AAH Lesions in the Same Lobe

AAH Lesions in the Same Lobe

January 2017 Abstracts Conclusion: DNA aneuploidy correlates with poor and moderately differentiated tumors. CPA4 and Rel B positive expression is i...

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January 2017

Abstracts

Conclusion: DNA aneuploidy correlates with poor and moderately differentiated tumors. CPA4 and Rel B positive expression is in relation to well differentiated carcinomas and nodal status Keywords: NSCLC, DNA ploidy, CPA4, Rel B

P1.02-080 Genomic Relationship between Lung Adenocarcinoma and Synchronous AIS/ AAH Lesions in the Same Lobe Topic: Other Mutations in Thoracic Malignancies Laura Tafe,1 Francine De Abreu,1 Jason Peterson,1 David Finley,2 Candice Black1 1Department of Pathology and Laboratory Medicine, DartmouthHitchcock Medical Center, Lebanon/NH/United States of America, 2Department of Thoracic Surgery, DartmouthHitchcock Medical Center, Lebanon/NH/United States of America Background: Atypical adenomatous hyperplasia (AAH) is considered the precursor lesion of adenocarcinoma (ADC), and adenocarcinoma in-situ (AIS) the pre-invasive phase of invasive ADC. Finding incidental synchronous AIS/AAH within lung resection specimens of ADC is an opportunity to evaluate and compare the genomic profiles of the lesions. Different mutation profiles would suggest a field effect with the formation of an early second primary. Identical mutations might suggest a closer relationship with the primary tumor such as an early intrapulmonary metastasis from spread through air spaces. In this study we evaluate the genomic profiles of synchronous AIS/AAH lesions and separate primary ADC in the same lobe of resection specimens. Methods: We tested the 13 lesions from six patients identified between August 2015 and June 2016 by targeted next generation sequencing (NGS) using the 50 gene AmpliSeq Cancer Hotspot Panel v2 and FISH for ALK rearrangements. All of our patients had a single radiographically evident ADC and one patient had a

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second smaller lesion which was proven ADC at resection. All six patients had at least one additional incidental focus of AIS/AAH, not detected radiographically. Our patients ranged in age from 51-67. Five patients were female (83%) and all were current or former smokers. Results: All cases were successfully tested and somatic alterations were found in all ADC and three AAH/AIS lesions. None of the samples had an ALK rearrangement. Patient 3, with two ADC, had different profiles between all three lesions tested. In Patient 6, the ADC had an activating EGFR p.L858R mutation and the synchronous AAH lesion showed a KRAS p.G12D mutation. Conclusion: All of the synchronous lesions, including the AAH/AIS lesions, showed different genomic profiles supporting the concept of field cancerization, suggesting that these incidental AAH/AIS foci likely represent de novo secondary tumors. Keywords: synchronous tumors, adenocarcinoma in situ, Genomics, Adenocarcinoma

P1.02-081 The Relationship of CDH3 Expression and DNA Methylation in Thymic Epitherial Tumors Topic: Other Mutations in Thoracic Malignancies Koichiro Kajiura,1 Kazuya Kondo,2 Toru Sawada,1 Naoya Kawakita,1 Mitsuhiro Tsuboi,3 Hiromitsu Takizawa,4 Akira Tangoku5 1Department of Thoracid, Endocrine Surgery and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City/Japan, 2Department of Oncological Medical Services, Tokushima University, Tokushima/Japan, 3Department of Thoracic, Endocrine Surgery and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City/ Japan, 4University Tokushima, Tokushima/Japan, 5 Department of Thoracic and Endocrine Surgery and Oncology, Institute of Health Biosciences, the University of Tokushima Graduate School, Tokushima/Japan

Results Patient

ADC site

ADC molecular

AIS/AAH site

AIS/AAH molecular

1 2 3 4 5 6

RUL, ADC LUL, ADC LLL, ADC1 LLL, ADC2 LUL, ADC RUL, ADC LLL, ADC

STK11 p.E342Q TP53 p.R158L KRAS p.G12V KRAS G12V; PIK3CA p.H1047L TP53 p.V157F KRAS p.G12A; FLT3 p.Y599H EGFR p.L858R

RUL, AAH LUL, AIS LLL, AIS LUL, AIS RUL, AIS LLL, AAH

WT WT TP53 p.H168Q; TP53 p.S94fs ATM p.F858L WT KRAS p.G12D

RUL e right upper lobe; LUL/LLL e left upper/lower lobe; WT e wild-type