ArticleBlood science (Baltimore, Md.)2019
Molecular mechanisms for stemness maintenance of acute myeloid leukemia stem cells.
Article in Blood science (Baltimore, Md.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- KLF4/MLL3 complex axis drives NRBP2 transcription to eliminate acute myeloid leukemia cells.Leukemia · 2026Article
- Evolving landscape of targeted immunotherapeutic interventions and CAR-T therapy for acute myeloid leukemia.NPJ precision oncology · 2026Review
- Differentiation therapy in acute myeloid leukaemia: molecular basis, clinical progress, and future perspectives.Frontiers in medicine · 2026Review
- Reprogramming of RNA m6A Modification Is Required for Acute Myeloid Leukemia Development.Genomics, proteomics & bioinformatics · 2025Article
- ICAT mediates the inhibition of stemness and tumorigenesis in acute myeloid leukemia cells induced by 1,25-(OH)Oncology research · 2025Article
- The Ubiquitin-Conjugating Enzyme E2 O (UBE2O) and Its Therapeutic Potential in Human Leukemias and Solid Tumors.Cancers · 2024Review
- A stem cell epigenome is associated with primary nonresponse to CD19 CAR T cells in pediatric acute lymphoblastic leukemia.Blood advances · 2023Article
- Sox13 and M2-like leukemia-associated macrophages contribute to endogenous IL-34 caused accelerated progression of acute myeloid leukemia.Cell death & disease · 2023Article
- Review
- Interplay between endoplasmic reticulum stress and non-coding RNAs in cancer.Journal of hematology & oncology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human acute myeloid leukemia (AML) is a fatal hematologic malignancy characterized with accumulation of myeloid blasts and differentiation arrest. The development of AML is associated with a serial of genetic and epigenetic alterations mainly occurred in hematopoietic stem and progenitor cells (HSPCs), which change HSPC state at the molecular and cellular levels and transform them into leukemia stem cells (LSCs). LSCs play critical roles in leukemia initiation, progression, and relapse, and need to be eradicated to achieve a cure in clinic. Key to successfully targeting LSCs is to fully understand the unique cellular and molecular mechanisms for maintaining their stemness. Here, we discuss LSCs in AML with a focus on identification of unique biological features of these stem cells to decipher the molecular mechanisms of LSC maintenance.
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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.