Case report: durable response to osimertinib, radiotherapy, and chemotherapy combination in advanced non-small cell lung cancer with atypical metastasis

Introduction

In recent years, comprehensive genomic profiling has transformed the management of non-small cell lung cancer (NSCLC), particularly for patients with actionable driver mutations (1). Among these, EGFR mutations are among the most clinically significant, found in 10–15% of NSCLC cases in Western populations and up to 50% in East Asian populations (2). These mutations, especially exon 19 deletions and exon 21 L858R substitutions, are more common in never-smokers and predict sensitivity to EGFR tyrosine kinase inhibitors (TKIs) (3). Osimertinib, a third-generation EGFR TKI, has demonstrated superior efficacy and central nervous system (CNS) penetration compared to earlier agents, becoming the standard first-line treatment for EGFR-mutated NSCLC (4-6). However, tumor behavior within this molecular subgroup is heterogeneous, as is their progression. While metastases in EGFR-mutated NSCLC typically involve the brain, bone, liver, or adrenal glands, rare presentations involving the pancreas, ocular structures, masticator space, and calvarium have also been reported (7-9). Some of these sites, including the masticator space, are more commonly involved in other malignancies such as head and neck cancers (HNCs), whereas calvarial involvement remains uncommon across most cancer types (10,11). In lung adenocarcinoma, craniofacial metastatic involvement of this kind is rare, with the literature limited to a small number of case reports summarized in Table 1 (8,9,12-16). Here, we report the case of a 71-year-old never-smoking female diagnosed with EGFR exon 19-mutated lung adenocarcinoma who presented with rare craniofacial metastases without brain involvement, achieving a durable systemic response following treatment with osimertinib, stereotactic body radiation therapy (SBRT), and platinum-doublet chemotherapy. We present this article in accordance with the CARE reporting checklist (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0139/rc).

Case presentation

A 71-year-old female never-smoker, with a remote history of secondhand smoke exposure from her father and occupational exposure while working in a restaurant, presented with a sudden-onset fever. Her medical history included hyperlipidemia, hypertension, fatty liver, and chronic thrombocytopenia. Her family history was significant for multiple first-degree relatives with malignancy, including two sisters, a father with lung cancer, and a brother with non-Hodgkin lymphoma. Following the onset of fatigue and dyspnea, the patient was initially evaluated by her primary care provider, and a chest radiograph was unremarkable. As part of the workup for elevated liver function tests, abdominal ultrasound (US) revealed multiple hepatic lesions concerning for metastatic disease (Week 0.0, Figure 1). Computed tomography (CT) of the abdomen and pelvis (CTAP) performed the following day confirmed multiple bilobar liver metastases (Figure 2).

Figure 1 Timeline of imaging assessments, molecular testing, and treatment course. Bx, biopsy; CTAP, Computed tomography of the abdomen and pelvis; CTCAP, computed tomography of the chest; EGD, esophagogastroduodenoscopy; EGFR, epidermal growth factor receptor; FDG, fluorodeoxyglucose; IHC, immunohistochemistry; LMD, leptomeningeal disease; LNs, lymph nodes; MRI, magnetic resonance imaging; PET-CT, positron emission tomography-computed tomography; R maxilla, right maxilla; RUL, right upper lobe; SBRT, stereotactic body radiotherapy; US, ultrasound.

Figure 2 Comparison of CT findings from pre-treatment, on-treatment, and post-treatment imaging showing improvement in hepatic lesions, pulmonary lesions, and mediastinal/hilar lymphadenopathy. Arrows indicate representative hepatic metastases in the upper row and pulmonary lesions in the lower row. CT, computed tomography.

