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Focal adhesion kinase-YAP signaling axis drives drug-tolerant persister cells and residual disease in lung cancer

Nature Communications(2024)10.1038/s41467-024-47423-0Source: DataRank Database

Focal adhesion kinase-YAP signaling axis drives drug-tolerant persister cells and residual disease in lung cancer is a research paper published in Nature Communications (2024). On theSindex it has a DataRank of 1.7. It has been cited 93 times, with 78 citing works in its 1-hop citation network.

N/A

1.7DataRank · unranked

Scored on demand from live citation data

Open Access93 citations · 78 citing works in its network

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›Methodology & internals

datarank_citation_only_1hop_v6· scope data_onlyMethodology

Pipeline:MetadataData-paper checkEnrichmentCitation networkScoring

Enrichment:Funding (11 grants)Impact (FWCI 20.61)OA: goldTopics (64)IDs (PubMed, OpenAlex)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 40%Citation Network 60%

Base Score Contribution

0.681

From this paper's citation signal

Citation Network Contribution

1.0

From 54 citing papers with measurable signal

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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 78 citers.

Mechanisms of Adaptive Resistance to Targeted Therapy in RET -Aberrant Cancers
Clinical Cancer Research20252 citations7 referencesContributes 0.157
Direct and selective pharmacological disruption of the YAP–TEAD interface by IAG933 inhibits Hippo-dependent and RAS–MAPK-altered cancers
Nature Cancer2024140 citations72 referencesContributes 0.069
Hippo pathway activation mediates cardiomyocyte ferroptosis to promote dilated cardiomyopathy through downregulating NFS1
Redox Biology202523 citations51 referencesContributes 0.062
Mitochondrial fatty acid oxidation as the target for blocking therapy-resistance and inhibiting tumor recurrence: The proof-of-principle model demonstrated for ovarian cancer cells
Journal of Advanced Research20259 citations47 referencesContributes 0.049
Long non-coding RNA LRTOR drives osimertinib resistance in non-small cell lung cancer by boosting YAP positive feedback loop
Drug Resistance Updates202510 citations52 referencesContributes 0.046

Authors (35)

Yu‐Ting Chou ORCID,Lauren Čech ORCID,Celia Fernández-Méndez ORCID,Johnny Yu ORCID,Victor Olivas

Live enrichment

PubMed:38702301 OpenAlex:https://openalex.org/W4396605932

National Institutes of Health

Grant: 5R01CA169338-02

Rational Combined Inhibition of NF-kB and EGFR to Optimize Lung Cancer Treatment

National Institutes of Health

Grant: 5R01HL120724-02

Balanced signaling cues to guide cell transitions in the blood lineage continuum

National Institutes of Health

Grant: 5U01CA217851-05

Organoid-based Discovery of Oncogenic Drivers and Treatment Resistance Mechanisms

National Institutes of Health

Grant: 1U54CA224065-01

University of Texas PDX Development and Trial Center

National Institutes of Health

Grant: 5R01CA211052-03

Optimizing biologically-based rational polytherapy in ALK+ lung cancer

National Institutes of Health

Grant: 1R01CA204302-01A1

Characterization of YAP as a rational companion target in lung cancer

National Institutes of Health

Grant: 1U01CA217882-01

The Cancer Target Discovery and Development Network at UCSF

National Institutes of Health

Grant: 5R01CA231300-03

(PQ7) Defining a new mode of RAS signaling in cancer from cytoplasmic protein granules

National Institutes of Health

Grant: 5R01GM131641-06

Mapping endogenous protein dynamics in living cells

National Institutes of Health

Grant: 5R01AI104789-05

Loss of Intrinsic Control in Autoimmune T Helper Cells with Signaling Variants

National Institutes of Health

Grant: 3U54CA224081-01S1

Bay Area Team Against Resistance

FWCI

20.61

Citation Percentile

1.0%

Citation Trend

2022

2023

2024

2025

2026

goldLicense: cc-by

journalhttps://doi.org/10.1038/s41467-024-47423-0

repositoryhttps://pubmed.ncbi.nlm.nih.gov/38702301

repositoryhttps://www.ncbi.nlm.nih.gov/pmc/articles/11068778

repositoryhttps://digitalcommons.library.tmc.edu/uthgsbs_docs/2835

repositoryhttp://hdl.handle.net/10261/371377

Fields of Study

Hippo pathway signaling and YAP/TAZFibroblast Growth Factor ResearchCancer-related gene regulation0301 basic medicine03 medical and health sciences0303 health sciences

MeSH Terms

Anaplastic Lymphoma KinaseYAP-Signaling ProteinsAnimalsAntineoplastic AgentsCarcinoma, Non-Small-Cell LungHumansLung NeoplasmsTranscription FactorsSignal TransductionProto-Oncogene Proteins p21(ras)Neoplasm, ResidualDrug Resistance, NeoplasmXenograft Model Antitumor AssaysCell Line, TumorAdaptor Proteins, Signal TransducingMiceFocal Adhesion Protein-Tyrosine KinasesFocal Adhesion Kinase 1ErbB Receptors

Keywords

KRASTargeted therapyCancer researchLung cancerMedicineMinimal residual diseaseCancerSignal transductionFocal adhesionOncologyBiologyImmunologyInternal medicineColorectal cancerCell biologyLeukemiaLung NeoplasmsNeoplasm, ResidualScienceAntineoplastic AgentsArticleProto-Oncogene Proteins p21(ras)MiceCarcinoma, Non-Small-Cell LungCell Line, TumorHumansAnimalsAnaplastic Lymphoma KinaseAdaptor Proteins, Signal TransducingQYAP-Signaling ProteinsXenograft Model Antitumor AssaysErbB ReceptorsCancer therapeutic resistanceDrug Resistance, NeoplasmFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesNon-small-cell lung cancerTranscription Factors

Sustainable Development Goals

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