Evidence map›Paper›PMID 30591422›Full record

ArticleNeoplasia (New York, N.Y.)2019

Trabectedin Reduces Skeletal Prostate Cancer Tumor Size in Association with Effects on M2 Macrophages and Efferocytosis.

J D Jones, B P Sinder, D Paige, F N Soki, A J Koh, S Thiele, Y Shiozawa, L C Hofbauer, S Daignault, H Roca and 1 more

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

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  15. Mechanobiology of Bone Metastatic Cancer.Current osteoporosis reports · 2021
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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

11 authors at 2 institutions in 2 countries.

J D JonesDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI.
B P SinderDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI.
D PaigeDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI.
F N SokiDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI.
A J KohDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI.
S ThieleDepartment of Endocrinology, Diabetes, and Bone Disease, Technische Universität Dresden Medical Center, Dresden, Germany; German Cancer Consortium (DKTK), partner site Dresden and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Y ShiozawaDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI; Department of Cancer Biology and Comprehensive Cancer Center, Wake Forest University School of Medicine, Winston-Salem, NC.
L C HofbauerDepartment of Endocrinology, Diabetes, and Bone Disease, Technische Universität Dresden Medical Center, Dresden, Germany; German Cancer Consortium (DKTK), partner site Dresden and German Cancer Research Center (DKFZ), Heidelberg, Germany.
S DaignaultDepartment of Biostatistics, Center for Cancer Biostatistics, University of Michigan, Ann Arbor, MI.
H RocaDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI.
L K McCauleyDepartment of Periodontics and Oral Medicine, University of Michigan School of Dentistry, Ann Arbor, MI; Department of Pathology, University of Michigan Medical School, Ann Arbor, MI. Electronic address: mccauley@umich.edu.
University of Michigan–Ann Arbor · USHeidelberg University · DE

Funding

Tumor microvesicle-mediated modulation of the bone microenvironmentP01CA093900 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PIENTA, KENNETH J. · 2004 to 2024
$29.6M
Tissue/InformaticsP50CA186786 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Robert Timothy Dess · 2014 to 2026
$27.6M
Osteomacs and Skeletal MetastasisF32CA168269 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SOKI, FABIANA NAOMI · 2013 to 2014
$121k
NCI NIH HHS F32 CA168269NCI NIH HHS P01 CA093900NCI NIH HHS P50 CA186786
6 · The paper itself

Abstract

Macrophages play a dual role in regulating tumor progression. They can either reduce tumor growth by secreting antitumorigenic factors or promote tumor progression by secreting a variety of soluble factors. The purpose of this study was to define the monocyte/macrophage population prevalent in skeletal tumors, explore a mechanism employed in supporting prostate cancer (PCa) skeletal metastasis, and examine a novel therapeutic target. Phagocytic CD68+ cells were found to correlate with Gleason score in human PCa samples, and M2-like macrophages (F4/80

Indexed as

AnimalsAntigens, CDAntigens, Differentiation, MyelomonocyticBone MarrowBone NeoplasmsCD68 MoleculeCell Line, TumorCell ProliferationCytokinesDisease Models, AnimalHumansImmunohistochemistryMacrophage ActivationMacrophagesMaleMiceAntigens, CDAntigens, Differentiation, MyelomonocyticCD68 antigen, humanCD68 MoleculeCytokinesTrabectedin

Identifiers

PMID30591422
PMCPMC6314218
OpenAlexW2908179060

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.