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J. Le Quesne
MINI 01 - Pathology (ID 93)
- Event: WCLC 2015
- Type: Mini Oral
- Track: Biology, Pathology, and Molecular Testing
- Presentations: 1
- Moderators:W.A. Franklin, A.G. Nicholson
- Coordinates: 9/07/2015, 10:45 - 12:15, Mile High Ballroom 2c-3c
MINI01.13 - Biologically Driven Sub-Classification of Early Lung Adenocarcinomas (ID 2418)
10:45 - 12:15 | Author(s): J. Le Quesne
Early lung adenocarcinomas have previously been successfully sub-classified by Noguchi et al on the basis of histopathological characteristics, in particular the pattern of growth exhibited by the tumour and the response of the adjacent stroma. A wholly in situ pattern of growth characterises preinvasive lung lesions, namely atypical adenomatous hyperplasia (AAH) and adenocarcinoma in situ (AIS). It is not uncommon for large areas of an invasive tumour to show this in situ pattern of growth. Metastases to the lung from other organs can also show areas of in situ spread, and this shows that truly invasive malignant clones of cells can grow along the alveolar surface. This study aimed to identify whether the characteristics of in situ growth in an individual tumour may give an indication of the underlying tumour biology, and be of prognostic value.
We reviewed all small (sub 35 mm) lung adenocarcinomas resected with curative intent over a 4 year period from our thoracic surgical centre. Nodal metastasis data was also collected, which the reviewing pathologists were blinded to. All tumour sections were reviewed by 2 thoracic histopathologists, who separated these into 4 categories, based on the patterns of growth, stromal changes, cytological changes between in situ and invasive components and overall symmetry of the lepidic growth. On the basis of these appearances early lung adenocarcinomas were divided into 4 groups. Type 1 showed minimal stromal reaction analogous to Noguchi A/B tumours. Types 2 and 3 are subdivisions of mixed in situ/invasive adenocarcinomas (equivalent to the Noguchi C group). Type 2 showed marked stromal changes in the invasive component and a cytologically lower grade asymmetrical lepidic component. Type 3 showed a concentric rim of lepidic growth cytologically similar to the invasive disease. Type 4 were wholly invasive tumours. Tumour type was subsequently correlated to pathological lymph node staging.
156 tumours were included and sub-classified. Of these 12 were type 1, 30 were type 2, 46 were type 3 and 68 were type 4. The rate of nodal metastasis was increased across the tumour types from 1 to 4, at 0%, 7%, 24% and 29% respectively.
We find that partly invasive lung adenocarcinomas fall into two histologically and biologically distinct groups with different potential toward nodal metastasis. We suggest the type 2 tumours represent the emergence of an invasive subclone in an in situ adenocarcinoma lacking this property. The type 3 tumours have a lepidic region at their edge which represents infiltration of normal structures by migratory malignant cells but may have no truly biologically ‘in situ’ disease. This group also shows more tendency toward metastasis. Type 4 lesions without any kind of lepidic growth have the highest rate of nodal involvement, and their destructive pattern of growth represents the most aggressive form of early tumours. Future molecular characterisation of these lesions and their various components may further inform our understanding of the pathways of tumorigenesis in lung adenocarcinoma.
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