Evidence map›Paper›PMID 10200307›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

A synthetic inhibitor of histone deacetylase, MS-27-275, with marked in vivo antitumor activity against human tumors.

A Saito, T Yamashita, Y Mariko, Y Nosaka, K Tsuchiya, T Ando, T Suzuki, T Tsuruo, O Nakanishi

2 registry-linked trialsOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 216 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
216citing papers in PubMed, 2 pooled it
10.3field-weighted citation impact, top 1% 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.

NCT01136499 phase2completednot on this mapstarted 2010, after this paper: background citation

Efficacy and Safety Assessment of Oral LBH589 in Adult Patients With Advanced Soft Tissue Sarcoma After Pre-treatment Failure: an Open-label, Multicenter Phase II Study

TypeinterventionalSponsorCentre Leon BerardRan2010 to 2013Enrolled53ConditionsSoft Tissue SarcomaArmsLBH589 (Panobinostat®)
NCT03829930 phase1terminatednot on this mapstarted 2019, after this paper: background citation

A Phase I Study of Entinostat in Combination With Enzalutamide for Treatment of Patients With Castration-Resistant Prostate Cancer

TypeinterventionalSponsorGeorge Washington UniversityRan2019 to 2020Enrolled6ConditionsProstate AdenocarcinomaArmsEntinostat, Enzalutamide
3 · Its place in the literature

Who cites it

216 citing papers in PubMed, 2 syntheses or guidelines pooled it, 696 citations in OpenAlex.

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156 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

A SaitoInstitute of Biological Science, Mitsui Pharmaceuticals, 1900-1 Togo, Mobara-shi, Chiba 297-0017, Japan.
T Yamashita
Y Mariko
Y Nosaka
K Tsuchiya
T Ando
T Suzuki
T Tsuruo
O Nakanishi
The University of Tokyo · JPMitsui Chemicals (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synthetic benzamide derivatives were investigated for their ability to inhibit histone deacetylase (HDA). In this study, one of the most active benzamide derivatives, MS-27-275, was examined with regard to its biological properties and antitumor efficacy. MS-27-275 inhibited partially purified human HDA and caused hyperacetylation of nuclear histones in various tumor cell lines. It behaved in a manner similar to other HDA inhibitors, such as sodium butyrate and trichostatin A; MS-27-275 induced p21(WAF1/CIP1) and gelsolin and changed the cell cycle distribution, decrease of S-phase cells, and increase of G1-phase cells. The in vitro sensitivity spectrum of MS-27-275 against various human tumor cell lines showed a pattern different than that of a commonly used antitumor agent, 5-fluorouracil, and, of interest, the accumulation of p21(WAF1/CIP1) tended to be faster and greater in the cell lines sensitive to MS-27-275. MS-27-275 administered orally strongly inhibited the growth in seven of eight tumor lines implanted into nude mice, although most of these did not respond to 5-fluorouracil. A structurally analogous compound to MS-27-275 without HDA-inhibiting activity showed neither the biological effects in cell culture nor the in vivo therapeutic efficacy. These results suggest that MS-27-275 acts as an antitumor agent through HDA inhibition and may provide a novel chemotherapeutic strategy for cancers insensitive to traditional antitumor agents.

Indexed as

Histone Deacetylase InhibitorsAnimalsAntineoplastic AgentsBenzamidesButyratesCell CycleCell SurvivalColonic NeoplasmsCyclin-Dependent Kinase Inhibitor p21CyclinsEnzyme InhibitorsFemaleFluorouracilGelsolinHL-60 CellsHumansAntineoplastic AgentsBenzamidesButyratesCDKN1A protein, humanCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21CyclinsentinostatEnzyme InhibitorsFluorouracilGelsolinHistone Deacetylase InhibitorsHydroxamic AcidsPyridinestrichostatin A

Identifiers

PMID10200307
PMCPMC16377
OpenAlexW2082739830

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.