Evidence map›Paper›PMID 40597785›Full record

ReviewBMC cancer2025

The complex journey of targeting RAS in oncology.

Katarzyna Wasiak, Damian Ciunowicz, Amelia Kierasińska-Kałka, Marta Węgierska, Marcin Pacholczyk, Piotr Rieske, Ewelina Stoczyńska-Fidelus

Abstract readReview
In one paragraph

Review in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. 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

7 authors.

Katarzyna WasiakDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland. katarzyna.wasiak@umed.lodz.pl.
Damian CiunowiczDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland.
Amelia Kierasińska-KałkaDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland.
Marta WęgierskaDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland.
Marcin PacholczykDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland.
Piotr RieskeDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland.
Ewelina Stoczyńska-FidelusDepartment of Research and Development, Personather Ltd., Inwestycyjna 7, Konstantynow Lodzki, 95 - 050, Poland.

Funding

Narodowe Centrum Badań i Rozwoju POIR.01.02.00-00-0034/15
6 · The paper itself

Abstract

Given the prevalence of RAS mutations in various cancers, personalized therapeutic approaches, guided by molecular markers, are essential. Farnesyltransferase inhibitors (FTIs) have emerged as potential therapeutic options; however, they also face obstacles such as toxicity and limited efficacy. Alternative strategies, such as direct inhibitors combined with pathway modulators, RNA interference, and gene-editing technologies, are under clinical investigation. The targeting of RAS, complicated by its structural nuances, particularly in the G domain, has advanced with the identification of druggable pockets such as the SW-II pocket. This breakthrough has led to the development of targeted therapeutics, such as sotorasib and adagrasib, for KRAS G12C-mutated non-small cell lung cancer (NSCLC). However, these advancements face challenges, including adaptive resistance and the necessity for isoform selectivity. New inhibitors, such as LY3537982 or GDC-6036, are promising, but achieving effective and selective RAS inhibition remains a significant challenge. Additionally, clinical trials have highlighted variability in patient responses, attributing limited treatment efficacy to resistance mechanisms, including on-target mutations and off-target pathway activations. Finally, the RAS oncogene, traditionally viewed as predominantly pro-cancerous, plays a complex role in oncogenesis, with recent evidence suggesting context-dependent effects, such as inducing senescence in certain cells. This shift in understanding underscores the therapeutic potential of manipulating the interplay between RAS and TP53 mutations in cancer. In conclusion, the complexity of effectively targeting the RAS-RAF-ERK pathway is exacerbated by the diverse resistance mechanisms. Challenges such as off-target effects and delivery issues remain significant barriers in the introduction of effective therapies based on RAS inhibitors. This overview highlights the evolving nature of targeting RAS in cancer therapy.

Indexed as

Antineoplastic AgentsMolecular Targeted TherapyNeoplasmsras ProteinsFarnesyltranstransferaseHumansMutationAntineoplastic AgentsFarnesyltranstransferaseras ProteinsCancerDrug discoveryHRASKRASNRASOncogeneProtein structureRAS proteinsSenescenceTherapy

Identifiers

PMID40597785
PMCPMC12211582

What OpenQuestion holds

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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.