Evidence map›Paper›PMID 40330550›Full record

ArticleNAR cancer2025

A systematic evaluation of the therapeutic potential of endogenous-ADAR editors in cancer prevention and treatment.

Rona Merdler-Rabinowicz, Ariel Dadush, Sumeet Patiyal, Padma Sheila Rajagopal, Gulzar N Daya, Shay Ben-Aroya, Alejandro A Schäffer, Eli Eisenberg, Eytan Ruppin, Erez Y Levanon

Abstract read
In one paragraph

Article in NAR cancer, 2025. 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

10 authors.

Rona Merdler-RabinowiczCancer Data Science Lab, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.ORCID 0000-0002-6133-8158
Ariel DadushMina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, 5290002, Israel.ORCID 0009-0000-2197-3889
Sumeet PatiyalCancer Data Science Lab, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Padma Sheila RajagopalCancer Data Science Lab, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Gulzar N DayaCancer Data Science Lab, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Shay Ben-AroyaMina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, 5290002, Israel.ORCID 0000-0002-6425-4259
Alejandro A SchäfferCancer Data Science Lab, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.
Eli EisenbergRaymond and Beverly Sackler School of Physics and Astronomy, Tel-Aviv University, Tel Aviv, 6997801, Israel.ORCID 0000-0001-8681-3202
Eytan RuppinCancer Data Science Lab, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, United States.ORCID 0000-0002-3390-110X
Erez Y LevanonMina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan, 5290002, Israel.ORCID 0000-0002-3641-4198

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenosine deaminases acting on RNA (ADAR) enzymes constitute a natural cellular mechanism that induces A-to-I(G) editing, introducing genetic changes at the RNA level. Recently, interest in the endogenous-ADAR editor has emerged for correcting genetic mutations, consisting of a programmed oligonucleotide that attracts the native ADAR, thereby offering opportunities for medical therapy. Here, we systematically chart the scope of cancer mutations that endogenous-ADAR can correct. First, analyzing germline single nucleotide variants in cancer predisposition genes, we find that endogenous-ADAR can revert a fifth of them, reducing the risk of cancer development later in life. Second, examining somatic mutations across various cancer types, we find that it has the potential to correct at least one driver mutation in over a third of the samples, suggesting a promising future treatment strategy. We also highlight key driver mutations that are amenable to endogenous-ADAR, and are thus of special clinical interest. As using endogenous-ADAR entails delivering relatively small payloads, the prospects of delivering endogenous-ADAR to various cancers seem promising. We expect that the large scope of correctable mutations that are systematically charted here for the first time will pave the way for a new era of cancer treatment options.

Indexed as

Adenosine DeaminaseNeoplasmsRNA-Binding ProteinsRNA EditingGenetic Predisposition to DiseaseGerm-Line MutationHumansMutationADAR protein, humanAdenosine DeaminaseRNA-Binding Proteins

Identifiers

PMID40330550
PMCPMC12053386

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.