Evidence map›Paper›PMID 42807855›Full record

ArticleInternational journal of biological sciences2026

Anlotinib enhances the sensitivity to docetaxel in lung cancer through inhibiting DDR1-mediated glycolytic pathway.

Xueqin Chen, Juan Shen, Zhifei Xu, Bo Xu, Jie Huang, Jingjing Jiang, Yidan Chen, Xin Li, Shaoyu Yang, Kan Wu and 6 more

Abstract read
In one paragraph

Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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

16 authors.

Xueqin ChenDepartment of Thoracic Oncology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang 310006, PR China.
Juan ShenDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, PR China.
Zhifei XuCenter for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, PR China.
Bo XuCenter for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, PR China.
Jie HuangDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, PR China.
Jingjing JiangInnovation Institute for Artificial Intelligence in Medicine of Zhejiang University, Hangzhou, Zhejiang 310018, PR China.
Yidan ChenDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, PR China.
Xin LiDepartment of Thoracic Oncology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang 310006, PR China.
Shaoyu YangDepartment of Thoracic Oncology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang 310006, PR China.
Kan WuDepartment of Thoracic Oncology, Hangzhou Cancer Hospital, Hangzhou, Zhejiang 310002, PR China.
Jiaoli WangDepartment of Thoracic Oncology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang 310006, PR China.
Peihua LuoCenter for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, PR China.
Qiaojun HeCenter for Drug Safety Evaluation and Research of Zhejiang University, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, PR China.
Shenglin MaDepartment of Thoracic Oncology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang 310006, PR China.
Bing XiaDepartment of Thoracic Oncology, Affiliated Hangzhou First People's Hospital, School of Medicine, Westlake University, Hangzhou, Zhejiang 310006, PR China.
Bo YangInstitute of Pharmacology & Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou, Zhejiang 310058, PR China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Discoidin domain receptor 1 (DDR1), a collagen-activated receptor tyrosine kinase, is essential for tumor cell proliferation, invasion and drug resistance. Our study demonstrated that the expression and phosphorylation of DDR1 were associated not only with the poor outcome of non-small cell lung cancer (NSCLC), but also with low sensitivity to docetaxel. Moreover, our kinase profiling identified that anlotinib, an oral small-molecule tyrosine kinase inhibitor, could significantly inhibit DDR1 phosphorylation. Further data revealed that anlotinib could increase the sensitivity to docetaxel in cell lines, cell-derived and patient-derived tumor xenografts through down-regulating DDR1 phosphorylation, which no longer existed in

Indexed as

Carcinoma, Non-Small-Cell LungDiscoidin Domain Receptor 1DocetaxelIndolesLung NeoplasmsQuinolinesAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationGlycolysisHumansMiceMice, NudePhosphorylationanlotinibAntineoplastic AgentsDDR1 protein, humanDiscoidin Domain Receptor 1DocetaxelIndolesQuinolinesanlotinibDDR1docetaxelglycolysissensitivity

Identifiers

PMID42807855
PMCPMC13617657

What OpenQuestion holds

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Registered trials

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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.