ECP 2022 Abstract Book

Virchows Archiv (2022) 481 (Suppl 1):S1–S364 13 types of lung carcinomas. It is probably caused by genetic predilection, immunosuppression, infectious agents such as EBV and radiotherapy/ chemotherapy given for the treatment of the first neoplasm. The thera- peutic management of such a combination requires separate considera- tion of the different coexisting neoplasms. E-PS-21-017 Adenosquamous carcinoma of the lung - biopsy: MET exon 14 skipping mutation V. Sousa*, A. Alarcão, A. Ladeirinha, M. Reis Silva, T. Ferreira, A. Rodrigues, C. Vilasboas, L. Carvalho *Institute of Anatomical and Molecular Pathology, Faculty of Medicine of the University of Coimbra; CIMAGO – Research Center for Environment, Genetics and Oncobiology, Faculty of Medicine, University of Coimbra; University Hospital Anatomical Pathology Coimbra, Portugal Background & objectives: MET exon14 skipping mutation (METex14) occurs in 3% in NSCLCs and coexists rarely with other oncogenic drivers. METex14/MET amplifications indicate poor prognosis. Recent approvals of capmatinib and tepotinib for metastatic NSCL METex14 depend on this biomarker in metastatic NSCLC. Methods: A 85-years-old woman - adenosquamous carcinoma of the lung (CK5.6/TTF1/ CK7 expression). NGS and Idylla techniques - FFPE macrodissected tumoral tissue with 40% representation of tumoral cells from biopsy. Oncomine Precision Assay (Thermo Fisher Scientific, Waltham, MA, USA) was performed according to manufacturer’s instruc- tion by Next Generation Sequencing (NGS) in Genexus. Idylla TM Gene Fusion Assay performed according to manufacturer’s instruction. Results: METex14 was detected by both techniques, Idylla and NGS. NGS made it possible to identify C.3082G>C;p.(Asp1028His) mutation with 35% allelic frequency. The two most clinically relevant MET alterations are METex14 mutations as the primary oncogenic driver and MET amplification as acquired resistance to tyrosine kinase inhibitors (TKI). Conclusion: MET-TKIs, capmatinib and tepotinib, for NSCLCs with METex14 marked a new step of MET-targeted therapy. METex14 alterations - point mutations/deletions/insertions/com- plex mutations lead to MET receptor decreased degradation, fol- lowed by MET signalling and tumourigenesis. The evaluation methods for METex14 include differential MET exon expression, quantitative reverse transcription polymerase chain reaction (qRT- PCR) or direct RNA sequencing. METex14 are the most commonly reported oncogenic MET mutations. MET mutations should be tested in the context of targeted therapy together with other molecular markers. E-PS-21-018 Swyer James MacLeod Syndrome: an uncommon phenomenon I. Eremia*, C. Anghel, S. Nica *University of Medicine Bucharest, Romania Background & objectives: Swyer James MacLeod syndrome is an uncommon lung condition characterized by pulmonary vascular reduc- tion and alveolar hyperdistention, with or without bronchiectasis. The radiographic appearance of a single pulmonary lobe or the entire lung is characteristic of this rare lung ailment. Methods: We present the case of a 43-year-old man who presented himself to the ER for: low fever and chills, dyspnea, wheezes, pleuritic chest pain and cough. The patient was examined in the ER with EKG, blood tests, a chest radiograph, and a CT scan. The patient’s respiratory func- tion was then assessed using spirometry in the internal medicine department. Results: Chest radiograph: right apico-axillary-laterothoracic hypertransparency that causes passive collapse of the underlying parenchyma - pneumothorax. Cord enlarged by lengthening and accentuating the convexity of the lower left arch. Left pulmonary hilum with increased density and projection area; accentuation of peribronchovascular and basal interstitial pattern. CT scan: multiple bubbles of emphysema, some with thick walls, at the level of both lung fields, predominantly on the right, the largest of about 9 / 8.5 cm. Right pulmonary sequestration of 9/4 cm. Moderately enlarged heart. Without pleural or pericardial effu- sions. Nonspecific mediastinal infracentimetric lymphadenopathy. Without changes in bone structure with oncological visa at the level of the scanned segment. Conclusion: The cause of Swyer James MacLeod syndrome is not completely understood. It seems that the initial abnormality occurs in the distal bronchi after an infection during early childhood. The clinic and the totality of the investigations carried out plead for the following diagnoses: Swyer James MacLeod syndrome (right pulmonary artery hypoplasia, bilateral diffuse pulmonary emphy- sema, bilateral bronchiectasis), moderate pulmonary hypertension. Treatment is conservative and preventative, focused primarily on controlling pulmonary infections. Inhaled corticosteroids may have a limited role in treatment. E-PS-21-019 A contemporary view at the pulmonary collapse Y. Kirillov, D. Protsenko, A. Avdalyan, V. Sokov, S. Timofeev* *Moscow MCC Kommunarka, Russia Background & objectives: Atelectasis or pulmonary collapse is a common complication after upper body radiation therapy and may be clinically noticeable in up to 30% of cases. However, early morphological changes in the lung tissue are not well clear. Methods: We researched early phases of pulmonary collapse in rats through radiation exposure in a dose of 12Gy on their chest. We took samples of lung tissue and bronchoalveolar washing (BAL) on the various days after exposure. We used electron microscopy (Zeiss-EVO-LS1), routine histology technique, morphometric anal- ysis (Aperio AT2 and NIH ImageJ), and detected the surfactant level in BAL in our study. Results: We detected initial signs of lung tissue damage by electron microscopy in 24 hours after exposure. Type-II pneumocytes appeared swelling and lamellar bodies looked damaged. Then we observed the significant decline of surfactant level on day-3. We identified atelectasis by light microscopy on the seventh day after the beginning the experiment. In most cases areas of pulmonary collapse were localized in the subpleural regions. Atelectatic area had been doubled in two weeks by adding intrapulmonary regions. By statistical analysis we revealed that changes of thickness of alveolar wall, square, and smooth muscle shortening of the airway had no significant role in the pulmonary collapse on day-7 but dominated on day-14. Conclusion: In this research we found out that destruction of type II pneumocytes and following reducing the total amount of surfactant level played a key role in pulmonary collapse on day 7. However, the morphometric changes in lung tissue such as S333