Evidence map›Paper›PMID 33065029›Full record

ReviewCell2020

Targeting KRAS(G12C): From Inhibitory Mechanism to Modulation of Antitumor Effects in Patients.

Dongsung Kim, Jenny Yaohua Xue, Piro Lito

Open access · bronzeAbstract readReview
In one paragraph

Review in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 135 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
135citing papers in PubMed, 1 pooled it
12.0field-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

135 citing papers in PubMed, 1 synthesis or guideline pooled it, 234 citations in OpenAlex.

  1. KRAS G12C inhibitors in KRASFrontiers in immunology · 2026
    Pooled it
  2. Trial
  3. Review
  4. A dual assault on KRAS.Nature chemical biology · 2026
    Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Systematic and precise interventions for KRAS-mutant cancers.Experimental hematology & oncology · 2026
    Review
  13. Therapeutic advances with KRASCancer gene therapy · 2026
    Review
  14. Article
  15. KRASScience advances · 2026
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

75 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

3 authors at 1 institution in 1 country.

Dongsung KimHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer, New York, NY, USA.
Jenny Yaohua XueHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer, New York, NY, USA; Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program, New York, NY, USA.
Piro LitoHuman Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer, New York, NY, USA; Weill Cornell/Rockefeller/Sloan Kettering Tri-Institutional MD-PhD Program, New York, NY, USA; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA; Department of Medicine, Weill Cornell Medical College, New York, NY, USA. Electronic address: litop@mskcc.org.
Memorial Sloan Kettering Cancer Center · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Dissecting KRAS oncoprotein signaling with small molecule inhibitorsR01CA230745 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI Piro Lito · 2018 to 2026
$3.8M
Studies on the effects of a novel intermittent therapy on intratumoral clonal architecture and resistanceR01CA230267 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LITO, PIRO · 2019 to 2023
$2.0M
Elucidating the regulation of mitosis by BRAF V600E in lung cancerK08CA191082 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI LITO, PIRO · 2015 to 2019
$872k
Dissecting the evolution of targeted therapy resistance in BRAFV600E-mutant cancerF30CA232549 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI XUE, JENNY YAOHUA · 2018 to 2021
$191k
NCI NIH HHS F30 CA232549NCI NIH HHS K08 CA191082NCI NIH HHS R01 CA230267NCI NIH HHS R01 CA230745NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

KRAS mutations are among the most common genetic alterations in lung, colorectal, and pancreatic cancers. Direct inhibition of KRAS oncoproteins has been a long-standing pursuit in precision oncology, one established shortly after the discovery of RAS mutations in human cancer cells nearly 40 years ago. Recent advances in medicinal chemistry have established inhibitors targeting KRAS(G12C), a mutation found in ∼13% of lung adenocarcinomas and, at a lower frequency, in other cancers. Preclinical studies describing their discovery and mechanism of action, coupled with emerging clinical data from patients treated with these drugs, have sparked a renewed enthusiasm in the study of KRAS and its therapeutic potential. Here, we discuss how these advances are reshaping the fundamental aspects of KRAS oncoprotein biology and the strides being made toward improving patient outcomes in the clinic.

Indexed as

Molecular Targeted TherapyAntineoplastic AgentsClinical Trials as TopicDrug Resistance, NeoplasmHumansMutationProto-Oncogene Proteins p21(ras)Antineoplastic AgentsKRAS protein, humanProto-Oncogene Proteins p21(ras)

Identifiers

PMID33065029
PMCPMC7669705
OpenAlexW3093242429

What OpenQuestion holds

Textmetadata
LicenceTDM
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.