Further imaging with CT of the chest, abdomen, and pelvis (CTCAP) revealed a 50 mm × 39 mm medial right upper lobe (RUL) pleural-based mass with mediastinal invasion, an additional approximately 20 mm RUL nodule, numerous other bilateral subcentimeter pulmonary nodules, mediastinal and hilar lymphadenopathy, cervical lymphadenopathy, scattered osseous metastases, and numerous hypoenhancing hepatic metastases. Representative liver lesions included a segment 5/right hepatic lobe lesion measuring 43 mm × 42 mm and a medial hepatic dome lesion measuring 35 mm × 20 mm (Figure 2). Esophagogastroduodenoscopy (EGD) showed negative results for gastrointestinal malignancy. A US-guided liver biopsy revealed adenocarcinoma involving the liver parenchyma; immunohistochemistry (IHC) was positive for TTF-1 and Napsin A, supporting pulmonary origin (Figure 3). Negative markers included CDX2, GATA3, HepPar-1, and neuroendocrine markers. Comprehensive molecular profiling of the liver biopsy specimen revealed an EGFR exon 19 deletion (p.E746_P753delinsVS) with an allele frequency (AF) of 60%. The additional molecular findings are summarized in Table S1.

Figure 3 Histopathology and IHC findings from the liver biopsy supporting pulmonary origin. (A) Hematoxylin and eosin-stained section showing adenocarcinoma involving the liver parenchyma. (B) IHC demonstrating tumor cell positivity for TTF-1. (C) Higher-power IHC image demonstrating faint, dot-like Napsin A staining in tumor cells. IHC, immunohistochemistry.

In week 3, the patient reported worsening fatigue and dyspnea as well as an unintentional weight loss of 10 pounds. Brain magnetic resonance imaging (MRI) revealed multiple infiltrative enhancing lesions within the calvarium and other visualized bony structures, some with epidural extension, including a heterogeneous enhancing right parietal bone lesion measuring approximately 24 mm × 19 mm with possible involvement of the superior sagittal sinus and epidural component, as well as an infiltrative enhancing left parietal bone lesion measuring approximately 34 mm × 16 mm with an epidural component (Figure 4). A large infiltrative, heterogeneously enhancing lesion centered within the right masticator space musculature, measuring 54 mm × 30 mm, with extension into the right maxilla, maxillary sinus, and nasal cavity, was also observed. She was subsequently referred to our hospital for head and neck surgery, radiation oncology, and neurosurgery. Positron emission tomography (PET)-CT confirmed fluorodeoxyglucose (FDG)-avid disease involving the lungs, liver, bone, lymph nodes, and right masticator space (Figure 5). Pulmonary findings included a primary lesion measuring 47 mm × 36 mm with a maximal standardized uptake value (SUV) of 11.2, likely corresponding to the medial RUL primary mass seen on CTCAP (Figure 2), and a separate RUL nodule measuring 18 mm × 16 mm with a maximal SUV of 6.5. Innumerable additional subcentimeter bilateral pulmonary nodules were also observed. Hepatic involvement included a necrotic right hepatic lobe metastasis measuring up to 46 mm × 40 mm with a maximal SUV of 9.1. Osseous disease consisted of innumerable FDG-avid lytic and mixed lytic-sclerotic metastases throughout the visualized skeleton. The right masticator space lesion measured approximately 54 mm × 30 mm with a maximal SUV of 9.0. The final clinical stage was assigned as stage IVB, corresponding to cT3N3M1c. A blood-based next-generation sequencing (NGS) assay confirmed the previously detected EGFR exon 19 deletion. At week 4.9, germline NGS, including sequencing and copy number analysis of cancer-associated and American College of Medical Genetics and Genomics (ACMG)-recommended genes, identified no clinically significant variants. Additional molecular findings and assay metrics are provided in Table S1.

Figure 4 Comparison of brain MRI scans from pre-treatment and post-treatment imaging showing response to treatment, with improvement in bone metastases involving the skull, resolution of epidural extension, and improvement in the right masticator lesion. Arrows indicate the right masticator lesion in the upper panels and calvarial/skull involvement in the lower panels. MRI, magnetic resonance imaging.

Figure 5 Comparison of PET-CT scans from pre-treatment and post-treatment showing response to treatment (summary comparison images side by side). CT, computed tomography; PET, positron emission tomography.

Given her molecular profile, the patient was initiated on osimertinib (80 mg) by mouth once daily at week 5.9, a TKI that targets sensitizing EGFR mutations and the T790M resistance mutation. Prior to systemic therapy, local control radiation therapy was delivered to the right maxilla and skull base between weeks 4.9 and 6.7, with a total dose of 30 Gray (Gy) in five fractions using SBRT. Systemic intravenous (IV) chemotherapy with carboplatin (AUC 5) and pemetrexed (500 mg/m²) was initiated at week 9.0 and administered concurrently with ongoing osimertinib. She completed six cycles by week 24.9. Maintenance therapy with pemetrexed and osimertinib was initiated thereafter.

