ECP 2022 Abstract Book

Virchows Archiv (2022) 481 (Suppl 1):S1–S364 13 epithelioid patients after 2011 were 36% and 58 months. Many patients had occupational asbestos exposure. 9 patients were judged as environmental asbestos exposure. The median asbestos body number in one gram of dried lung was 7,189. The asbestos body numbers in one gram of dried lung of 13 patients (22%) were less than 1,000, and those of 35 patients (58%) were more than 5,000. Conclusion: Strong relationship between inhaled asbestos in the lung and MPM was re-confirmed. The representative occupations were construction worker, asbestos factory worker, plumber, and railroad car maker. Although the dried lung of MPM patients were investigated, the asbestos body numbers of 22% were less than 1,000/g, and those of only 58% were more than 5,000/g. OFP-06-011 Prevalence of TTF-1 negative lung adenocarcinoma on lung core biopsy with EGFR, ALK and PD-L1 status S. Sayeda*, A. Naqvi, H. Begum, C. Finley, C. Coschi, R. Juergens, M. Bonert *Pathology, McMaster University, Canada Background & objectives: TTF-1 negative (TTF1neg) lung adeno- carcinoma is relatively infrequent, typically CK7+ HepPar1+ and has SMARCA4 gene mutations. The objective was to retrospec- tively examine biomarkers/immunohistochemical characteristics of local TTF1neg lung adenocarcinomas. Locally, the TTF-1 immu- nostain clone in use is 8G7G3/1 (Dako). Methods: All in-house lung core biopsies (LCBs) from Jan 2011- Dec 2020 were retrieved and analysed using a hierarchical free text string matching algorithm (HFTSMA) to establish the diagnosis, and a logical text parsing tool (LTPT) to retrieve results for immu- nostains, PD-L1, EGFR, and ALK status. A full review/audit was done by pathologists on cases selected by the HFTSMA and LTPT. Results: Of 5,867 LCBs, 3,142 had immunostains (IHC) from 4,973 patients. The HFTSMA classified 5,725 (98%) LCBs. LTPT identified 85% of LCBs based on TTF-1 status. TTF-1 was done but not reported in 11%. 748 of 1,640 LCBs with adenocarcinoma were TTF-1 positive (TTF1+). 73 cases were TTF1neg, CK7+ and negative for non-lung markers. 50 of these 73 were deemed primary lung, of which 0/29 were EGFR+ and 0/28 were ALK+. PD-L1 was positive in 2/17 (11%), low posi- tive 3/17 (18%) and negative in 12/17 (71%) cases. Only 1/28 cases was positive for Napsin A. HepPar1 was done in only four cases; three matched the SMARCA4 deficient profile TTF1neg CK7+ HepPar1+. Conclusion: Using the HFTSMA and LTPT, additional TTF1neg lung adenocarcinomas were identified, and these were uniformly negative for EGFR and ALK. In the cohort, 6% (50/ (748+50)) are TTF1neg lung adenocarcinomas. PD-L1 appears to be frequently negative compared to TTF1+ adenocarcinomas. IHC reporting is uneven in our environment. The possible utility of HepPar1 positiv- ity in identifying TTF1neg LCBs appears to be underutilized in our environment. Napsin A negativity appears to be a common finding in TTF1neg lung adenocarcinomas. OFP-06-012 Histologic features, nuclear grading, BAP1 and PD-L1 expres- sion in malignant pleural mesothelioma: analysis of a mono- institutional series H.G. Terzioglu*, S. Onder *Hacettepe University, Turkey Background & objectives: The most common primary malignant tumour of the pleura is malignant pleural mesothelioma (MPM) which has a poor outcome. This study aims to identify any relation between histological features, nuclear grading, and expression sta- tus of BAP1 and PD-L1 in MPM. Methods: 52 tumour samples diagnosed as MPM between 2001- 2022 were re-evaluated and nuclear grading was performed. Whole sections were analysed for BAP1 and PD-L1 (73-10 clone) expression by using IHC assays. Presence or absence of the nuclear expression of BAP1 was noted. Any pattern of staining was accepted in PD-L1 the 73-10 clone, and cut-offs were set as ≥1%, ≥50%, ≥80%. Results: Male/female ratio was 27:25 and age range was 33-83 (mean:60). Forty-nine cases were epithelioid and 3 were biphasic. Among epithelioid MPMs, 37/49 were low grade(LG). BAP1 expression was lost in 69%(67% of epithelioid, 100% of biphasic) of cases. There was no statistically significant correlation between BAP1 loss and nuclear grade or overall tumour grade. PD-L1 was negative in 43%(95% epithelioid, 84% LG, 65% BAP1-lost); ≥1% positive in 40%(95% epithelioid, 74% LG, 65% BAP1-lost); ≥50% positive in 11%(75% epithelioid,33% LG, 100% BAP1 lost) and ≥80% positive in 6%(100% epithelioid, 67% LG, 67% BAP1-lost) of the cases. Rhabdoid features were seen in 5/49 cases all of which were BAP1-lost, and PD-L1 positive. Conclusion: MPM is an aggressive tumour. BAP1 is the most common somatic mutation, and its loss of expression remains to be common regardless of tumour grade or PD-L1 status. In epithelioid MPMs, expression of PD-L1 seems to be associated with certain histologic features such as rhabdoid morphology, but not with tumour grade or BAP1 expression. Immune checkpoint inhibitors were shown to be effective for some aggressive tumour types, and it may be promising for a subset of MPM patients as well. OFP-06-013 Evaluation of predictive markers for the patterns of metastatic disease in patients with pulmonary adenocarcinoma J. Wolf*, P. Clahsen, E. Andrinopoulou, D. Mustafa, M. Kros, J. von der Thüsen *Department of Pathology, Erasmus Medical Center, Rotterdam, The Netherlands Background & objectives: The majority of patients diagnosed with pulmonary adenocarcinoma present at an advanced stage of the disease or will develop metastases during follow-up. Find- ing predictive biomarkers for the development of metastatic dis- ease during diagnostic workup is important to guide therapeutic strategies. Methods: Histologic growth pattern and a diagnostic genetic panel customized for lung cancer alterations, were evaluated in biopsy and resection specimens of 319 patients presenting with metasta- ses from pulmonary adenocarcinoma. A subset of patients with early-stage lung adenocarcinoma who developed metastasis during follow up was compared to a group who did not develop metastatic disease. Results: Primary lung tumours presenting with a dominant solid growth pattern and absence of driver mutations correlate with brain metastasis and are found predominantly in early brain metastasis. EGFR mutations are found in early metastasis of brain and non- brain origin irrespectively of the growth pattern. MET mutations were seen in early non-brain metastasis. We observed a major change of the dominant growth pattern between the primary lung tumour and the corresponding metastasis. Both, early and late brain metastasis show more often a papillary dominant growth pattern whereas the acinar dominant pattern is found in early brain and non-brain metastasis. Conclusion: Routine histopathology and genetic biomarkers of pri- mary pulmonary adenocarcinoma specimens predict to some extent the development of metastasis. These parameters are by themselves S26