Evidence map›Paper›PMID 40442405›Full record

ReviewBritish journal of cancer2025

An FDA-approved drug library screening identifies proteasome inhibitors as selective cytotoxic agents for angiosarcoma cells.

Che-Yuan Hsu, Teruki Yanagi, Kodai Miyamoto, Satoko Otsuguro, Katsumi Maenaka, Hiroshi Nishihara, Hideki Nakamura, Kenzo Takahashi, Hideyuki Ujiie

Abstract readReview
In one paragraph

Review in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Che-Yuan HsuDepartment of Dermatology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Teruki YanagiDepartment of Dermatology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan. tyanagi@med.u-ryukyu.ac.jp.ORCID 0000-0003-2196-7600
Kodai MiyamotoDepartment of Dermatology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Satoko OtsuguroCenter for Research and Education on Drug Discovery, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Katsumi MaenakaCenter for Research and Education on Drug Discovery, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
Hiroshi NishiharaCenter for Cancer Genomics, Keio University School of Medicine, Tokyo, Japan.
Hideki NakamuraCentral Research Institute, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.
Kenzo TakahashiDepartment of Dermatology, Graduate School of Medicine, University of the Ryukyus, Okinawa, Japan.
Hideyuki UjiieDepartment of Dermatology, Faculty of Medicine and Graduate School of Medicine, Hokkaido University, Sapporo, Japan.

Funding

MEXT | Japan Society for the Promotion of Science (JSPS) JP20H05873MEXT | Japan Society for the Promotion of Science (JSPS) JP23K07757
6 · The paper itself

Abstract

Cutaneous angiosarcoma (CAS) is a life-threatening neoplasm with a 5-year survival rate of under 40% in advanced cases. As available treatments for CAS are limited, novel therapeutics must be explored. To identify potential therapeutic candidates, we conducted a drug screening analysis using an angiosarcoma cell line, HAMON. Cancer-related gene analysis revealed alterations in FGFR4, MYCN, CDKN2A, NF1, TP53, KDM6A, ATRX, MSH6, ATM, and NOTCH1 in HAMON cells. Screening of 4681 FDA-approved drugs identified four candidate compounds, with the proteasome inhibitor bortezomib selected for further study. ATP and MTT assays revealed bortezomib to be the most effective candidate against HAMON cells. Clonogenic assays revealed fewer HAMON cell colonies in the range of 1-10 nM bortezomib. DNA-content fluorescence-activated cell sorting analysis revealed a notable increase in the sub-G0/G1 phases, suggesting cell death without cell cycle arrest. Annexin V-propidium iodide staining revealed a significant increase in the percentage of early and late apoptotic cells in the bortezomib group. Mechanistically, bortezomib induced activation of NF-κB and endoplasmic reticulum stress signaling. The administration of bortezomib to immunocompromised mice implanted with HAMON cells induced apoptosis of tumor cells. This study identified the proteasome inhibitor bortezomib as a potential candidate for angiosarcoma in vitro and in vivo.

Indexed as

Antineoplastic AgentsBortezomibHemangiosarcomaProteasome InhibitorsSkin NeoplasmsAnimalsApoptosisCell Line, TumorDrug Screening Assays, AntitumorHumansMiceUnited StatesXenograft Model Antitumor AssaysAntineoplastic AgentsBortezomibProteasome Inhibitors

Identifiers

PMID40442405
PMCPMC12238406

What OpenQuestion holds

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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.