The DOI matches its Crossref record; 74 of the 74 references it cites were found in a registry or an index.
A YAP/FOXM1 axis mediates EMT-associated EGFR inhibitor resistance and increased expression of spindle assembly checkpoint components
Open accessAbstract
YAP and FOXM1 are mediators of EGFR inhibitor resistance, and spindle proteins are therapeutic targets for this multidrug-resistant phenotype.
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“Particularly, YAP/TAZ plays a crucial role in the intrinsic and acquired resistance to inhibitors targeting RTK/MAPK pathway (24, 28–32).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [28]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“accumulating evidence suggests that the dysregulation of the Hippo-YAP/TAZ pathway serves as a central resistance mechanism in multiple therapies, particularly in the intrinsic and acquired resistance to RTK, RAF, or MEK inhibitors (24, 28, 29).”
From YAP/TAZ mediates resistance to KRAS inhibitors through inhibiting proapoptosis and activating the SLC7A5/mTOR axis (2024) · cites this paper as [28]
Experimental — accuracy not yet measuredIn the citing paper
“Nilsson et al. identified activation of a YAP/FOXM1 axis in EMT EGFR TKI-resistant models [91]. This was associated with dysregulation of spindle assembly checkpoint (SAC) proteins, including polo-like kinase 1, aurora kinases, and kinesin spindle protein, and rendered cells vulnerable to SAC inhibitors.”
From Emerging Insights into Targeted Therapy-Tolerant Persister Cells in Cancer (2021) · cites this paper as [91]
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Cites
The Sequence Alignment/Map format and SAMtools
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ANNOVAR: functional annotation of genetic variants from high-throughput sequencing data
Wang, K., Li, M., & Hakonarson, H. H. (2010) · Nucleic Acids Research · doi:10.1093/nar/gkq603 · Cited by 14,724
Fast and accurate long-read alignment with Burrows-Wheeler transform.
Li, H., & Durbin, R. (2010) · Bioinformatics · doi:10.1093/bioinformatics/btp698 · Cited by 12,063
Gefitinib or Carboplatin–Paclitaxel in Pulmonary Adenocarcinoma
Mok, T. S., Wu, Y.-L., Thongprasert, S., Yang, C.-H., Chu, D.-T., Saijo, N., Sunpaweravong, P., Han, B., Margono, B., Ichinose, Y., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0810699 · Cited by 8,261
Comprehensive molecular profiling of lung adenocarcinoma
The Cancer Genome Atlas Research Network (2014) · Nature · doi:10.1038/nature13385 · Cited by 5,732
Gefitinib or Chemotherapy for Non–Small-Cell Lung Cancer with Mutated EGFR
Maemondo, M., Inoue, A., Kobayashi, K., Sugawara, S., Oizumi, S., Isobe, H., Gemma, A., Harada, M., Yoshizawa, H., Kinoshita, I., et al. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa0909530 · Cited by 5,525
Osimertinib in Untreated EGFR -Mutated Advanced Non–Small-Cell Lung Cancer
Soria, J.-C., Ohe, Y., Vansteenkiste, J., Reungwetwattana, T., Chewaskulyong, B., Lee, K. H., Dechaphunkul, A., Imamura, F., Nogami, N., Kurata, T., et al. (2018) · New England Journal of Medicine · doi:10.1056/nejmoa1713137 · Cited by 5,508
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Research works printed but not linked: 1
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Tang, T. T., Konradi, A. W., Feng, Y., Peng, X., Ma, M., Li, J., Yu, F.-X., Guan, K.-L., & Post, L. (2021) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.mct-20-0717 · Cited by 245
Coordinating gene expression during the cell cycle
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Hagenbeek, T. J., Zbieg, J. R., Hafner, M., Mroue, R., Lacap, J. A., Sodir, N. M., Noland, C. L., Afghani, S., Kishore, A., Bhat, K. P., et al. (2023) · Nature Cancer · doi:10.1038/s43018-023-00577-0 · Cited by 215
Insights into recent findings and clinical application of YAP and TAZ in cancer
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Metadata
- Authors
- Nilsson, M. B., Sun, H., Robichaux, J., Pfeifer, M., McDermott, U., Travers, J., Diao, L., Xi, Y., Tong, P., Shen, L., Hofstad, M., Kawakami, M., Le, X., Liu, X., Fan, Y., Poteete, A., Hu, L., Negrao, M. V., Tran, H., Dmitrovsky, E., Peng, D., Gibbons, D. L., Wang, J., & Heymach, J. V.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- AstraZeneca (United Kingdom) (GB)
- Departments of Thoracic/Head and Neck Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
- Corresponding author
- Heymach, John V.
- ORCID
- Nilsson, Monique B.
- Sun, Huiying
- Robichaux, Jacqulyne
- Pfeifer, Matthias
- McDermott, Ultan
- Travers, Jon
- Diao, Lixia
- Xi, Yuanxin
- Tong, Pan
- Shen, Li
- Hofstad, Mia
- Kawakami, Masanori
- Le, Xiuning
- Liu, Xi
- Fan, Youhong
- Poteete, Alissa
- Hu, Limei
- Negrao, Marcelo V.
- Tran, Hai
- Dmitrovsky, Ethan
- Peng, David
- Gibbons, Don L.
- Wang, Jing
- Heymach, John V.
- Venue
- Science Translational Medicine
- Published
- 2020-09-02
- Volume
- 12
- Issue
- 559
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC8269000
- OpenAlex
- W3082143929
- Cited by
- 177
- References
- 74
- Citations by year
- 2026: 15 · 2025: 34 · 2024: 29 · 2023: 40 · 2022: 31 · 2021: 26 · 2020: 2
- FWCI
- 14.23
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Lung SPORE grant P50 CA070907, NIH CCSG (CA016672), CA016672, 1R01 CA190628)
- National Cancer Institute (HHSN261200800001E)
- LUNGevity Foundation
- University of Texas MD Anderson Cancer Center (Lung Cancer Moon Shot Program)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- epithelial-mesenchymal transition, EGFR tyrosine kinase inhibitor resistance, spindle assembly checkpoint, multidrug resistance, therapeutic vulnerabilities, non-small cell lung cancer, clinical outcomes
- MeSH terms
- Forkhead Box Protein M1, Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Humans, Lung Neoplasms, Drug Resistance, Neoplasm, Proteomics, Cell Line, Tumor, Protein Kinase Inhibitors, Epithelial-Mesenchymal Transition, M Phase Cell Cycle Checkpoints, ErbB Receptors
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