Follow-up imaging revealed an encouraging response. A chest, abdomen, and pelvis (CTCAP) scan at week 19.0 showed interval reduction of the medial RUL mass with mediastinal extension to 24 mm × 14 mm from 50 mm × 39 mm, as well as decrease in a separate RUL nodule to 16 mm × 14 mm from approximately 20 mm at baseline. Hepatic metastases also decreased in size and number, including a representative right hepatic lobe lesion measuring 22 mm × 21 mm compared with 43 mm × 42 mm at baseline, along with increased sclerosis of multiple axial and appendicular osseous metastatic lesions, suggestive of treatment response (Figure 2). At week 31.1, brain and spine MRI demonstrated improvement in the previously noted infiltrative enhancing calvarial and other visualized osseous lesions, with complete resolution of prior epidural extension (Figure 4). The previously described 24 mm × 19 mm right parietal bone lesion with epidural component had resolved, and another calvarial lesion, previously measuring 34 mm × 16 mm and described on baseline imaging in the left parietal bone, had decreased to 16 mm × 10 mm with resolution of its epidural component. The right masticator space lesion had also largely resolved, leaving only a 13 mm residual enhancing lesion involving the right maxilla. No leptomeningeal disease (LMD) was identified (Figure 4). PET-CT performed simultaneously demonstrated a marked metabolic response across most disease sites, including a marked response in skeletal metastases (Figure 5). The primary RUL mass extending into the mediastinum and right hilum decreased from 47 mm × 36 mm to 20 × 13 mm, with a maximal SUV falling from 11.2 to 3.0. The satellite RUL nodule similarly decreased from 18 mm × 16 mm to 13 mm × 11 mm, with a maximal SUV declining from 6.5 to 2.4. The other tiny bilateral pulmonary nodules resolved, as did the minimally FDG-avid small right pleural effusion. Hepatic disease also showed marked regression, with only a faint residual FDG-avid focus in the lateral right hepatic lobe (maximal SUV 4.1) without a measurable CT correlate. In contrast, mildly increased uptake persisted in the right masticator space despite interval decrease in lesion size from 54 mm × 30 mm to 37 mm × 11 mm, with a maximal SUV rising from 9.0 to 10.8. As of week 62.0, the patient maintains their durable response and is on maintenance therapy with osimertinib and pemetrexed. Treatment was overall well tolerated within the reported timeframe, with no documented severe treatment-related adverse events, dose holds, or dose reductions. Based on chart review, osimertinib appeared to be continued without interruption during chemotherapy and maintenance. Laboratory monitoring showed no thrombocytopenia or neutropenia during treatment, although anemia progressed over time, with hemoglobin declining to 8.4 g/dL by final follow-up. Minor symptoms documented in the chart included upper palate irritation and transient left upper arm pain, both of which were managed conservatively. The patient demonstrated sustained clinical and radiographic response, and discussions regarding treatment duration and supportive care remain ongoing.

All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the City of Hope Institutional Review Board (IRB# 07047). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

Metastases to the masticator space and calvarium are two highly uncommon sites in NSCLC. The masticator space is a deep facial compartment often involved in advanced HNC through direct extension or perineural spread, particularly in buccal mucosa oral cavity squamous cell carcinoma (OCSCC) and nasopharyngeal carcinoma (NPC) (10,17,18). In salivary gland carcinomas (SGCs), involvement is rare but has been documented in isolated cases (19). Calvarial metastases may occur through hematogenous spread, retrograde venous flow, or direct extension via cranial foramina (20). In a review of 175 skull metastases, only one originated from a head and neck primary (11).

