Evidence map›Paper›PMID 35581303›Full record

ArticleScientific reports2022

The K-Ras(G12D)-inhibitory peptide KS-58 suppresses growth of murine CT26 colorectal cancer cell-derived tumors.

Kotaro Sakamoto, Bangzhong Lin, Kazuto Nunomura, Takeshi Izawa, Shinsaku Nakagawa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
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  9. KRASJournal of translational medicine · 2023
    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

5 authors at 3 institutions in 1 country.

Kotaro SakamotoResearch & Development Department, Ichimaru Pharcos Company Limited, 318-1 Asagi, Motosu, Gifu, 501-0475, Japan. sakamoto-kotaro@ichimaru.co.jp.
Bangzhong LinCenter for Supporting Drug Discovery and Life Science Research, Graduate School of Pharmaceutical Science, Osaka University, 1-6 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Kazuto NunomuraCenter for Supporting Drug Discovery and Life Science Research, Graduate School of Pharmaceutical Science, Osaka University, 1-6 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Takeshi IzawaLaboratory of Veterinary Pathology, Osaka Prefecture University, 1-58 Rinku-Orai-Kita, Izumisano, Osaka, 598-8531, Japan.
Shinsaku NakagawaCenter for Supporting Drug Discovery and Life Science Research, Graduate School of Pharmaceutical Science, Osaka University, 1-6 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Osaka University · JPIchimaru Pharcos (Japan) · JPOsaka Prefecture University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the cell proliferation regulator K-Ras are found with a variety of cancer types, so drugs targeting these mutant proteins could hold great clinical potential. Very recently, a drug targeting the K-Ras(G12C) mutant observed in lung cancer gained regulatory approval and several clinical trials are currently underway to examine the efficacy of this agent when combined with other drugs such as a monoclonal antibody inhibitor of programmed cell death 1 receptor (anti-PD-1). Alternatively, there are currently no approved drugs targeting K-Ras(G12D), the most common cancer-associated K-Ras mutant. In 2020, we described the development of the K-Ras(G12D) inhibitory bicyclic peptide KS-58 and presented evidence for anticancer activity against mouse xenografts derived from the human pancreatic cancer cell line PANC-1 stably expressing K-Ras(G12D). Here, we show that KS-58 also possess anticancer activity against mouse tumors derived from the colorectal cancer cell line CT26 stably expressing K-Ras(G12D). Further, KS-58 treatment reduced phosphorylation of ERK, a major downstream signaling factor in the Ras pathway, confirming that KS-58 inhibits K-Ras(G12D) function. Unexpectedly; however, KS-58 did not show additive or synergistic anticancer activity with mouse anti-PD-1. Morphological analysis and immunostaining demonstrated no obvious differences in CD8

Indexed as

Colorectal NeoplasmsPeptidesProto-Oncogene Proteins p21(ras)AnimalsCell Line, TumorCell ProliferationMiceMutant ProteinsMutationPeptides, CyclicKS-58Mutant ProteinsPeptidesPeptides, CyclicProto-Oncogene Proteins p21(ras)

Identifiers

PMID35581303
PMCPMC9114382
OpenAlexW4280571262

What OpenQuestion holds

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LicenceCC BY
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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.