Evidence map›Paper›PMID 39542653›Full record

ArticleJournal for immunotherapy of cancer2024

DLL4-targeted CAR-T therapy sensitizes neoadjuvant chemotherapy via eliminating cancer stem cells and reshaping immune microenvironment in HER2

Jingrui Yan, Yongjie Xie, Ziyun Liu, Yanfang Yang, Tianxing Zhou

Abstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

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  9. Identification ofFrontiers in pharmacology · 2026
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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

5 authors.

Jingrui YanDepartment of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yongjie XieDepartment of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Ziyun LiuDepartment of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yanfang YangSecond Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, China zhoutianxing@tjmuch.com tjyangyf@126.com.
Tianxing ZhouDepartment of Pancreatic Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer; Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China zhoutianxing@tjmuch.com tjyangyf@126.com.ORCID 0009-0006-0150-1343

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeoadjuvant therapy with trastuzumab, pertuzumab and paclitaxel (THP) has significantly improved the prognosis of patients with human epidermal growth factor receptor 2 (HER2)

methodsThe Cancer Genome Atlas database, Gene Expression Omnibus and membrane protein database were used to identify the key regulator of THP neoadjuvant resistance. The biological functions and mechanisms of delta-like 4 proteins (DLL4) in THP therapy resistance were investigated in vitro and in vivo using the bioinformatic analysis, multiplex immunofluorescence, flow cytometry, sphere formation assays and chromatin immunoprecipitation, etc. Furthermore, DLL4-targeted chimeric antigen receptor (CAR)-T cells were established to sensitize THP therapy.

resultsDLL4 was identified as a key target in THP neoadjuvant therapy resistance for HER2

conclusionsOur study revealed novel functions of DLL4 in cell stemness and immune infiltration, including NET formation and T cell exclusion, which collectively contributed to THP neoadjuvant therapy resistance in HER2

Indexed as

Breast NeoplasmsErb-b2 Receptor Tyrosine KinasesNeoadjuvant TherapyNeoplastic Stem CellsTumor MicroenvironmentAdaptor Proteins, Signal TransducingAnimalsAntineoplastic Combined Chemotherapy ProtocolsCalcium-Binding ProteinsCell Line, TumorDrug Resistance, NeoplasmFemaleHumansImmunotherapy, AdoptiveMicePaclitaxelAdaptor Proteins, Signal TransducingCalcium-Binding ProteinsDLL4 protein, humanERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesPaclitaxelReceptors, Chimeric AntigenBreast CancerChemotherapyImmunotherapyStem Cell

Identifiers

PMID39542653
PMCPMC11575309

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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.