Our patient underwent SBRT to the base of the skull and right maxilla early in the treatment course to achieve local control of craniofacial disease involving anatomically critical structures, including the right maxilla and possible cavernous sinus extension, in the setting of documented local discomfort and possible cranial nerve VI involvement. Surgical management was not pursued because the patient was deemed a poor operative candidate. Osimertinib was started concurrently for systemic EGFR-directed therapy to maintain EGFR inhibition during local treatment. Prospective trials have shown that adding SBRT to EGFR-TKI therapy can significantly prolong progression-free survival in NSCLC (21,22). While data supporting SBRT for NSCLC metastases to the head and neck are limited, radiation is a well-established modality in these anatomical regions (21,23). Platinum-doublet chemotherapy was added at week 9 given the patient’s high metastatic burden, reflecting a decision to intensify systemic therapy while continuing EGFR-directed treatment. The FLAURA2 trial demonstrated that adding platinum-pemetrexed to osimertinib improved median overall survival from 37.6 to 47.5 months (hazard ratio for death, 0.77; 95% confidence interval: 0.61–0.96) (5). In the present case, substantial radiographic and metabolic regression was observed across widespread disease sites, including craniofacial metastases, over 33.4 weeks, with an ongoing response at 62 weeks. However, this response should be interpreted cautiously. Given the known intrinsic sensitivity of EGFR exon 19 deletion NSCLC to osimertinib, much of the observed benefit may have been attributable to targeted therapy alone, and the incremental contribution of SBRT and chemotherapy cannot be determined from a single case.

Unlike NSCLC, EGFR aberrations in head and neck malignancies are primarily characterized by protein overexpression and gene amplification rather than true activating kinase domain mutations (2,3,24,25) In NPC, for example, EGFR overexpression is common, but activating mutations are rare, with one study reporting 4.3% of cases (26). Within SGC, salivary duct carcinoma (SDC) demonstrates a higher frequency of activating EGFR variants; in one study of 66 EGFR-expressing SDC tumors, 5 cases [9.4%; exon 18 (n=3) and exon 19 (n=2)] harbored activating mutations (27). Activating EGFR mutations are otherwise uncommon across head and neck malignancies, aside from the inverted sinonasal papilloma (ISP)-associated sinonasal squamous cell carcinoma (SNSCC) spectrum in which EGFR driver alterations have been reported at high frequency. In a widely cited molecular analysis, sequencing of EGFR exons 18 to 21 identified activating EGFR mutations in 88% of ISP and 77% of ISP-associated SNSCC (28). However, these alterations were predominantly EGFR exon 20 insertions, a genotype with therapeutic implications distinct from exon 19 deletion disease, which provides a closer molecular analogue to the present case (28,29).

SDC represents a clinically aggressive and molecularly diverse HNC subtype with limited systemic options. While surgery and radiation are standard treatments for localized disease, systemic therapy is typically biomarker-driven. Responses to androgen deprivation or HER2-targeted therapies have been documented, but no standard exists for EGFR-mutant SDC (22). In the subset of SDCs that harbor activating EGFR mutations, this case suggests a plausible role for an osimertinib-based multimodal treatment strategy, while underscoring the need for further study before any claims regarding efficacy or optimal sequencing can be made.

Although limited to a single case, this report is informative not because it introduces a novel treatment combination, but because it shows how multimodal therapy can be deployed in an uncommon and anatomically high-risk metastatic presentation for which guidance remains sparse. These findings add to the growing evidence supporting combined systemic and local therapy in EGFR-mutant NSCLC and suggest that that early multimodal treatment may be a practical strategy for simultaneously addressing anatomically threatening craniofacial disease and systemic tumor burden. More broadly, this case illustrates a potential framework for extending genotype-matched strategies to rare, molecularly defined tumor subsets, including EGFR-mutant SDC. Several limitations should be emphasized. As a single-patient observation, this case does not permit inference regarding comparative efficacy or optimal sequencing, and the relative contributions of osimertinib, SBRT, and platinum-pemetrexed cannot be disentangled. In addition, formal serial molecular monitoring, such as circulating tumor DNA assessment, was not available to correlate treatment exposure with molecular response or resistance dynamics. Long-term follow-up and further studies are needed to refine patient selection and optimize treatment intensity.

