Synchronous occurrence of squamous-cell carcinoma “transformation” and EGFR exon 20 S768I mutation as a novel mechanism of resistance in EGFR-mutated lung adenocarcinoma

Longo, Lucia; Mengoli, Maria Cecilia; Bertolini, Federica; Bettelli, Stefania; Manfredini, Samantha; Rossi, Giulio

doi:10.1016/j.lungcan.2016.11.012

Cited by 25 publications

(15 citation statements)

References 5 publications

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“…Notably, the computational data on rare EGFR mutations also correlated well with the clinical data (see Supplementary Table 6). [9][10][11][12][13] Furthermore, the data also correlated well with previous computational studies that analyzed the drug sensitivity or resistance of a limited number of EGFR mutants. 14 Only those mutants that displayed a higher RIBA toward a particular inhibitor than that of the WT kinase were considered sensitive in this study.…”

Section: Resultssupporting

confidence: 78%

Computational Analysis of Epidermal Growth Factor Receptor Mutations Predicts Differential Drug Sensitivity Profiles toward Kinase Inhibitors

Akula

Kamasani

Sivan

et al. 2018

Journal of Thoracic Oncology

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Section: Resultssupporting

confidence: 78%

Computational Analysis of Epidermal Growth Factor Receptor Mutations Predicts Differential Drug Sensitivity Profiles toward Kinase Inhibitors

Akula

Kamasani

Sivan

et al. 2018

Journal of Thoracic Oncology

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“…Another challenging situation is the recurrence of EGFR-mutated adenocarcinomas after targeted therapy, resulting in a pure squamous cell carcinoma that may be p40 positive and TTF1 negative while retaining the original EGFR mutation, sometimes with an additional T790M mutation. 22,23 This transition of histologic differentiation may represent a mechanism of resistance to tyrosine kinase inhibitors.…”

Section: Key Questionsmentioning

confidence: 99%

Best Practices Recommendations for Diagnostic Immunohistochemistry in Lung Cancer

Yatabe

Đačić

Borczuk

et al. 2019

Journal of Thoracic Oncology

241

221

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Since the 2015 WHO classification was introduced into clinical practice, immunohistochemistry (IHC) has figured prominently in lung cancer diagnosis. In addition to distinction of small cell versus non-small cell carcinoma, patients' treatment of choice is directly linked to histologic subtypes of non-small cell carcinoma, which pertains to IHC results, particularly for poorly differentiated tumors. The use of IHC has improved diagnostic accuracy in the classification of lung carcinoma, but the interpretation of IHC results remains challenging in some instances. Also, pathologists must be aware of many interpretation pitfalls, and the use of IHC should be efficient to spare the tissue for molecular testing. The International Association for the Study of Lung Cancer Pathology Committee received questions on practical application and interpretation of IHC in lung cancer diagnosis. After discussions in several International Association for the Study of Lung Cancer Pathology Committee meetings, the issues and caveats were summarized in terms of 11 key questions covering common and important diagnostic situations in a daily clinical practice with some relevant challenging queries. The questions cover topics such as the best IHC markers for distinguishing NSCLC subtypes, differences in thyroid transcription factor 1 clones, and the utility of IHC in diagnosing uncommon subtypes of lung cancer and distinguishing primary from metastatic tumors. This article provides answers and explanations for the key questions about the use of IHC in diagnosis of lung carcinoma, representing viewpoints of experts in thoracic pathology that should assist the community in the appropriate use of IHC in diagnostic pathology.

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“…Pathological transformation after EGFR‐TKI treatment has not been adequately studied, but transformation to small cell carcinoma and epithelial–mesenchymal transition are the most common . Although pathological transformation to squamous cell carcinoma has been described in some case reports , the details have not been elucidated. Here, we report two cases with transformation to squamous cell carcinoma after treatment with EGFR‐TKIs.…”

Section: Introductionmentioning

confidence: 99%

Squamous cell transformation as a mechanism of acquired resistance to tyrosine kinase inhibitor in EGFR‐mutated lung adenocarcinoma: a report of two cases

Uruga

Fujii²,

Nakamura

et al. 2020

Respirology Case Reports

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Pathological transformation to squamous cell carcinoma after epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor treatment has been reported, but details of the transformation remain unclear. We report two cases with transformation to squamous cell carcinoma. The first case was a 61-year-old man who was an ex-smoker with stage IV lung adenocarcinoma harbouring EGFR exon 19 insertion. He experienced squamous cell transformation after 28 months of erlotinib therapy. Next-generation sequencing (NGS) analysis showed EGFR T790M and genomic alterations in PTEN, PDGFR, and HRAS. The second case was a 72-year-old man who was an ex-smoker with stage IV lung adenocarcinoma harbouring EGFR exon 21 L858R. He experienced squamous cell transformation after nine months of erlotinib therapy. NGS analysis showed EGFR T790M and genomic alterations in PTEN, SMARCB1, TP53, and KIT. Both patients had PTEN genomic alterations and the PI3K/AKT/mTOR (mammalian target of rapamycin) pathway might play an important role in squamous cell transformation. Case ReportCase 1 A 61-year-old man who was an ex-smoker underwent computed tomography-guided percutaneous lung biopsy. On the basis of the American Joint Committee on Cancer staging

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Synchronous occurrence of squamous-cell carcinoma “transformation” and EGFR exon 20 S768I mutation as a novel mechanism of resistance in EGFR-mutated lung adenocarcinoma

Cited by 25 publications

References 5 publications

Computational Analysis of Epidermal Growth Factor Receptor Mutations Predicts Differential Drug Sensitivity Profiles toward Kinase Inhibitors

Computational Analysis of Epidermal Growth Factor Receptor Mutations Predicts Differential Drug Sensitivity Profiles toward Kinase Inhibitors

Best Practices Recommendations for Diagnostic Immunohistochemistry in Lung Cancer

Squamous cell transformation as a mechanism of acquired resistance to tyrosine kinase inhibitor in EGFR‐mutated lung adenocarcinoma: a report of two cases

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