Evidence map›Paper›PMID 36284306›Full record

ReviewJournal of hematology & oncology2022

Drugging KRAS: current perspectives and state-of-art review.

Kaushal Parikh, Giuseppe Banna, Stephen V Liu, Alex Friedlaender, Aakash Desai, Vivek Subbiah, Alfredo Addeo

Open access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
13.0field-weighted citation impact, top 1% 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

91 citing papers in PubMed, 136 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Targeted therapeutic strategies forTranslational lung cancer research · 2026
    Review
  8. Article
  9. Review
  10. CSIE: cancer subtyping via inference and ensemble.Briefings in bioinformatics · 2026
    Article
  11. Article
  12. Article
  13. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. KRAS Clinical Trial Finder: A Patient-Centered Platform for Improving Access to Clinical Trial Information.AMIA Joint Summits on Translational Science proceedings. AMIA Joint Summits on Translational Science · 2026
    Article
  19. Development andTheranostics · 2026
    Article
  20. Article

31 more citing papers are in PubMed but not listed here.

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 at 6 institutions in 3 countries.

Kaushal ParikhMayo Clinic, Rochester, USA.
Giuseppe BannaPortsmouth University Hospitals NHS Trust, Portsmouth, UK.
Stephen V LiuGeorgetown University, Washington, DC, USA.
Alex FriedlaenderClinique General Beaulieu, Geneva, Switzerland.
Aakash DesaiMayo Clinic, Rochester, USA.
Vivek Subbiah *MD Anderson Cancer Center, Houston, USA.
Alfredo Addeo *University Hospital Geneva, Geneva, Switzerland. alfredo.addeo@hcuge.ch.
Mayo Clinic in Florida · USGénérale-Beaulieu Clinic · CHGeorgetown University · USPortsmouth Hospitals NHS Trust · GBThe University of Texas MD Anderson Cancer Center · USUniversity Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

After decades of efforts, we have recently made progress into targeting KRAS mutations in several malignancies. Known as the 'holy grail' of targeted cancer therapies, KRAS is the most frequently mutated oncogene in human malignancies. Under normal conditions, KRAS shuttles between the GDP-bound 'off' state and the GTP-bound 'on' state. Mutant KRAS is constitutively activated and leads to persistent downstream signaling and oncogenesis. In 2013, improved understanding of KRAS biology and newer drug designing technologies led to the crucial discovery of a cysteine drug-binding pocket in GDP-bound mutant KRAS G12C protein. Covalent inhibitors that block mutant KRAS G12C were successfully developed and sotorasib was the first KRAS G12C inhibitor to be approved, with several more in the pipeline. Simultaneously, effects of KRAS mutations on tumour microenvironment were also discovered, partly owing to the universal use of immune checkpoint inhibitors. In this review, we discuss the discovery, biology, and function of KRAS in human malignancies. We also discuss the relationship between KRAS mutations and the tumour microenvironment, and therapeutic strategies to target KRAS. Finally, we review the current clinical evidence and ongoing clinical trials of novel agents targeting KRAS and shine light on resistance pathways known so far.

Indexed as

Antineoplastic AgentsNeoplasmsCysteineGuanosine TriphosphateHumansImmune Checkpoint InhibitorsMutationProto-Oncogene Proteins p21(ras)Tumor MicroenvironmentAntineoplastic AgentsCysteineGuanosine TriphosphateImmune Checkpoint InhibitorsKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID36284306
PMCPMC9597994
OpenAlexW4307201601

What Socratic 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 Socratic graph.