Evidence map›Paper›PMID 35046095›Full record

ReviewCancer discovery2022

Expanding the Reach of Precision Oncology by Drugging All KRAS Mutants.

Marco H Hofmann, Daniel Gerlach, Sandra Misale, Mark Petronczki, Norbert Kraut

Abstract readReview
In one paragraph

Review in Cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 1 pooled it
–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

197 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Design, synthesis and biological evaluation of novel KRAS-G12D inhibitors.Journal of enzyme inhibition and medicinal chemistry · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. The SOS1 Inhibitor BI 1701963 as Monotherapy or in Combination with Trametinib in Patients with KRAS Mutation-Positive Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026
    Article
  9. Review
  10. Article
  11. Article
  12. Precision Targeting ofInternational journal of molecular sciences · 2026
    Review
  13. Targeting WFS1 overcomes KRASNPJ precision oncology · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

137 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

5 authors.

Marco H HofmannDiscovery Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria.ORCID 0000-0001-7557-1156
Daniel GerlachDiscovery Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria.ORCID 0000-0001-9338-3765
Sandra MisaleMolecular Pharmacology Program, Memorial Sloan-Kettering Cancer Center, New York, New York.
Mark PetronczkiDiscovery Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria.ORCID 0000-0003-0139-5692
Norbert KrautDiscovery Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria.ORCID 0000-0003-3941-7105

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

KRAS is the most frequently mutated oncogene, harboring mutations in approximately one in seven cancers. Allele-specific KRASG12C inhibitors are currently changing the treatment paradigm for patients with KRASG12C-mutated non-small cell lung cancer and colorectal cancer. The success of addressing a previously elusive KRAS allele has fueled drug discovery efforts for all KRAS mutants. Pan-KRAS drugs have the potential to address broad patient populations, including KRASG12D-, KRASG12V-, KRASG13D-, KRASG12R-, and KRASG12A-mutant or KRAS wild-type-amplified cancers, as well as cancers with acquired resistance to KRASG12C inhibitors. Here, we review actively pursued allele-specific and pan-KRAS inhibition strategies and their potential utility. SIGNIFICANCE: Mutant-selective KRASG12C inhibitors target a fraction (approximately 13.6%) of all KRAS-driven cancers. A broad arsenal of KRAS drugs is needed to comprehensively conquer KRAS-driven cancers. Conceptually, we foresee two future classes of KRAS medicines: mutant-selective KRAS drugs targeting individual variant alleles and pan-KRAS therapeutics targeting a broad range of KRAS alterations.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsHumansMutationOncogenesPrecision MedicineProto-Oncogene Proteins p21(ras)KRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID35046095
PMCPMC9394389

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.