The DOI matches its Crossref record; 16 of the 16 references it cites were found in a registry or an index.
Transformation from non-small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of origin
Open accessAbstract
Lung cancer is the most common cause of cancer deaths worldwide. The two broad histological subtypes of lung cancer are small-cell lung cancer (SCLC), which is the cause of 15% of cases, and non-small-cell lung cancer (NSCLC), which accounts for 85% of cases and includes adenocarcinoma, squamous-cell carcinoma, and large-cell carcinoma. Although NSCLC and SCLC are commonly thought to be different diseases owing to their distinct biology and genomic abnormalities, the idea that these malignant disorders might share common cells of origin has been gaining support. This idea has been supported by the unexpected findings that a subset of NSCLCs with mutated EGFR return as SCLC when resistance to EGFR tyrosine kinase inhibitors develops. Additionally, other case reports have described the coexistence of NSCLC and SCLC, further challenging the commonly accepted view of their distinct lineages. Here, we summarise the published clinical observations and biology underlying tumours with combined SCLC and NSCLC histology and cancers that transform from adenocarcinoma to SCLC. We also discuss pre-clinical studies pointing to common potential cells of origin, and speculate how the distinct paths of differentiation are determined by the genomics of each disease.
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Cites
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
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
Rosell, R., Carcereny, E., Gervais, R., Vergnenegre, A., Massuti, B., Felip, E., Palmero, R., Garcia-Gomez, R., Pallares, C., Sanchez, J. M., et al. (2012) · The Lancet Oncology · doi:10.1016/s1470-2045(11)70393-x · Cited by 5,489
MET Amplification Leads to Gefitinib Resistance in Lung Cancer by Activating ERBB3 Signaling
Engelman, J. A., Zejnullahu, K., Mitsudomi, T., Song, Y., Hyland, C., Park, J. O., Lindeman, N., Gale, C.-M., Zhao, X., Christensen, J., et al. (2007) · Science · doi:10.1126/science.1141478 · Cited by 4,496
Self-citationMitsudomi, T., Morita, S., Yatabe, Y., Negoro, S., Okamoto, I., Tsurutani, J., Seto, T., Satouchi, M., Tada, H., Hirashima, T., et al. (2010) · The Lancet Oncology · doi:10.1016/s1470-2045(09)70364-x · Cited by 4,090
Genotypic and Histological Evolution of Lung Cancers Acquiring Resistance to EGFR Inhibitors
Sequist, L. V., Waltman, B. A., Dias-Santagata, D., Digumarthy, S., Turke, A. B., Fidias, P., Bergethon, K., Shaw, A. T., Gettinger, S., Cosper, A. K., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002003 · Cited by 3,499
Self-citationSequist, L. V., Yang, J. C.-H., Yamamoto, N., O'Byrne, K., Hirsh, V., Mok, T., Geater, S. L., Orlov, S., Tsai, C.-M., Boyer, M., et al. (2013) · Journal of Clinical Oncology · doi:10.1200/jco.2012.44.2806 · Cited by 3,228
Self-citationScagliotti, G. V., Parikh, P., von Pawel, J., Biesma, B., Vansteenkiste, J., Manegold, C., Serwatowski, P., Gatzemeier, U., Digumarti, R., Zukin, M., et al. (2008) · Journal of Clinical Oncology · doi:10.1200/jco.2007.15.0375 · Cited by 3,203
The T790M mutation in EGFR kinase causes drug resistance by increasing the affinity for ATP
Yun, C.-H., Mengwasser, K. E., Toms, A. V., Woo, M. S., Greulich, H., Wong, K.-K., Meyerson, M., & Eck, M. J. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0709662105 · Cited by 2,118
Wu, Y.-L., Zhou, C., Hu, C.-P., Feng, J., Lu, S., Huang, Y., Li, W., Hou, M., Shi, J. H., Lee, K. Y., et al. (2014) · The Lancet Oncology · doi:10.1016/s1470-2045(13)70604-1 · Cited by 1,978
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Vasan, N., Baselga, J., & Hyman, D. M. (2019) · Nature · doi:10.1038/s41586-019-1730-1 · Cited by 2,770
Burr, M. L., Sparbier, C. E., Chan, K. L., Chan, Y.-C., Kersbergen, A., Lam, E. Y. N., Azidis-Yates, E., Vassiliadis, D., Bell, C. C., Gilan, O., et al. (2019) · Cancer Cell · doi:10.1016/j.ccell.2019.08.008 · Cited by 649
Third-generation EGFR and ALK inhibitors: mechanisms of resistance and management
Cooper, A. J., Sequist, L. V., & Lin, J. J. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00639-9 · Cited by 508
Self-citationNotch signaling pathway in cancer: from mechanistic insights to targeted therapies
Shi, Q., Xue, C., Zeng, Y., Yuan, X., Chu, Q., Jiang, S., Wang, J., Zhang, Y., Zhu, D., & Li, L. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01828-x · Cited by 401
Megyesfalvi, Z., Gay, C. M., Popper, H., Pirker, R., Ostoros, G., Heeke, S., Lang, C., Hoetzenecker, K., Schwendenwein, A., Boettiger, K., et al. (2023) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.21785 · Cited by 369
Metadata
- Authors
- Oser, M. G., Niederst, M. J., Sequist, L. V., & Engelman, J. A.
- Venue
- The Lancet Oncology
- Publisher
- Elsevier BV
- Published
- 2015-04
- Volume
- 16
- Issue
- 4
- Pages
- e165-e172
- ISSN
- 1470-2045 (ISSN-L)
- OpenAlex
- W2061932411
- Cited by
- 942
- References
- 16
- FWCI
- 23.40
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: Transformation from non-small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of origin. https://app.cochat.ai/papers/10.1016/s1470-2045(14)71180-5
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- Oser, M. G., Niederst, M. J., Sequist, L. V., & Engelman, J. A. (2015). Transformation from non-small-cell lung cancer to small-cell lung cancer: molecular drivers and cells of origin. The Lancet Oncology. https://doi.org/10.1016/s1470-2045(14)71180-5
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
