Evidence map›Paper›PMID 39740910›Full record

ArticleIn vivo (Athens, Greece)

Tadashi Ashizawa, Akira Iizuka, Akari Kanematsu, Takayuki Ando, Chie Maeda, Haruo Miyata, Kazue Yamashita, Tomoatsu Ikeya, Yasufumi Kikuchi, Kouji Maruyama and 4 more

Abstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

14 authors.

Tadashi AshizawaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Akira IizukaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Akari KanematsuImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Takayuki AndoDepartment of Drug and Food Science, Shizuoka Institute of Environment and Hygiene, Shizuoka, Japan.
Chie MaedaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Haruo MiyataImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Kazue YamashitaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Tomoatsu IkeyaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Yasufumi KikuchiImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Kouji MaruyamaExperimental Animal Facility, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Takeshi NagashimaSRL, Tokyo, Japan.
Kenichi UrakamiCancer Diagnostic Research Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan.
Ken YamaguchiOffice of the President Emeritus, Shizuoka Cancer Center Hospital, Shizuoka, Japan.
Yasuto AkiyamaImmunotherapy Division, Shizuoka Cancer Center Research Institute, Shizuoka, Japan; y.akiyama@scchr.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimImmune checkpoint blockade has achieved great success as a targeted immunotherapy for solid cancers. However, small molecules that inhibit programmed death 1/programmed death ligand 1 (PD-1/PD-L1) binding are still being developed and have several advantages, such as high bioavailability. Previously, we reported a novel PD-1/PD-L1-inhibiting small compound, SCL-1, which showed potent antitumor effects on PD-L1 MATERIALS AND

methodsTwelve syngeneic mice models of tumors, such as colon, breast, bladder, kidney, pancreatic, non-small cell lung cancers, melanoma, and lymphomas, were used for in vivo experiments. Tumor mutation burden (TMB) was analyzed by whole exome sequencing (WES) using reference DNA from mouse blood. The proportion of CD8

resultsSCL-1 had a markedly greater antitumor effect (11 sensitive tumors and 1 resistant tumor among the 12 tumor types) than the anti-mouse PD-1 antibody (8 sensitive tumors and 4 resistant tumors). In addition, the tumor growth inhibition rate (%) was more closely associated with TMB in the SCL-1 group than in the anti-PD-1 antibody group. Furthermore, in vivo experiments using PD-L1 gene knockout and lymphocyte-depletion technologies demonstrated that the antitumor activity of SCL-1 was dependent on CD8

conclusionSCL-1 has great potential as an oral immunotherapy that targets immune checkpoint molecules in cancer treatment.

Indexed as

B7-H1 AntigenCD8-Positive T-LymphocytesDisease Models, AnimalImmune Checkpoint InhibitorsLymphocytes, Tumor-InfiltratingProgrammed Cell Death 1 ReceptorAnimalsCell Line, TumorFemaleHumansImmunotherapyMiceNeoplasmsB7-H1 AntigenImmune Checkpoint InhibitorsProgrammed Cell Death 1 Receptormouse syngeneic tumorsPD-1/PD-L1 inhibitorsmall chemical compoundtumor-infiltrating lymphocyte (TIL)tumor mutation burden (TMB)

Identifiers

PMID39740910
PMCPMC11705142

What OpenQuestion holds

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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.