Article in British journal of haematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
0numbers the graph read from it
0cells of the map it votes in
1citing 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
9 authors.
Chiqi ChenKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0001-7220-8212
Xuanyi ZhouKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Liyuan CaoKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Wenqian YangKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lietao WengKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jin YuanSchool of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Wen ZhouHaihe Laboratory of Cell Ecosystem, State Key Laboratory of Experimental Hematology, Key Laboratory for Carcinogenesis and Invasion, Chinese Ministry of Education, Key Laboratory of Carcinogenesis, Chinese Ministry of Health, Department of Hematology, Xiangya Hospital, Central South University, Changsha, Hunan, China.ORCID https://orcid.org/0000-0003-4085-7714
Zhuo YuKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Junke ZhengKey Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Faculty of Basic Medicine, Hongqiao International Institute of Medicine, Shanghai Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0002-7023-2400
Funding
National Basic Research Program of China 2024YFA1803500National Natural Science Foundation of China 32030030National Natural Science Foundation of China 32371160National Natural Science Foundation of China 82170175National Natural Science Foundation of China 82370180National Natural Science Foundation of China 82430007National Postdoctoral Science Foundation of China 2021T140454Shanghai Municipal Health Commission 20204Y0008
6 · The paper itself
Abstract
Multiple myeloma (MM) is a haematological malignancy characterized by the clonal expansion of plasma cells within the bone marrow, thus resulting in the overproduction of monoclonal immunoglobulins. Despite the availability of various immunotherapeutic strategies, patient survival rates remain disappointingly low, thus underscoring the need for innovative immunotherapies to improve outcomes. Leukocyte Ig-like receptor subfamily B (LILRB1), which is a recently identified immune checkpoint, has an undefined role and molecular mechanism in MM. Herein, we demonstrated that LILRB1 was significantly upregulated in MM patients and MM cell lines and was negatively correlated with patient survival. The knockdown of LILRB1 promoted apoptosis in MM cells, enhanced sensitivity to bortezomib and diminished tumourigenicity in a subcutaneous mouse model. Mechanistically, LILRB1 triggers downstream GATA Binding Protein 2 (GATA2) and sustains MM cell proliferation via the GATA2-Sarcoma Antigen 1 (SAGE1) signalling pathway. Consequently, the targeting of LILRB1 may represent a promising therapeutic approach for MM.
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.