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Introduction Epithelial myoepithelial carcinoma (EMC) of the nasal cavity is a rare tumor, and here we describe the first case of EMC of the nasal cavity presenting with epiphora. A case presentation and review of the literature is provided. Methods A case report is described of a 63-year-old man who presented with unilateral epiphora and was found via a thorough history and physical examination to have a nasal tumor. The physical examination consisted of an ocular examination, including probing and irrigation, and a detailed nasal examination (anterior rhinoscopy, nasal endoscopy). The nasal examination was prompted by the patient's report of concurrent nasal symptoms during history taking. Immunohistochemistry subsequently identified the nasal tumor as EMC. A literature search was performed to gain insights into similar malignancies of the nasal cavity. Results Eight cases of EMC of the nasal cavity were identified in the literature, none of the patients presented with epiphora. The case presented here resulted in resolution of the patient's symptoms and no evidence of disease after surgical excision. Conclusion Epithelial myoepithelial is a rare salivary gland malignancy that can arise in the nasal cavity. Unilateral epiphora with concurrent nasal symptoms should prompt nasal cavity examination for the possibility of an obstructive tumor.

Abstract Background Lung cancer is the number one cancer killer worldwide. A major drawback in the lung cancer treatment field is the lack of realistic mouse models that replicate the complexity of human malignancy and immune contexture within the tumor microenvironment. Such models are urgently needed. Mutations of the tumor protein p53 are among the most common alterations in human lung cancers. Methods Previously, we developed a line of lung cancer mouse model where mutant human TP53-273H is expressed in a lung specific manner in FVB/N background. To investigate whether the human TP53 mutant has a similar oncogenic potential when it is expressed in another strain of mouse, we crossed the FVB/N-SPC-TP53-273H mice to A/J strain and created A/J-SPC-TP53-273H transgenic mice. We then compared lung tumor formation between A/J-SPC-TP53-273H and FVB/N-SPC-TP53-273H. Results We found the TP53-273H mutant gene has a similar oncogenic potential in lung tumor formation in both mice strains, although A/J strain mice have been found to be a highly susceptible strain in terms of carcinogen-induced lung cancer. Both transgenic lines survived more than 18 months and developed age related lung adenocarcinomas. With micro CT imaging, we found the FVB-SPC-TP53-273H mice survived more than 8 weeks after initial detection of lung cancer, providing a sufficient window for evaluating new anti-cancer agents. Conclusions Oncogenic potential of the most common genetic mutation, TP53-273H, in human lung cancer is unique when it is expressed in different strains of mice. Our mouse models are useful tools for testing novel immune checkpoint inhibitors or other therapeutic strategies in the treatment of lung cancer.