Evidence map›Paper›PMID 27885740›Full record

ArticleCancer science2017

ASP5878, a selective FGFR inhibitor, to treat FGFR3-dependent urothelial cancer with or without chemoresistance.

Aya Kikuchi, Tomoyuki Suzuki, Taisuke Nakazawa, Masateru Iizuka, Ayako Nakayama, Tohru Ozawa, Minoru Kameda, Nobuaki Shindoh, Tadashi Terasaka, Masaaki Hirano and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.5field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. The FGF/FGFR/c-Myc axis as a promising therapeutic target in multiple myeloma.Journal of experimental & clinical cancer research : CR · 2024
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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.

Aya KikuchiDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Tomoyuki SuzukiDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Taisuke NakazawaDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Masateru IizukaDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Ayako NakayamaDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Tohru OzawaDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Minoru KamedaDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Nobuaki ShindohDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Tadashi TerasakaDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Masaaki HiranoDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Sadao KuromitsuDrug Discovery Research, Astellas Pharma Inc., Tsukuba-shi, Ibaraki, Japan.
Astellas Pharma (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FGF/FGFR gene aberrations such as amplification, mutation and fusion are associated with many types of human cancers including urothelial cancer. FGFR kinase inhibitors are expected to be a targeted therapy for urothelial cancer harboring FGFR3 gene alternations. ASP5878, a selective inhibitor of FGFR1, 2, 3 and 4 under clinical investigation, selectively inhibited cell proliferation of urothelial cancer cell lines harboring FGFR3 point mutation or fusion (UM-UC-14, RT-112, RT4 and SW 780) among 23 urothelial cancer cell lines. Furthermore, ASP5878 inhibited cell proliferation of adriamycin-resistant UM-UC-14 cell line harboring MDR1 overexpression and gemcitabine-resistant RT-112 cell line. The protein expression of c-MYC, an oncoprotein, in gemcitabine-resistant RT-112 cell line was higher than that in RT-112 parental cell line and ASP5878 decreased the c-MYC expression in both RT-112 parental and gemcitabine-resistant RT-112 cell lines. Once-daily oral administration of ASP5878 exerted potent antitumor activities in UM-UC-14, RT-112 and gemcitabine-resistant RT-112 xenograft models without affecting body weight. These findings suggest that ASP5878 has the potential to be an oral targeted therapy against urothelial cancer harboring FGFR3 fusion or FGFR3 point mutation after the acquisition of gemcitabine- or adriamycin-resistance.

Indexed as

Molecular Targeted TherapyAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BBody WeightCell Line, TumorCell ProliferationDeoxycytidineDNA-Binding ProteinsDoxorubicinDrug Resistance, NeoplasmGemcitabineGene FusionHumansPoint MutationPyrazolesPyrimidinesABCB1 protein, humanAntineoplastic AgentsASP5878ATP Binding Cassette Transporter, Subfamily BDeoxycytidineDNA-Binding ProteinsDoxorubicinFGFR3 protein, humanGemcitabineMYCBP protein, humanPyrazolesPyrimidinesReceptor, Fibroblast Growth Factor, Type 3Transcription FactorsChemotherapyFGFR3-fusion or -mutationmolecular targeted drug therapyoral dosingurothelial cancer

Identifiers

PMID27885740
PMCPMC5329164
OpenAlexW2552600856

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.