Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.
2 · The registry
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.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
15 authors.
He-Zhou GuoShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0001-6405-396X
Zi-Hua GuoShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-4192-7713
Shan-He YuShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-0268-7374
Li-Ting NiuShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-6987-3585
Wan-Ting QiangShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-4308-166X
Meng-Meng HuangShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0003-2765-3530
Yuan-Yuan TianFels Institute, Department of Microbiology and Immunology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.
Juan ChenShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.
Hui YangShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.
Xiang-Qin WengShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.
Yi ZhangFels Institute, Department of Microbiology and Immunology, Lewis Katz School of Medicine, Temple University, Philadelphia, PA 19140, USA.ORCID 0000-0002-3456-2728
Wu ZhangShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.
Shao-Yan HuDepartment of Hematology and Oncology, Children's Hospital of Soochow University, No 92, Zhongnan Street, Suzhou 215025, China.ORCID 0000-0002-3386-6957
Jun ShiDepartment of Hematology, Shanghai Ninth People's Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai 200011, China.ORCID 0000-0003-0780-5242
Jiang ZhuShanghai Institute of Hematology and State Key Laboratory of Medical Genomics, National Research Center for Translational Medicine (Shanghai), Collaborative Innovation Center of Hematology, Ruijin Hospital affiliated with Shanghai Jiao-Tong University School of Medicine, Shanghai 200025, China.ORCID 0000-0002-2976-1175
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
Chemotherapy can effectively reduce the leukemic burden and restore immune cell production in most acute myeloid leukemia (AML) cases. Nevertheless, endogenous immunosurveillance usually fails to recover after chemotherapy, permitting relapse. The underlying mechanisms of this therapeutic failure have remained poorly understood. Here, we show that abnormal IL-36 production activated by NF-κB is an essential feature of mouse and human leukemic progenitor cells (LPs). Mechanistically, IL-36 directly activates inflammatory monocytes (IMs) in bone marrow, which then precludes clearance of leukemia mediated by CD8
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.
Leukemic progenitor cells enable immunosuppression and post-chemotherapy relapse via IL-36-inflammatory monocyte axis. · full record | OpenQuestion