Evidence map›Paper›PMID 28454247›Full record

ArticleOncology letters2017

AMPD3 is associated with the malignant characteristics of gastrointestinal stromal tumors.

Meihong Wong, Kohei Funasaka, Tomohiko Obayashi, Ryoji Miyahara, Yoshiki Hirooka, Michinari Hamaguchi, Hidemi Goto, Takeshi Senga

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 18 citations in OpenAlex.

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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 1 institution in 1 country.

Meihong WongDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Kohei FunasakaDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Tomohiko ObayashiDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Ryoji MiyaharaDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Yoshiki HirookaDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Michinari HamaguchiDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Hidemi GotoDepartment of Gastroenterology and Hepatology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Takeshi SengaDivision of Cancer Biology, Nagoya University Graduate School of Medicine, Nagoya 466-8550, Japan.
Nagoya University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors of the gastrointestinal tract. It is well known that activating mutations in the receptor tyrosine kinases KIT and platelet-derived growth factor receptor-α have essential roles in the pathogenesis of GISTs. The activation of these receptor protein kinases triggers multiple signaling pathways that promote cell proliferation and survival; however, the exact mechanism by which the activation of these kinases promotes the progression of GISTs remains uncertain. The aim of the present was to search for genes that are associated with the progression of GIST. The present study used reverse transcription-quantitative polymerase chain reaction to demonstrate that adenosine monophosphate deaminase 3 (AMPD3) was highly expressed in GISTs. Furthermore, transfection of GIST-T1 cells with KIT-specific small interfering RNA (siRNA) demonstrated that the expression of AMPD3 was dependent on KIT expression, while the depletion of AMPD3 in human GIST-T1 cells using AMPD3-specific siRNA resulted in the suppression of cell migration and invasion. In addition, AMPD3 depletion sensitized GIST-T1 cells to the tyrosine kinase inhibitor imatinib. The results of the present suggested that the combined inhibition of tyrosine kinases and AMPD3 may be effective for the treatment of GISTs.

Indexed as

adenosine monophosphate deaminase 3gastrointestinal stromal tumorsimatinibinvasionKITmigration

Identifiers

PMID28454247
PMCPMC5403233
OpenAlexW2565099855

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.