Evidence map›Paper›PMID 41478991›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2026

High-Throughput RNA Interference Screen Targeting Synthetic-Lethal Gain-of-Function of Oncogenic Mutant TP53 in Triple-Negative Breast Cancer.

Susumu Rokudai

Abstract read
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In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

1 author.

Susumu RokudaiDepartment of Molecular Pharmacology and Oncology, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan. srokudai@gunma-u.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNBC is an aggressive and metastatic subtype of breast cancer in which the TP53 mutation occurs frequently and is associated with particularly poor outcomes. Mutations in TP53 can disrupt the intrinsic function of the tumor suppressor as well as acquire oncogenic gain-of-function (GOF) activities. However, little is known about its oncogenic GOF mediators and functions. Targeted therapy for TNBC patients is thus one of the most urgent needs in breast cancer therapeutics, and identifying genes that have synthetic lethal interactions with mutant TP53 may be a promising approach. Sequential analysis of RNA-seq followed by high-throughput RNA interference screening (HTS-RNAi screening), as an intrinsic cellular mechanism for the identification of genes with synthetic lethality of mutant TP53, is a promising strategy for the treatment of mutant TP53 in TNBC and determining its impact on tumorigenesis.

Indexed as

Gain of Function MutationHigh-Throughput Screening AssaysRNA InterferenceSynthetic Lethal MutationsTriple Negative Breast NeoplasmsTumor Suppressor Protein p53Cell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMutationTP53 protein, humanTumor Suppressor Protein p53Adenosine receptorHigh-throughput RNA interference screens (HTS-RNAi screens)Molecular-targeting cancer therapyMutant TP53Triple-negative breast cancer (TNBC)

Identifiers

PMID41478991

What OpenQuestion holds

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Registered trials

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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.