Author of

• 16549

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  P1.02 - Poster Session with Presenters Present (ID 454)

  • Event: WCLC 2016
  • Type: Poster Presenters Present
  • Track: Biology/Pathology
  • Presentations: 1
  • Moderators:
  • Coordinates: 12/05/2016, 14:30 - 15:45, Hall B (Poster Area)

  • 16629

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    P1.02-080 - Genomic Relationship between Lung Adenocarcinoma and Synchronous AIS/AAH Lesions in the Same Lobe (ID 5776)

    14:30 - 14:30  |  Author(s): J. Peterson
    • Abstract

    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 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.

    Results

    Patient	ADC site	ADC molecular	AIS/AAH site	AIS/AAH molecular
    1	RUL, ADC	STK11 p.E342Q	RUL, AAH	WT
    2	LUL, ADC	TP53 p.R158L	LUL, AIS	WT
    3	LLL, ADC1 LLL, ADC2	KRAS p.G12V KRAS G12V; PIK3CA p.H1047L	LLL, AIS	TP53 p.H168Q; TP53 p.S94fs
    4	LUL, ADC	TP53 p.V157F	LUL, AIS	ATM p.F858L
    5	RUL, ADC	KRAS p.G12A; FLT3 p.Y599H	RUL, AIS	WT
    6	LLL, ADC	EGFR p.L858R	LLL, AAH	KRAS p.G12D

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