RESUMO
BACKGROUND: Estrogens are steroid hormones that affect a number of physiological functions in cells; these compounds play an irreplaceable role in the reproductive system. Their effects are mediated by the estrogen receptor (ER), of which there are two subtypes - ERα and ERβ. ERs are expressed in regions outside the reproductive system, including bone, brain, intestine, endothelium, kidney, and lung. Expression of ER by lung cancer (LC) cells was first described in the early 1980s. The experimental literature also describes co-expression of ERβ and an epidermal growth factor activating mutation, and the additive antiproliferative effects of anti-estrogens plus tyrosine kinase inhibitors during treatment of lung adenocarcinoma. However, coincident expression of ER and ALK translocation were not decribed. The 4-year survival for generalized non-small cell lung cancer indicates the possibility that both molecular features (ER and ALK positivity) may be a favorable prognostic biomarker for this tumor. CASE: A 69-year-old patient presented with generalized lung adenocarcinoma that was positive for ERb and the ALK-EML4 fusion gene. The tumor was stage IV. Additional examinations excluded malignancy of the gynecological area. The patient was treated with chemotherapy and a tyrosine kinase ALK inhibitor. CONCLUSION: The role of individual ER subtypes in LC carcinogenesis, and the possible therapeutic effects, is unclear. This is the first documented case of co-occurrence of ALK-EML4 and ERβ in LC. Key words non-small cell lung cancer - estrogen receptors - ALK translocation - prognosis - treatment This work was supported by Ministry of Health of the Czech Republic, grant AZV 16-32318A, and by Ministry of Education, Youth and Sports of the Czech Republic, grant NPU I LO1304. The authors declare they have no potential conflicts of interest concerning drugs, products, or services used in the study. The Editorial Board declares that the manuscript met the ICMJE recommendation for biomedical papers. Submitted: 23. 9. 2018 Accepted: 25. 10. 2018.
