Evidence map›Paper›PMID 24403861›Full record

ArticleNeoplasia (New York, N.Y.)2013

Combining molecular targeted drugs to inhibit both cancer cells and activated stromal cells in gastric cancer.

Mieko Onoyama, Yasuhiko Kitadai, Yuichiro Tanaka, Ryo Yuge, Kei Shinagawa, Shinji Tanaka, Wataru Yasui, Kazuaki Chayama

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  7. The Emerging Roles of Pericytes in Modulating Tumor Microenvironment.Frontiers in cell and developmental biology · 2021
    Review
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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

8 authors at 2 institutions in 1 country.

Mieko OnoyamaDepartment of Gastroenterology and Metabolism, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yasuhiko KitadaiDepartment of Gastroenterology and Metabolism, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Yuichiro TanakaDepartment of Gastroenterology and Metabolism, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Ryo YugeDepartment of Gastroenterology and Metabolism, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kei ShinagawaDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.
Shinji TanakaDepartment of Endoscopy, Hiroshima University Hospital, Hiroshima, Japan.
Wataru YasuiDepartment of Molecular Pathology, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Kazuaki ChayamaDepartment of Gastroenterology and Metabolism, Graduate School of Biomedical and Health Sciences, Hiroshima University, Hiroshima, Japan.
Hiroshima University · JPHiroshima University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have revealed that PDGF plays a role in promoting progressive tumor growth in several cancers, including gastric cancer. Cancer-associated fibroblasts, pericytes, and lymphatic endothelial cells in stroma express high levels of PDGF receptor (PDGF-R); cancer cells and vascular endothelial cells do not. Mammalian target of rapamycin (mTOR) is a serine/threonine kinase that increases the production of proteins that stimulate key cellular processes such as cell growth and proliferation, cell metabolism, and angiogenesis. In the present study, we examined the effects of PDGF-R tyrosine kinase inhibitor (nilotinib) and mTOR inhibitor (everolimus) on tumor stroma in an orthotopic nude mice model of human gastric cancer. Expression of PDGF-B and PDGF-Rβ mRNAs was associated with stromal volume. Treatment with nilotinib did not suppress tumor growth but significantly decreased stromal reactivity, lymphatic invasion, lymphatic vessel area, and pericyte coverage of tumor microvessels. In contrast, treatment with everolimus decreased tumor growth and microvessel density but not stromal reactivity. Nilotinib and everolimus in combination reduced both the growth rate and stromal reaction. Target molecule-based inhibition of cancer-stromal cell interaction appears promising as an effective antitumor therapy.

Indexed as

AdenocarcinomaAnimalsAntineoplastic Combined Chemotherapy ProtocolsCell Line, TumorDrug SynergismEverolimusFemaleGene ExpressionHumansMiceMice, Inbred BALB CMice, NudeMolecular Targeted TherapyProto-Oncogene Proteins c-sisPyrimidinesReceptor, Platelet-Derived Growth Factor betaEverolimusMTOR protein, humannilotinibProto-Oncogene Proteins c-sisPyrimidinesReceptor, Platelet-Derived Growth Factor betaSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID24403861
PMCPMC3884530
OpenAlexW1887041030

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.