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The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.

Concurrent RB1 and TP53 Alterations Define a Subset of EGFR-Mutant Lung Cancers at risk for Histologic Transformation and Inferior Clinical Outcomes

Open access
Offin, Michael, Chan, Joseph M., Tenet, Megan, Rizvi, Hira A., Shen, Ronglai, Riely, Gregory J., Rekhtman, Natasha, Daneshbod, Yahya, Quintanal-Villalonga, Alvaro, Penson, Alexander, Hellmann, Matthew D., Arcila, Maria E., Ladanyi, Marc, Pe’er, Dana, Kris, Mark G., Rudin, Charles M., Yu, Helena A.·2019·Journal of Thoracic Oncology
DOI 10.1016/j.jtho.2019.06.002
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Abstract

Introduction: EGFR-mutant lung cancers are clinically and genomically heterogeneous with concurrent RB1/TP53 alterations identifying a subset at increased risk for small cell transformation. The genomic alterations that induce lineage plasticity are unknown. Methods: Patients with EGFR/RB1/TP53-mutant lung cancers, identified by NGS from 2014–2018, were compared to patients with untreated, metastatic EGFR-mutant lung cancers without both RB1- and TP53-alterations. Time to EGFR-tyrosine kinase inhibitor (EGFR-TKI) discontinuation (TTD), overall survival, SCLC transformation rate, and genomic alterations were evaluated. Results: Patients with EGFR/RB1/TP53-mutant lung cancers represented 5% (43/863) of EGFR-mutant lung cancers but were uniquely at risk for transformation (18%, 7/39), with no transformations in EGFR-mutant lung cancers without baseline TP53 and RB1 alterations. Irrespective of transformation, patients with EGFR/TP53/RB1-mutant lung cancers had a shorter TTD than EGFR/TP53 and EGFR-mutant only cancers (9.5 vs 12.3 vs 36.6 months respectively, p = 2×10−9). The triple-mutant population had a higher incidence of whole genome doubling (WGD) compared to NSCLC and SCLC at large (80% vs 34%, p < 5×10−9; vs 51%, p < 0.002 respectively) and further enrichment in triple-mutant cancers with eventual small cell histology (7/7 pre-transformed plus 4/4 baseline SCLC vs 23/32 never transformed respectively, p = 0.05). AID/APOBEC mutation signature was also enriched in triple-mutant lung cancers that transformed (FDR = 0.03). Conclusions: EGFR/TP53/RB1-mutant lung cancers are at unique risk of histologic transformation, with 25% presenting with de novo SCLC or eventual small cell transformation. Triple-mutant lung cancers are enriched in WGD and AID/APOBEC hypermutation which may represent early genomic determinants of lineage plasticity.

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Metadata

Authors
Offin, M., Chan, J. M., Tenet, M., Rizvi, H. A., Shen, R., Riely, G. J., Rekhtman, N., Daneshbod, Y., Quintanal-Villalonga, A., Penson, A., Hellmann, M. D., Arcila, M. E., Ladanyi, M., Pe’er, D., Kris, M. G., Rudin, C. M., & Yu, H. A.
Venue
Journal of Thoracic Oncology
Publisher
Elsevier BV
Published
2019-10
Volume
14
Issue
10
Pages
1784-1793
ISSN
1556-0864 (ISSN-L)
DOI
10.1016/j.jtho.2019.06.002
OpenAlex
W2952506496
Cited by
444
References
29
FWCI
28.33
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Concurrent RB1 and TP53 Alterations Define a Subset of EGFR-Mutant Lung Cancers at risk for Histologic Transformation and Inferior Clinical Outcomes. https://app.cochat.ai/papers/10.1016/j.jtho.2019.06.002
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Offin, M., Chan, J. M., Tenet, M., Rizvi, H. A., Shen, R., Riely, G. J., Rekhtman, N., Daneshbod, Y., Quintanal-Villalonga, A., Penson, A., Hellmann, M. D., Arcila, M. E., Ladanyi, M., Pe’er, D., Kris, M. G., Rudin, C. M., & Yu, H. A. (2019). Concurrent RB1 and TP53 Alterations Define a Subset of EGFR-Mutant Lung Cancers at risk for Histologic Transformation and Inferior Clinical Outcomes. Journal of Thoracic Oncology. https://doi.org/10.1016/j.jtho.2019.06.002

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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