Evidence map›Paper›PMID 36358848›Full record

ReviewCancers2022

KRAS in NSCLC: State of the Art and Future Perspectives.

Priscilla Cascetta, Arianna Marinello, Chiara Lazzari, Vanesa Gregorc, David Planchard, Roberto Bianco, Nicola Normanno, Alessandro Morabito

Abstract readReview
In one paragraph

Review in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing 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

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

  1. Pooled it
  2. Phase I/II Trial of Exportin 1 Inhibitor Selinexor plus Docetaxel in Previously Treated, Advanced KRAS-Mutant Non-Small Cell Lung Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
    Trial
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  16. Observational
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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

8 authors.

Priscilla CascettaDepartment of Medical Oncology, Gustave Roussy Cancer Campus, 114 rue Edouard Vaillant, 94850 Villejuif, France.ORCID 0000-0002-4252-7543
Arianna MarinelloDepartment of Medical Oncology, Gustave Roussy Cancer Campus, 114 rue Edouard Vaillant, 94850 Villejuif, France.
Chiara LazzariDepartment of Medical Oncology, Candiolo Cancer Institute, FPO-IRCCS, Candiolo, 10060 Turin, Italy.
Vanesa GregorcDepartment of Medical Oncology, Candiolo Cancer Institute, FPO-IRCCS, Candiolo, 10060 Turin, Italy.
David PlanchardDepartment of Medical Oncology, Gustave Roussy Cancer Campus, 114 rue Edouard Vaillant, 94850 Villejuif, France.
Roberto BiancoDepartment of Clinical Medicine and Surgery, Oncology Division, University of Naples Federico II, Via Sergio Pansini 5, 80131 Naples, Italy.
Nicola NormannoCellular Biology and Biotherapy, Istituto Nazionale Tumori, IRCCS, Fondazione G. Pascale, Via Mariano Semmola 53, 80131 Naples, Italy.ORCID 0000-0002-7158-2605
Alessandro MorabitoThoracic Medical Oncology, Istituto Nazionale Tumori, IRCCS, Fondazione G. Pascale, Via Mariano Semmola 53, 80131 Naples, Italy.ORCID 0000-0002-1319-9608

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In NSCLC, KRAS mutations occur in up to 30% of all cases, most frequently at codon 12 and 13. KRAS mutations have been linked to adenocarcinoma histology, positive smoking history, and Caucasian ethnicity, although differences have been described across KRAS mutational variants subtypes. KRAS mutations often concur with other molecular alterations, notably TP53, STK11, and KEAP1, which could play an important role in treatment efficacy and patient outcomes. For many years, KRAS mutations have been considered undruggable mainly due to a high toxicity profile and low specificity of compounds. Sotorasib and adagrasib are novel KRAS inhibitors that recently gained FDA approval for pre-treated KRAS mutant NSCLC patients, and other molecules such as GDC-6036 are currently being investigated with promising results. Despite their approval, the efficacy of these drugs is lower than expected and progression among responders has been reported. Mechanisms of acquired resistance to anti-KRAS molecules typically involves either on target secondary mutations (e.g., G12, G13, Q61H, R68S, H95, Y96C, V8L) or off-target alterations. Ongoing trials are currently evaluating strategies for implementing efficacy and overcoming acquired resistance to these compounds. Finally, the efficacy of immune-checkpoint inhibitors still needs to be completely assessed and responses to anti-PD-1/PD-L1 agents may strongly depend on concomitant mutations.

Indexed as

acquired resistanceadagrasibAMG 510immune-checkpoint inhibitorsKRASlung cancerMRTX849NSCLCsotorasib

Identifiers

PMID36358848
PMCPMC9656434

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.