Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
0numbers the graph read from it
0cells of the map it votes in
2citing 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
12 authors.
Song'en Xu *Division of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.
Jiaxin Hong *Division of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.ORCID 0000-0002-4399-9083
Meimei DongyeState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangdong Provincial Key Laboratory of Ophthalmology and Visual Science, Guangzhou 510060, China.
Jiehao LinDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.
Rongtao XueDepartment of Hematology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Zhibin HuangDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.ORCID 0000-0003-4286-4002
Jin XuDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.ORCID 0000-0002-6840-1359
Yiyue ZhangDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.ORCID 0000-0002-9402-3523
Anskar Yu-Hung LeungDivision of Hematology, Department of Medicine, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, Special Administrative Region of China.
Juan ShenDepartment of Marine Pharmacy, School of Life Science and Biopharmaceutics, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Wenqing ZhangDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.ORCID 0000-0002-3636-7133
Wei LiuDivision of Cell, Developmental and Integrative Biology, School of Medicine, South China University of Technology, Guangzhou 510006, China.ORCID 0000-0003-3660-5514
Funding
MOST | National Key Research and Development Program of China (NKPs) 2018YFA0801000MOST | National Natural Science Foundation of China (NSFC) 81770167MOST | National Natural Science Foundation of China (NSFC) 82070163MOST | National Natural Science Foundation of China (NSFC)/Research Grants Council (RGC) Joint Research Scheme 32161160326
6 · The paper itself
Abstract
Approximately 30% of patients with myelodysplastic syndrome (MDS) progress to secondary acute myeloid leukemia (sAML) via accumulating gene mutations. Genomic analyses reveal a complex interplay among mutant genes, with co-occurring and mutually exclusive patterns. Hyperactivation of c-MYB and deficiency of PU.1 have been linked to myeloid disorders. We report a case of AML with concurrent
Indexed as
Leukemia, Myeloid, AcuteMyelodysplastic SyndromesProto-Oncogene ProteinsProto-Oncogene Proteins c-mybTrans-ActivatorsAnimalsHumansMaleMutationProto-Oncogene Protein Spi-1ZebrafishProto-Oncogene ProteinsProto-Oncogene Proteins c-mybProto-Oncogene Protein Spi-1Trans-Activatorsc-MybPelger–Huët anomaly cellsPu.1sAMLzebrafish
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.
The synergistic effect of c-Myb hyperactivation and Pu.1 deficiency induces Pelger-Huët anomaly and promotes sAML. · full record | OpenQuestion