Evidence map›Paper›PMID 42490143›Full record

ArticleThe Journal of clinical investigation2026

PAX5 modulates vascularization and contributes to neuroendocrine lineage transition during carcinoma progression.

Ailing Wu, Yujie Hao, Xuemiao Yan, Junrong Liu, Lin Wang, Yan Jin, Wenxu Liu, Xiyue Chen, Yuan Jiang, Luc Girard and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical investigation, 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

20 authors.

Ailing WuZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Yujie HaoZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Xuemiao YanZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Junrong LiuZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Lin WangZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Yan JinZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Wenxu LiuZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Xiyue ChenZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Yuan JiangDepartment of Lung Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Luc GirardHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Zhiqun ShangTianjin Institute of Urology, the 2nd Hospital of Tianjin Medical University, Tianjin, China.
Jun YanDepartment of Pathology, Tianjin First Center Hospital, Tianjin, China.
Zhenfa ZhangDepartment of Lung Cancer Center, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Wenchen GongDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Yuanjie NiuTianjin Institute of Urology, the 2nd Hospital of Tianjin Medical University, Tianjin, China.
Benjamin J DrapkinHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
John D MinnaHamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Lance S TeradaDepartment of Internal Medicine, Division of Pulmonary and Critical Care, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Zhenyi MaZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.
Zhe LiuZhejiang Key Laboratory of Medical Epigenetics, Jiande Hospital, Department of Cell Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China.

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V., MINNA, JOHN D. · 1996 to 2024
$57.4M
Coordinating center for the NCI small cell lung cancer research consortiumU24CA213274 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Lauren Averett Byers, JOHN D. MINNA · 2017 to 2026
$12.9M
Developing ASCL1 and NeuroD1 lineage oncogene targeted therapy for small cell lung cancerU01CA213338 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI MINNA, JOHN D. · 2017 to 2021
$3.0M
(PQ1) Epigenetic effects of the premalignant fieldR01CA208620 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TERADA, LANCE S · 2016 to 2020
$1.9M
NCI NIH HHS P50 CA070907NCI NIH HHS R01 CA208620NCI NIH HHS U01 CA213338NCI NIH HHS U24 CA213274
6 · The paper itself

Abstract

Human carcinomas often gain aggressive characteristics and escape cell type-specific treatment regimens through cryptic shifts in lineage states. However, the underlying mechanisms that govern lineage plasticity in carcinomas are undefined. Here in this study, we found that PAX5, a neural/lymphatic transcription factor, contributed to neuroendocrine (NE) lineage transition. PAX5 was highly expressed in aggressive human NE carcinoma cells and tissues but not in non-NE cancer cells and tissues. Deletion of Pax5 in Rb1fl/fl Trp53fl/fl mice caused a reduction of tumor vessels, loss of NE morphologic features, and decreased expression of ASCL1, NCAM, and SYP, whereas ectopic expression of PAX5 in CC10-rtTA TetO-hEGFRex19del/T790M mouse adenocarcinomas and in LNCAP prostate cancer xenografts induced an angiogenic microenvironment and NE morphology. Importantly, antiangiogenic drugs reduced NE features of Rb1fl/fl Trp53fl/fl tumors and blocked PAX5-induced NE transformation. These studies demonstrate an essential role of an angiogenic microenvironment in transition/maintenance of NE lineage, suggesting that targeting PAX5 and its downstream signaling may modulate lineage transitions responsible for treatment failure in both small cell neuroendocrine carcinoma and adenocarcinomas.

Indexed as

Carcinoma, NeuroendocrineCell LineageNeoplasm ProteinsNeovascularization, PathologicPAX5 Transcription FactorProstatic NeoplasmsAnimalsBasic Helix-Loop-Helix ProteinsCell Line, TumorDisease ProgressionHumansMaleMiceMice, KnockoutTumor Suppressor Protein p53Basic Helix-Loop-Helix ProteinsNeoplasm ProteinsPAX5 protein, humanPAX5 Transcription FactorTrp53 protein, mouseTumor Suppressor Protein p53AngiogenesisLung cancerMouse modelsNeuroendocrine regulationOncology

Identifiers

PMID42490143
PMCPMC13574158

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.