196 Chapter 14 The maximum degree of iatrogenic collapse that may occur is influenced by the thickness of both the alveolar epithelial lining and wall. In cases of lepidic adenocarcinoma, the increased thickness of the lining reduces the flexibility of the alveolar walls, but the tumour cells themselves remain relatively flexible. This also explains the difficulty for surgeons to localize, i.e., by palpation, ground glass opacities during surgery. On the other hand, acquired desmoplastic stroma has a solid texture that cannot be compressed, making it easier to feel during palpation. The physiological variation in surface and volume during breathing is neglectable. In contrast, the morphology drastically changes during iatrogenic collapse, not only at architectural, but also at cellular level. A possible minor adaptation during collapse of the peripheral pulmonary parenchyma may be that the recoil of the elastic fibers support surface reduction to some extent. The contracting activity of myofibroblasts, normally placed under the pneumocytes, and adaptation in length of the smaller airways may also play a minor role.318 However, this is not sufficient to prevent the here described wavy/undulatory appearance of the alveolar walls. Tangential cutting leads to pseudostratification, which may add to the confusion with invasive adenocarcinoma. In practice, this tangential cutting effect is present in focal areas of the collapsed alveolar space, and not in the whole alveolar space. The biology of the lesion is likely to be represented by the monolayer, whereby focal cell overlap or mild stratification is a known feature19. Undulating appearance may give rise to over-interpreting collapsed AIS as a papillary or acinar predominant pattern332. Therefore, to understand the in-vivo growth patterns of pulmonary adenocarcinomas, the pathologist requires beside a mental image of the normal microanatomy of the inflated lung, also a mental image of the deflated wrinkled alveolar walls as this modification inevitably occurs during the surgical procedure. The presence of (discontinuous) elastin fibers in a tumour with fibrovascular cores lined by tumour cells, denotes the fibrovascular core as a 2-dimensional cross cut of alveolar wall. Without other invasion characteristics, the diagnosis is than (iatrogenic collapsed) AIS. The minimum criterion of alveolar filling growth patterns as surrogate marker of invasion is that at least a few adjacent alveoli should contain this pattern, to avoid overdiagnosis of invasive adenocarcinoma. This approach is in line with that in the breast: e.g. in the diagnosis of lobular carcinoma in situ333 and the differentiation from (atypical) hyperplasia. In such cases, the criteria is that more than 50% of the acini in a terminal duct lobular unit must be filled and expanded by the neoplastic cells to qualify as lobular carcinoma in situ. MIA is not used in the revised classification, as 2 mm true invasion may be associated with a recurrence in the follow-up. In addition, the recognition of elastin in pre-existing alveolar wall may induce downgrading to AIS if signs of invasion are absent. The overdiagnosis in application of the WHO classification explains the improved prognosis of papillary carcinoma and some acinar carcinomas and also the recognition of the MIA category.
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