Evidence map›Paper›PMID 25557115›Full record

ReviewActa pharmacologica Sinica2015

The RAS-RAL axis in cancer: evidence for mutation-specific selectivity in non-small cell lung cancer.

Sunny Guin, Dan Theodorescu

Open access · bronzeAbstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
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  14. KRAS, NRAS and BRAF mutations in colorectal cancer and melanoma.Medical oncology (Northwood, London, England) · 2017
    Review
  15. Article
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  18. The higher level of complexity of K-Ras4B activation at the membrane.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  19. Article
  20. 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

2 authors at 2 institutions in 1 country.

Sunny Guin1] Department of Surgery, University of Colorado, Aurora, CO 80045, USA [2] Department of Pharmacology, University of Colorado, Aurora, CO 80045, USA.
Dan Theodorescu1] Department of Surgery, University of Colorado, Aurora, CO 80045, USA [2] Department of Pharmacology, University of Colorado, Aurora, CO 80045, USA [3] University of Colorado Comprehensive Cancer Center, Aurora, CO 80045, USA.
University of Colorado Anschutz Medical Campus · USUniversity of Colorado Denver · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activating RAS mutations are common in human tumors. These mutations are often markers for resistance to therapy and subsequent poor prognosis. So far, targeting the RAF-MEK-ERK and PI3K-AKT signaling pathways downstream of RAS is the only promising approach in the treatment of cancer patients harboring RAS mutations. RAL GTPase, another downstream effector of RAS, is also considered as a therapeutic option for the treatment of RAS-mutant cancers. The RAL GTPase family comprises RALA and RALB, which can have either divergent or similar functions in different tumor models. Recent studies on non-small cell lung cancer (NSCLC) have showed that different RAS mutations selectively activate specific effector pathways. This observation requires broader validation in other tumor tissue types, but if true, will provide a new approach to the treatment of RAS-mutant cancer patients by targeting specific downstream RAS effectors according to the type of RAS mutation. It also suggests that RAL GTPase inhibition will be an important treatment strategy for tumors harboring RAS glycine to cysteine (G12C) or glycien to valine (G12V) mutations, which are commonly found in NSCLC and pancreatic cancer.

Indexed as

MutationAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungEnzyme InhibitorsHumansLung NeoplasmsMolecular Targeted Therapyral GTP-Binding Proteinsras ProteinsSignal TransductionAntineoplastic AgentsEnzyme Inhibitorsral GTP-Binding Proteinsras Proteins

Identifiers

PMID25557115
PMCPMC4349922
OpenAlexW2008183550

What OpenQuestion holds

Textmetadata
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.