ReviewTherapeutic advances in hematology2021
Advances in therapeutic options for newly diagnosed, high-risk AML patients.
Review in Therapeutic advances in hematology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
12 citing papers in PubMed, 37 citations in OpenAlex.
- The role of SLC22A4 in Acute Myeloid Leukaemia.Mediterranean journal of hematology and infectious diseases · 2025Article
- Prognostic impact ofTherapeutic advances in hematology · 2024Article
- Literature review and expert opinion on the treatment of high-risk acute myeloid leukemia in patients who are eligible for intensive chemotherapy.Frontiers in oncology · 2024Review
- Granulocyte-Macrophage-Colony-Stimulating-Factor Combined with Prostaglandin E1 Create Dendritic Cells of Leukemic Origin from AML Patients' Whole Blood and Whole Bone Marrow That Mediate Antileukemic Processes after Mixed Lymphocyte Culture.International journal of molecular sciences · 2023Article
- Using published pathway figures in enrichment analysis and machine learning.BMC genomics · 2023Article
- Article
- Comprehensive bioinformatic analysis of the expression and prognostic significance of TSC22D domain family genes in adult acute myeloid leukemia.BMC medical genomics · 2023Article
- Bioinformatic analysis reveals the clinical value of SASH3 in survival prognosis and immune infiltration of acute myelocytic leukemia (AML).American journal of translational research · 2023Article
- Curcumin activates NLRC4, AIM2, and IFI16 inflammasomes and induces pyroptosis by up-regulated ISG3 transcript factor in acute myeloid leukemia cell lines.Cancer biology & therapy · 2022Article
- Super-enhancer profiling identifies novel critical and targetable cancer survival gene LYL1 in pediatric acute myeloid leukemia.Journal of experimental & clinical cancer research : CR · 2022Article
- BRD4 Inhibitor GNE-987 Exerts Anticancer Effects by Targeting Super-Enhancer-Related Gene LYL1 in Acute Myeloid Leukemia.Journal of immunology research · 2022Article
- CEBPG promotes acute myeloid leukemia progression by enhancing EIF4EBP1.Cancer cell international · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) is an aggressive malignancy characterized by clonal proliferation of neoplastic immature precursor cells. AML impacts older adults and has a poor prognosis. Despite recent advances in treatment, AML is complex, with both genetic and epigenetic aberrations in the malignant clone and elaborate interactions with its microenvironment. We are now able to stratify patients on the basis of specific clinical and molecular features in order to optimize individual treatment strategies. However, our understanding of the complex nature of these molecular abnormalities continues to expand the defining characteristics of high-risk mutations. In this review, we focus on genetic and microenvironmental factors in adverse risk AML that play critical roles in leukemogenesis, including those not described in an European LeukemiaNet adverse risk group, and describe therapies that are currently in the clinical arena, either approved or under development.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.