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H. Nitanda
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P2.02 - Poster Session/ Treatment of Localized Disease – NSCLC (ID 210)
- Event: WCLC 2015
- Type: Poster
- Track: Treatment of Localized Disease - NSCLC
- Presentations: 1
- Moderators:
- Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)
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P2.02-004 - Clinicopathological Features and Outcomes of AAH, AIS and MIA in Resected Lung Adenocarcinoma (ID 2644)
09:30 - 09:30 | Author(s): H. Nitanda
- Abstract
Background:
After proposal of a new histologic classification of lung adenocarcinoma from the IASLC/ATS/ERS in 2011, the 2015 WHO classification of lung cancer new defines the new subtypes of adenocarcinoma in situ (AIS) and minimally invasive adenocarcinoma (MIA). The former shows a lepidic growth pattern without invasion (BAC) and the latter a lepidic growth pattern with <= 5mm invasion. Atypical adenomatous hyperplasia (AAH) and AIS（previously, bronchioloalveolar carcinoma）are categorized as preinvasive lesions of adenocarcinoma. Recent studies have shown that patients with AIS and MIA had nearly 100% disease-free survival (DFS), if complete resection was achieved, though the details of the surgical procedures were not mentioned.
Methods:
We reviewed 93 patients with AAH, AIS or MIA, enrolled from among 629 lung adenocarcinoma patients who underwent resection at our hospital from 2007 to 2014. We retrospectively investigated clinical features, pathological findings and the presence of epidermal growth factor (EGFR) mutations, as well as the surgical procedures of wedge resection, segmentectomy and lobectomy. The results were compared with clinical outcomes.
Results:
The patients ranged in age from 40 to 82 years (median 66) and included 40 males and 53 females. Synchronous or metachronous multiple primary lung carcinomas were documented in 15 (16%) patients, who had undergone resections of one to four lesions. Seven of 15 patients had combined lesions of AAH, AIS and MIA, and 8 of 15 had invasive adenocarcinoma combined with AIS or MIA. The total numbers of resected lesions were 7 AAHs, 28 AISs, and 70 MIAs. The diameters of the AAH, AIS and MIA were 4 to 10 mm (median 7), 5 to 20 mm (median 8) and 4 to 23 mm (median 11), respectively. In gene analysis for each lesion, the EGFR mutations were detected in one of five AAH lesions (20%), in eight of 28 AIS lesions (28%) and in 34 of 67 MIA lesions (50%). It was confirmed that both tumor size and the frequency of EGFR mutations gradually increased in the direction from AAH to MIA. As for surgical procedures, we performed 1) wedge resection for 5 AAH lesions, 12 AIS lesions and 22 MIA lesions, 2) segmentectomy with N1 lymph node sampling for 1 AAH, 6 AIS and 15 MIA and 3) lobectomy with N2 lymph node dissection for 1 AAH, 10 AIS and 33 MIA. None of the cases had lymph node metastasis pathologically and all were p-Stage IA. The median follow-up duration from the date of surgery was 31 months (1.7-86 months). Two patients with MIA died 22 and 29 months after surgery due to other malignancies, but none of the patients experienced recurrence and the 5-year DFS rate was 100%. Of 70 MIA lesions, 37 (53%) were removed by wedge resection or segmentectomy.
Conclusion:
AAH/AIS/MIA lesions were related to multiple primary lung carcinomas. Gradual malignant progression from AAH to AIS to MIA was verified. Although accumulation of further cases and long-term follow-up are needed, a subset of these lesions might be treated by wedge resection or segmentectomy.