Conclusions

This case highlights a rare presentation of EGFR-mutated lung adenocarcinoma with metastatic involvement of the masticator space and calvarium in the absence of brain metastases. Early multimodal treatment with osimertinib, SBRT, and platinum-doublet chemotherapy was associated with meaningful regression of anatomically high-risk craniofacial disease and a durable systemic response. Although no conclusions regarding comparative efficacy can be drawn from a single case, this report adds to the limited literature on rare craniofacial metastatic patterns in lung adenocarcinoma and suggests that combined local and systemic therapy may be a reasonable strategy in selected patients. Further study is needed to better define optimal treatment intensity, sequencing, and applicability to related molecularly defined tumor subsets.

Acknowledgments

The authors thank the City of Hope nursing and support teams for their unwavering dedication to the patients they serve.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0139/rc

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0139/prf

Funding: This research was funded in part by the U.S. government under Advanced Research Projects Agency for Health agreement 140D042590004. The views and conclusions contained in this document are those of the authors and should not be interpreted as representing the official policies, either expressed or implied, of the U.S. government.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2026-1-0139/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the Declaration of Helsinki and its subsequent amendments. This study was approved by the City of Hope Institutional Review Board (IRB# 07047). Written informed consent was obtained from the patient for the publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

References

1. Hirsch FR, Scagliotti GV, Mulshine JL, et al. Lung cancer: current therapies and new targeted treatments. Lancet 2017;389:299-311. [Crossref] [PubMed]
2. Watanabe K, Hosomi Y, Naoki K, et al. The Whole Picture of First-Line Osimertinib for EGFR Mutation-Positive Advanced NSCLC: Real-World Efficacy, Safety, Progression Pattern, and Posttreatment Therapy (Reiwa Study). JTO Clin Res Rep 2024;5:100720. [Crossref] [PubMed]
3. Li AR, Chitale D, Riely GJ, et al. EGFR mutations in lung adenocarcinomas: clinical testing experience and relationship to EGFR gene copy number and immunohistochemical expression. J Mol Diagn 2008;10:242-8. [Crossref] [PubMed]
4. Soria JC, Ohe Y, Vansteenkiste J, et al. Osimertinib in Untreated EGFR-Mutated Advanced Non–Small-Cell Lung Cancer. N Engl J Med 2018;378:113-25. [Crossref] [PubMed]
5. Jänne PA, Planchard D, Kobayashi K, et al. Survival with Osimertinib plus Chemotherapy in EGFR-Mutated Advanced NSCLC. N Engl J Med 2026;394:27-38. [Crossref] [PubMed]
6. Ballard P, Yates JW, Yang Z, et al. Preclinical Comparison of Osimertinib with Other EGFR-TKIs in EGFR-Mutant NSCLC Brain Metastases Models, and Early Evidence of Clinical Brain Metastases Activity. Clin Cancer Res 2016;22:5130-40. [Crossref] [PubMed]
7. Niu FY, Zhou Q, Yang JJ, et al. Distribution and prognosis of uncommon metastases from non-small cell lung cancer. BMC Cancer 2016;16:149. [Crossref] [PubMed]
8. Mengoli MC, Rossi G, Tiseo M, et al. 'Turban-like' skull metastasis from pulmonary adenocarcinoma. Thorax 2017;72:767-8. [Crossref] [PubMed]
9. Liu Y, Zhu Z, Lv W. Infratemporal Fossa Metastasis of Non-Small-Cell Lung Adenocarcinoma: A Case Report and Literature Review. Ear Nose Throat J 2024; Epub ahead of print. [Crossref]
10. Amit M, Eran A, Billan S, et al. Perineural Spread in Noncutaneous Head and Neck Cancer: New Insights into an Old Problem. J Neurol Surg B Skull Base 2016;77:86-95. [Crossref] [PubMed]
