ArticleThe Journal of clinical investigation2016
SLAMF1 regulation of chemotaxis and autophagy determines CLL patient response.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.
- Identification of 4 autophagy-related genetic variants as risk factors for chronic lymphocytic leukemia.Blood advances · 2025Pooled it
- PGE2 displays immunosuppressive effects during human active tuberculosis.Scientific reports · 2021Trial
- The Anti-SLAMF7 Antibody, Elotuzumab, Induces Antibody-Dependent Cellular Cytotoxicity Against CLL Cell Lines.Molecules (Basel, Switzerland) · 2026Article
- Radiation-induced SLAMF1 reconfigures the SLAM family receptors landscape in triple-negative breast cancer cells.Journal of Cancer · 2026Article
- SLAMF receptors: key regulators of tumor progression and emerging targets for cancer immunotherapy.Molecular cancer · 2025Review
- Crosstalk Between Autophagy and Oxidative Stress in Hematological Malignancies: Mechanisms, Implications, and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2025Review
- SLAM Family Receptors in B Cell Chronic Lymphoproliferative Disorders.International journal of molecular sciences · 2024Review
- CD44: a cancer stem cell marker and therapeutic target in leukemia treatment.Frontiers in immunology · 2024Review
- The role of CD180 in hematological malignancies and inflammatory disorders.Molecular medicine (Cambridge, Mass.) · 2023Review
- Identification of molecular subtypes of ischaemic stroke based on immune-related genes and weighted co-expression network analysis.IET systems biology · 2023Article
- SLAM-family receptors come of age as a potential molecular target in cancer immunotherapy.Frontiers in immunology · 2023Review
- Autophagy in Hematological Malignancies.Cancers · 2022Review
- Identification and Validation of Immune Molecular Subtypes and Immune Landscape Based on Colon Cancer Cohort.Frontiers in medicine · 2022Article
- Super-Enhancer-Associated nine-gene prognostic score model for prediction of survival in chronic lymphocytic leukemia patients.Frontiers in genetics · 2022Article
- Article
- Construction of a ceRNA network of hub genes affecting immune infiltration in ovarian cancer identified by WGCNA.BMC cancer · 2021Article
- Autophagy and Metabolism in Normal and Malignant Hematopoiesis.International journal of molecular sciences · 2021Review
- HELQ and EGR3 expression correlate with IGHV mutation status and prognosis in chronic lymphocytic leukemia.Journal of translational medicine · 2021Article
- SLAMF1 Promotes Methotrexate Resistance via Activating Autophagy in Choriocarcinoma Cells.Cancer management and research · 2020Article
- Increased Expression of Autophagy Protein LC3 in Two Patients With Progressing Chronic Lymphocytic Leukemia.Frontiers in endocrinology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic lymphocytic leukemia (CLL) is a variable disease; therefore, markers to identify aggressive forms are essential for patient management. Here, we have shown that expression of the costimulatory molecule and microbial sensor SLAMF1 (also known as CD150) is lost in a subset of patients with an aggressive CLL that associates with a shorter time to first treatment and reduced overall survival. SLAMF1 silencing in CLL-like Mec-1 cells, which constitutively express SLAMF1, modulated pathways related to cell migration, cytoskeletal organization, and intracellular vesicle formation and recirculation. SLAMF1 deficiency associated with increased expression of CXCR4, CD38, and CD44, thereby positively affecting chemotactic responses to CXCL12. SLAMF1 ligation with an agonistic monoclonal antibody increased ROS accumulation and induced phosphorylation of p38, JNK1/2, and BCL2, thereby promoting the autophagic flux. Beclin1 dissociated from BCL2 in response to SLAMF1 ligation, resulting in formation of the autophagy macrocomplex, which contains SLAMF1, beclin1, and the enzyme VPS34. Accordingly, SLAMF1-silenced cells or SLAMF1(lo) primary CLL cells were resistant to autophagy-activating therapeutic agents, such as fludarabine and the BCL2 homology domain 3 mimetic ABT-737. Together, these results indicate that loss of SLAMF1 expression in CLL modulates genetic pathways that regulate chemotaxis and autophagy and that potentially affect drug responses, and suggest that these effects underlie unfavorable clinical outcome experienced by SLAMF1(lo) patients.
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.