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Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy

Nature(2024)10.1038/s41586-024-07205-6Source: DataRank Database

Concurrent inhibition of oncogenic and wild-type RAS-GTP for cancer therapy is a research paper published in Nature (2024). On theSindex it has a DataRank of 4.2. It has been cited 326 times, with 100 citing works in its 1-hop citation network.

N/A

4.2DataRank · unranked

Scored on demand from live citation data

Deposits data Open Access326 citations · 100 citing works in its network

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Linked data & code

nct pdb

Data availability

Repositories this paper deposited data in (declared in PubMed).

ClinicalTrials.govNCT05379985

DataRank reads this dataset's downstream impact straight off the citation graph — no black box, no proprietary weighting. How is this computed?

›Methodology & internals

datarank_citation_only_1hop_v6· scope data_onlyMethodology

Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring

Enrichment:Funding (20 grants)Impact (FWCI 54.47)OA: hybridTopics (76)IDs (PubMed, PMC, OpenAlex)Annotations (2)SDGs (2)

FAIR Checklist

Context only (not used in score)

Findable (1/2)

Has DOI

Accessible (1/2)

Open Access

Interoperable (0/2)

Reusable (0/3)

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DataRank Breakdown

Base Score 20%Citation Network 80%

Base Score Contribution

0.868

From this paper's citation signal

Citation Network Contribution

3.4

From 100 citing papers with measurable signal

Learn more about DataRank methodology →

Top 5 citers driving the network score

Ranked by each citer's contribution to N(p) — log1p(C_q) divided by its reference count — out of 100 citers.

HRS-4642: The next piece of the puzzle to keep KRAS in check
Cancer Cell202411 citations10 referencesContributes 0.248
Finding the sweet spot: Targeting RAS in tumors while sparing normal tissue
Cancer Cell202411 citations11 referencesContributes 0.226
Unlocking the promise of RAS inhibition in pancreatic cancer
Nature Reviews Gastroenterology & Hepatology20247 citations10 referencesContributes 0.208
Beware of extreme calculated lipophilicity when designing cyclic peptides
Nature Chemical Biology20245 citations13 referencesContributes 0.138
Identification of Novel pan-KRAS Inhibitors via Structure-Based Drug Design, Scaffold Hopping, and Biological Evaluation
ACS Medicinal Chemistry Letters20255 citations16 referencesContributes 0.112

Authors (53)

Bianca J. Lee ORCID,Jingjing Jiang ORCID,Aidan C.A. Tomlinson ORCID,Kyle J. Seamon ORCID,Alessia Mira ORCID

Live enrichment

PubMed:38589574 PMC:PMC11111408 OpenAlex:https://openalex.org/W4394580100

NCI NIH HHS

Grant: F32 CA239328

NCI NIH HHS

Grant: R01 CA276268

NCI NIH HHS

Grant: K22 CA276632

NCI NIH HHS

Grant: R00 CA276700

NCI NIH HHS

Grant: R01 CA279264

NCI NIH HHS

Grant: R35 CA232113

NCI NIH HHS

Grant: K99 CA276700

NCI NIH HHS

Grant: P30 CA008748

NCI NIH HHS

Grant: R01 CA230745

NCI NIH HHS

Grant: P50 CA257911

NCI NIH HHS

Grant: T32 CA009156

National Institutes of Health

Grant: 5K99CA276700-02

Mechanistic Basis for ERK in driving KRAS-dependent pancreatic cancer

National Institutes of Health

Grant: 5R35CA232113-04

Targeting undruggable RAS for cancer treatment

National Institutes of Health

Grant: 1K22CA276632-01

Identification of resistance mechanisms to direct KRAS inhibition in pancreatic cancer

National Institutes of Health

Grant: 2P30CA008748-43

MOUSE GENETICS

National Institutes of Health

Grant: 1P50CA257911-01A1

Selective Targeting of Pancreatic Cancer SPORE

National Institutes of Health

Grant: 5T32CA009156-20

BASIC MECHANISMS OF VIRAL AND CHEMICAL CARCINOGENESIS

European Commission

Grant: 101001288

From the understanding of KRAS-RAF membrane dynamics to new therapeutic strategies in cancer

National Institutes of Health

Grant: 1F32CA239328-01

Defining the roles of ERK MAPK in driving KRAS-mutant pancreatic cancer growth.

National Institutes of Health

Grant: 1R01CA279264-01

Mechanisms of adaptation and resistance to emerging therapies for lung cancer

FWCI

54.47

Citation Percentile

1.0%

Citation Trend

2023

2024

2025

2026

hybridLicense: cc-by

journalhttps://www.nature.com/articles/s41586-024-07205-6.pdf

publisherhttps://www.nature.com/articles/s41586-024-07205-6.pdf

publisherhttps://www.nature.com/articles/s41586-024-07205-6

journalhttps://doi.org/10.1038/s41586-024-07205-6

repositoryhttps://pubmed.ncbi.nlm.nih.gov/38589574

Fields of Study

Protein Kinase Regulation and GTPase SignalingPI3K/AKT/mTOR signaling in cancerMelanoma and MAPK Pathways0301 basic medicine0303 health sciences03 medical and health sciencesAnimalsHumansMiceAntineoplastic AgentsCell Line, TumorGuanosine TriphosphateMice, Inbred BALB CMice, Inbred C57BLMutationNeoplasmsOncogene Protein p21(ras)PiperazinesProto-Oncogene Proteins p21(ras)Signal TransductionXenograft Model Antitumor AssaysMembrane ProteinsGTP Phosphohydrolases

MeSH Terms

AnimalsAntineoplastic AgentsFemaleGuanosine TriphosphateHumansMaleMembrane ProteinsMice, Inbred BALB CMice, Inbred C57BLMutationNeoplasmsPiperazinesSignal TransductionOncogene Protein p21(ras)Proto-Oncogene Proteins p21(ras)GTP PhosphohydrolasesXenograft Model Antitumor AssaysCell Line, TumorMice

Keywords

KRASHRASNeuroblastoma RAS viral oncogene homologCancer researchCancerBiologyEGFR inhibitorsTargeted therapyMutationMedicineGeneColorectal cancerGeneticsEpidermal growth factor receptorMice, Inbred BALB CMembrane ProteinsDrug developmentAntineoplastic AgentsOncogene Protein p21(ras)Xenograft Model Antitumor AssaysArticlePiperazinesGTP PhosphohydrolasesMice, Inbred C57BLProto-Oncogene Proteins p21(ras)Cancer therapeutic resistanceMiceTargeted therapiesCell Line, TumorNeoplasmsAnimalsHumansGuanosine TriphosphateSignal Transduction

Sustainable Development Goals

SDG 3: 3. Good healthSDG 0: Good health and well-being