11. Mitsuya K, Nakasu Y, Horiguchi S, et al. Metastatic skull tumors: MRI features and a new conventional classification. J Neurooncol 2011;104:239-45. [Crossref] [PubMed]
12. Turner RC, Lucke-Wold BP, Hwang R, et al. Lung cancer metastasis presenting as a solitary skull mass. J Surg Case Rep 2016;2016:rjw116. [Crossref] [PubMed]
13. Altalhy A, Maghrabi Y, Almansouri Z, et al. Solitary Skull Metastasis as the First Presentation of a Metachronous Primary Lung Cancer in a Survivor from Pancreatic Cancer. Case Rep Oncol Med 2017;2017:5674749. [Crossref] [PubMed]
14. Pal S, Biswas B, Biswas RR, et al. Calvarial metastasis from adenocarcinoma of lung: An uncommon initial presentation diagnosed by cytology. J Cancer Res Ther 2020;16:935-7. [Crossref] [PubMed]
15. Patel S, Zaita B, Singh A, et al. Advanced non-small cell lung cancer treated with palliative systemic therapy complicated by calvarial metastasis: a case report. Transl Cancer Res 2022;11:3357-62. [Crossref] [PubMed]
16. Oh J, Choi E, Aggarwal R. Metastatic Lung Adenocarcinoma: A Case of Unusual Presentation With a Skull Mass. Cureus 2023;15:e42399.
17. Das S, Sharan R, Attakkil A, et al. Outcomes of clinico-radiologically advanced cancer (cT4b) of buccal mucosa: a retrospective analysis of 104 patients. Ecancermedicalscience 2022;16:1400. [Crossref] [PubMed]
18. Luo DH, Yang J, Qiu HZ, et al. A new T classification based on masticator space involvement in nasopharyngeal carcinoma: a study of 742 cases with magnetic resonance imaging. BMC Cancer 2014;14:653. [Crossref] [PubMed]
19. Pabbisetti D, Praharaju BS, Inampudi JV, et al. A rare case report of adenoid cystic carcinoma of parotid gland with perivascular and perineural spread. BJR Case Rep 2022;8:20210249. [Crossref] [PubMed]
20. Pesce A, Armocida D, Fiorentino F, et al. Full-Thickness Craniodural Metastasis with Leptomeningeal Infiltration of Salivary Origin: A Radiological Lesson and a Technical Remark. Tomography 2022;8:2164-70. [Crossref] [PubMed]
21. Peng P, Gong J, Zhang Y, et al. EGFR-TKIs plus stereotactic body radiation therapy (SBRT) for stage IV Non-small cell lung cancer (NSCLC): A prospective, multicenter, randomized, controlled phase II study. Radiother Oncol 2023;184:109681. [Crossref] [PubMed]
22. Masubuchi T, Tada Y, Maruya S, et al. Clinicopathological significance of androgen receptor, HER2, Ki-67 and EGFR expressions in salivary duct carcinoma. Int J Clin Oncol 2015;20:35-44. [Crossref] [PubMed]
23. De Felice F, Cattaneo CG, Franco P. Radiotherapy and Systemic Therapies: Focus on Head and Neck Cancer. Cancers (Basel) 2023;15:4232. [Crossref] [PubMed]
24. Nair S, Bonner JA, Bredel M. EGFR Mutations in Head and Neck Squamous Cell Carcinoma. Int J Mol Sci 2022;23:3818. [Crossref] [PubMed]
25. Perisanidis C. Prevalence of EGFR Tyrosine Kinase Domain Mutations in Head and Neck Squamous Cell Carcinoma: Cohort Study and Systematic Review. In Vivo 2017;31:23-34. [Crossref] [PubMed]
26. Zhang JW, Qin T, Hong SD, et al. Multiple oncogenic mutations related to targeted therapy in nasopharyngeal carcinoma. Chin J Cancer 2015;34:177-83. [Crossref] [PubMed]
27. Williams MD, Roberts DB, Kies MS, et al. Genetic and expression analysis of HER-2 and EGFR genes in salivary duct carcinoma: empirical and therapeutic significance. Clin Cancer Res 2010;16:2266-74. [Crossref] [PubMed]
28. Udager AM, Rolland DCM, McHugh JB, et al. High-Frequency Targetable EGFR Mutations in Sinonasal Squamous Cell Carcinomas Arising from Inverted Sinonasal Papilloma. Cancer Res 2015;75:2600-6. [Crossref] [PubMed]
29. Pacini L, Cabal VN, Hermsen MA, et al. EGFR Exon 20 Insertion Mutations in Sinonasal Squamous Cell Carcinoma. Cancers (Basel) 2022;14:394. [Crossref] [PubMed]