Evidence map›Paper›PMID 26114873›Full record

ArticlePloS one2015

Role of IL13RA2 in Sunitinib Resistance in Clear Cell Renal Cell Carcinoma.

Noboru Shibasaki, Toshinari Yamasaki, Toru Kanno, Ryuichiro Arakaki, Hiromasa Sakamoto, Noriaki Utsunomiya, Takahiro Inoue, Tatsuaki Tsuruyama, Eijiro Nakamura, Osamu Ogawa and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. 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
2.4field-weighted citation impact, top 11% 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, 44 citations in OpenAlex.

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  12. Molecular therapy oncolytics · 2022
    Article
  13. Engineered IL13 variants direct specificity of IL13Rα2-targeted CAR T cell therapy.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
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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 1 institution in 1 country.

Noboru ShibasakiDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Toshinari YamasakiDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Toru KannoDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Ryuichiro ArakakiDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Hiromasa SakamotoDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Noriaki UtsunomiyaDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Takahiro InoueDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Tatsuaki TsuruyamaDepartment of Diagnostic Pathology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Eijiro NakamuraLaboratory for Malignancy Control Research, Medical Innovation Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Osamu OgawaDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Tomomi KambaDepartment of Urology, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Kyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular endothelial growth factor (VEGF) and mammalian target of rapamycin are well-known therapeutic targets for renal cell carcinoma (RCC). Sunitinib is an agent that targets VEGF receptors and is considered to be a standard treatment for metastatic or unresectable clear cell RCC (ccRCC). However, ccRCC eventually develops resistance to sunitinib in most cases, and the mechanisms underlying this resistance are not fully elucidated. In the present study, we established unique primary xenograft models, KURC1 (Kyoto University Renal Cancer 1) and KURC2, from freshly isolated ccRCC specimens. The KURC1 xenograft initially responded to sunitinib treatment, however finally acquired resistance. KURC2 retained sensitivity to sunitinib for over 6 months. Comparing gene expression profiles between the two xenograft models with different sensitivity to sunitinib, we identified interleukin 13 receptor alpha 2 (IL13RA2) as a candidate molecule associated with the acquired sunitinib-resistance in ccRCC. And patients with high IL13RA2 expression in immunohistochemistry in primary ccRCC tumor tends to have sunitinib-resistant metastatic site. Next, we showed that sunitinib-sensitive 786-O cells acquired resistance in vivo when IL13RA2 was overexpressed. Conversely, shRNA-mediated knockdown of IL13RA2 successfully overcame the sunitinib-resistance in Caki-1 cells. Histopathological analyses revealed that IL13RA2 repressed sunitinib-induced apoptosis without increasing tumor vasculature in vivo. To our knowledge, this is a novel mechanism of developing resistance to sunitinib in a certain population of ccRCC, and these results indicate that IL13RA2 could be one of potential target to overcome sunitinib resistance.

Indexed as

AnimalsAntineoplastic AgentsCarcinoma, Renal CellCell Line, TumorDrug Resistance, NeoplasmFemaleHumansIndolesInterleukin-13 Receptor alpha2 SubunitKidney NeoplasmsMice, Inbred BALB CMice, SCIDPyrrolesSunitinibXenograft Model Antitumor AssaysAntineoplastic AgentsIndolesInterleukin-13 Receptor alpha2 SubunitPyrrolesSunitinib

Identifiers

PMID26114873
PMCPMC4482605
OpenAlexW1526757159

What OpenQuestion holds

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LicenceCC BY
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.