ArticleThe Journal of experimental medicine2019
CD97 is a critical regulator of acute myeloid leukemia stem cell function.
Article in The Journal of experimental medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Efferocytosis triggered proteomic reprogramming of macrophages reveals CD97 as a novel apoptotic receptor.Cell death and differentiation · 2026Article
- CD97/Cells · 2026Review
- Multi-Omics Integration Reveals That SN-011 Targets JUNB to Upregulate ADGRE5 and Restore Vascular Endothelial Cell Communication in Ischemic Stroke.Chemical biology & drug design · 2026Article
- T cell-engaging bispecific antibodies for myeloid malignancies: Targets, formats, and clinical challenges.Cell reports. Medicine · 2026Review
- From complexity to clarity: aging bone marrow niche in bone and blood regeneration and malignancy.Bone research · 2026Review
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Prognostic impact of CD123 overexpression on the outcome of pediatric acute myeloid leukemia.Frontiers in oncology · 2026Article
- Engineering antibody-drug conjugates targeting an adhesion GPCR, CD97.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- CD97-directed CAR-T cells with enhanced persistence eradicate acute myeloid leukemia in diverse xenograft models.Cell reports. Medicine · 2025Article
- Mechanosensitive adhesion G protein-coupled receptors: Insights from health and disease.Genes & diseases · 2025Review
- Flow cytometric detection of leukemic stem cells in Acute Myeloid Leukemia: current status and future directions.Frontiers in pharmacology · 2025Review
- CD97 maintains tumorigenicity of glioblastoma stem cells via mTORC2 signaling and is targeted by CAR Th9 cells.Cell reports. Medicine · 2024Article
- Plasma Proteomic Signature Predicts Myeloid Neoplasm Risk.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Construction of a Cuproptosis-Related Gene Signature for Predicting Prognosis in Gastric Cancer.Biochemical genetics · 2024Article
- Emerging and Future Targeted Therapies for Pediatric Acute Myeloid Leukemia: Targeting the Leukemia Stem Cells.Biomedicines · 2023Review
- The expression profile and tumorigenic mechanisms of CD97 (ADGRE5) in glioblastoma render it a targetable vulnerability.Cell reports · 2023Article
- Retained functional normal and preleukemic HSCs at diagnosis are associated with good prognosis in DNMT3AmutNPM1mut AMLs.Blood advances · 2023Article
- Role of Adhesion G Protein-Coupled Receptors in Immune Dysfunction and Disorder.International journal of molecular sciences · 2023Review
- Pathophysiological impact of the adhesion G protein-coupled receptor family.American journal of physiology. Cell physiology · 2022Review
- Leukotrienes promote stem cell self-renewal and chemoresistance in acute myeloid leukemia.Leukemia · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Despite significant efforts to improve therapies for acute myeloid leukemia (AML), clinical outcomes remain poor. Understanding the mechanisms that regulate the development and maintenance of leukemic stem cells (LSCs) is important to reveal new therapeutic opportunities. We have identified CD97, a member of the adhesion class of G protein-coupled receptors (GPCRs), as a frequently up-regulated antigen on AML blasts that is a critical regulator of blast function. High levels of CD97 correlate with poor prognosis, and silencing of CD97 reduces disease aggressiveness in vivo. These phenotypes are due to CD97's ability to promote proliferation, survival, and the maintenance of the undifferentiated state in leukemic blasts. Collectively, our data credential CD97 as a promising therapeutic target on LSCs in AML.
Indexed as
Identifiers
What OpenQuestion holds
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.