Article in Science advances, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
0numbers the graph read from it
0cells of the map it votes in
4citing 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
14 authors.
Mei FengInternational Cancer Institute and Translational Cancer Research Center, Peking University First Hospital, Beijing, China.ORCID 0009-0000-2326-4875
Hong LiuThe Second Surgical Department of Breast Cancer, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute & Hospital, Tianjin, China.
Lu ZhengDepartment of Internal Medicine, The Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, Zhengzhou, Henan, China.
Yang LiuDepartment of Hepatobiliary Cancer, Liver Cancer Center, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.ORCID 0000-0001-6450-9509
Hao ZhuangDepartment of Hepatobiliopancreatic Surgery, Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, China.ORCID 0000-0002-7339-8211
Hao XuThe Second Surgical Department of Breast Cancer, National Clinical Research Center for Cancer, Tianjin Medical University Cancer Institute & Hospital, Tianjin, China.
Tingting ZhangDepartment of Hepatobiliopancreatic Surgery, Affiliated Cancer Hospital of Zhengzhou University and Henan Cancer Hospital, Zhengzhou, China.
Zhen WuState Key Laboratory of Genetic Engineering, Department of Biochemistry and Biophysics, School of Life Sciences, Fudan University, Shanghai, China.
Xiaolong QianKey Laboratory of Cancer Prevention and Therapy, Tianjin; Tianjin's Clinical Research Center for Cancer; Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education, Tianjin, China.
Huikai LiDepartment of Hepatobiliary Cancer, Liver Cancer Center, Tianjin Medical University Cancer Institute & Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.ORCID 0000-0003-4864-4991
Tengfei XiaoShanghai Xunbaihui Biotechnology Co. Ltd., Building #1, 4th floor, 88 Darwin Road, Pudong New Area, Shanghai, China.
Yisheng PanDivision of General Surgery, Peking University First Hospital, Peking University, Beijing, China.ORCID 0000-0002-8924-2342
Shaokun ShuState Key Laboratory of Molecular Oncology, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education/Beijing), Department of Lymphoma, Peking University Cancer Hospital & Institute, Beijing, China.ORCID 0000-0001-6839-2782
Ning ZhangInternational Cancer Institute and Translational Cancer Research Center, Peking University First Hospital, Beijing, China.ORCID 0000-0001-7182-0100
Funding
No grant is acknowledged in the PubMed record.
6 · The paper itself
Abstract
The nongenetic mechanisms by which cancer cells escape cell cycle inhibition remain inadequately understood. Here, we uncover an epigenetic pathway driving adaptive resistance to cyclin-dependent kinase 4/6 (CDK4/6) inhibitors in hepatobiliary cancers using integrative approach combining genome-wide CRISPR screenings with transcriptional, epigenetic, and proteomic profiling. Sustained CDK4/6 inhibition triggers BAP1-dependent chromatin remodeling that induces a stem cell-like epigenetic state. Specifically, BAP1 removes ubiquitin modification (H2AK119ub) at the
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 Socratic graph.
Genome-wide screenings identify BAP1 as a synthetic-lethality target with CDK4/6 inhibitors. · full record | Socratic