Evidence map›Paper›PMID 31285612›Full record

ArticleNature neuroscience2019

Genetic manipulation of autonomic nerve fiber innervation and activity and its effect on breast cancer progression.

Atsunori Kamiya, Yohsuke Hayama, Shigeki Kato, Akihiko Shimomura, Takushi Shimomura, Katsumasa Irie, Ryosuke Kaneko, Yuchio Yanagawa, Kazuto Kobayashi, Takahiro Ochiya

RetractedAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 175 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 1 pooled it
25.5field-weighted citation impact, top 1% of its field
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

175 citing papers in PubMed, 1 synthesis or guideline pooled it, 289 citations in OpenAlex.

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115 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 7 institutions in 1 country.

Atsunori KamiyaDepartment of Cellular Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan. kamiyaa@okayama-u.ac.jp.ORCID http://orcid.org/0000-0001-8160-0427
Yohsuke HayamaDepartment of Cardiovascular Dynamics, National Cerebral and Cardiovascular Center Research Institute, Suita, Japan.
Shigeki KatoDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, Japan.
Akihiko ShimomuraDepartment of Breast and Medical Oncology, National Cancer Center Hospital, Tokyo, Japan.
Takushi ShimomuraCellular and Structural Physiology Institute (CeSPI), Nagoya University, Furo-cho, Chikusa, Nagoya, Japan.
Katsumasa IrieCellular and Structural Physiology Institute (CeSPI), Nagoya University, Furo-cho, Chikusa, Nagoya, Japan.
Ryosuke KanekoDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
Yuchio YanagawaDepartment of Genetic and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Japan.
Kazuto KobayashiDepartment of Molecular Genetics, Institute of Biomedical Sciences, Fukushima Medical University School of Medicine, Fukushima, Japan.
Takahiro OchiyaDivision of Molecular and Cellular Medicine, National Cancer Center Research Institute, Tokyo, Japan.
Fukushima Medical University · JPGunma University · JPNagoya University · JPNational Cerebral and Cardiovascular Center · JPNational Institute for Physiological Sciences · JPOkayama University · JPTokyo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effects of autonomic innervation of tumors on tumor growth remain unclear. Here we developed a series of genetic techniques to manipulate autonomic innervation in a tumor- and fiber-type-specific manner in mice with human breast cancer xenografts and in rats with chemically induced breast tumors. Breast cancer growth and progression were accelerated following stimulation of sympathetic nerves in tumors, but were reduced following stimulation of parasympathetic nerves. Tumor-specific sympathetic denervation suppressed tumor growth and downregulated the expression of immune checkpoint molecules (programed death-1 (PD-1), programed death ligand-1 (PD-L1), and FOXP3) to a greater extent than with pharmacological α- or β-adrenergic receptor blockers. Genetically induced simulation of parasympathetic innervation of tumors decreased PD-1 and PD-L1 expression. In humans, a retrospective analysis of breast cancer specimens from 29 patients revealed that increased sympathetic and decreased parasympathetic nerve density in tumors were associated with poor clinical outcomes and correlated with higher expression of immune checkpoint molecules. These findings suggest that autonomic innervation of tumors regulates breast cancer progression.

Indexed as

Adrenergic AntagonistsAnimalsAutonomic Fibers, PreganglionicB7-H1 AntigenBreast NeoplasmsDenervationDisease ProgressionFemaleForkhead Transcription FactorsHeterograftsHumansMiceMice, Inbred BALB CNeoplasm TransplantationParasympathetic Nervous SystemProgrammed Cell Death 1 ReceptorAdrenergic AntagonistsB7-H1 AntigenCD274 protein, humanForkhead Transcription FactorsFOXP3 protein, humanPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID31285612
OpenAlexW2956383533

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.