biomarker associated with aneuploidy and disease progression. (PubMed, Front Cell Dev Biol)
Our findings suggest that reduced STAG2 protein expression plays a relevant role in MDS pathogenesis. Immunohistochemical assessment of STAG2 may be incorporated into the clinical workflows as a potential diagnostic and prognostic biomarker, as well as indicate therapeutic targets, particularly in association with complex karyotypes and trisomy 8.
Journal
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STAG2 (Stromal Antigen 2)
2d
IDH1 mutation creates a dependency on fatty acid metabolism that underlies sensitivity to cuproptosis in acute myeloid leukemia cells. (PubMed, Int J Med Sci)
In this study, we demonstrate that IDH1-mutant AML cells are markedly more sensitive to cuproptosis induced by the copper ionophore elesclomol (ES), compared to their wild-type counterparts...In vivo experiments confirm that ES more effectively suppresses tumor growth in IDH1-mutant xenografts. These findings uncover a copper-dependent metabolic vulnerability and provide a rationale for exploiting cuproptosis as a therapeutic strategy in IDH1-mutant AML.
Journal
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IDH1 (Isocitrate dehydrogenase (NADP(+)) 1)
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IDH1 mutation
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elesclomol (STA-4783)