Natural history of pure ground-glass opacity after long-term follow-up of more than 2 years

Kodama, Ken; Higashiyama, Masahiko; Yokouchi, Hideoki; Takami, Koji; Kuriyama, Kinya; Kusunoki, Yoko; Nakayama, Tomio; Imamura, Fumio

doi:10.1016/s0003-4975(01)03410-5

Cited by 151 publications

(117 citation statements)

References 13 publications

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“…Thus, the majority of pure GGNs remained stable on later follow-up. On the other hand, in study populations, which included patients with a history of malignancy, a much higher proportion (15%-58%) of pure GGNs showed interval growth (42,43). These studies indicate that a history of past malignancy is a risk factor for nodule growth.…”

Section: Natural Clinical Course Of Subsolid Nodulesmentioning

confidence: 83%

Pulmonary subsolid nodules: what radiologists need to know about the imaging features and management strategy

Kim¹,

Park²,

Koh³

et al. 2013

Diagn Interv Radiol

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Section: Natural Clinical Course Of Subsolid Nodulesmentioning

confidence: 83%

Pulmonary subsolid nodules: what radiologists need to know about the imaging features and management strategy

Kim¹,

Park²,

Koh³

et al. 2013

Diagn Interv Radiol

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“…A single pure GGN larger than 5 mm requires an initial follow-up CT at 3 months followed by yearly CT scans for a minimum of 3 years as long as the lesion is persistent and stable in size A pure GGN that is larger than 5 mm is likely to be a preinvasive AAH or AIS and is amenable to a conservative approach with CT surveillance [12] . The initial 3-month follow-up CT is done to identify the pure GGNs that spontaneously disappear, as well as the rapidly growing nodules.…”

Section: Recommendationmentioning

confidence: 99%

Incidental, subsolid pulmonary nodules at CT: etiology and management

Seidelman¹,

Quint²

2013

Cancer Imaging

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Pulmonary nodules, both solid and subsolid, are common incidental findings on computed tomography (CT) studies. Subsolid nodules (SSNs) may be further classified as either pure ground-glass nodules or part-solid nodules. The differential diagnosis for an SSN is broad, including infection, organizing pneumonia, inflammation, hemorrhage, focal fibrosis, and neoplasm. Adenocarcinomas of the lung are currently the most common type of lung cancer, representing 3035% of all primary lung tumors, and the subtype of bronchioloalveolar cell carcinoma (BAC) commonly presents as an SSN. In 2011, a new classification system for lung adenocarcinomas was proposed by the International Association for the Study of Lung Cancer, the American Thoracic Society, and the European Respiratory Society. An important feature of the new system is the relinquishment of the term BAC in favor of more specific histologic subtypes. It has been reported that these subtypes are associated with characteristic CT findings. This article reviews the new classification system of lung adenocarcinomas, discusses and illustrates the associated CT findings, and outlines the current recommendations for further diagnosis, treatment, and follow-up of SSNs based on computed tomography findings.

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“…This speculation matches the clinical observation that about half of pure groundglass opacities, identified on high-resolution computed tomography and usually diagnosed as atypical adenomatous hyperplasia or nonmucinous bronchioloalveolar carcinoma on histopathological examination, do not increase in size and density for more than 2 years. 23 However, we did not observed significant differences in histology, tumor maximum size, and proliferation activity (estimated by Ki-67 LI) between atypical adenomatous hyperplasias with and without EGFR mutations ( Figure 1; Table 3). Further studies are needed to determine the biological differences between atypical adenomatous hyperplasias with and without EGFR mutations.…”

Section: Egfr Mutation In Pulmonary Atypical Adenomatous Hyperplasia mentioning

confidence: 64%

Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung

et al. 2007

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Activating epidermal growth factor receptor (EGFR) gene mutations are frequently detected in lung adenocarcinomas, especially adenocarcinomas with a nonmucinous bronchioloalveolar carcinoma component. EGFR-mutated lung adenocarcinomas respond well to EGFR tyrosine kinase inhibitors. We previously found that most (88%) pure nonmucinous bronchioloalveolar carcinomas (adenocarcinoma in situ) already harbor EGFR mutations, indicating that the mutations are an early genetic event in the pathogenesis. We examined 54 atypical adenomatous hyperplasias, precursor lesions of lung adenocarcinomas, obtained from 28 Japanese patients for the hotspot mutations of EGFR exons 19 and 21 and K-ras codon 12. EGFR mutations were observed in 17 of the 54 (32%) atypical adenomatous hyperplasias examined: Ten and seven atypical adenomatous hyperplasias had deletion mutations at exon 19 or point mutations (L858R) at exon 21, respectively. We did not observe apparent histological differences between atypical adenomatous hyperplasias with and without EGFR mutations. K-ras mutation (G12S) was detected in only one atypical adenomatous hyperplasia. As EGFR mutational frequency of atypical adenomatous hyperplasias was much lower than that of nonmucinous bronchioloalveolar carcinomas, we surmise that EGFR-mutated atypical adenomatous hyperplasias, but not atypical adenomatous hyperplasias with wild-type EGFR, are likely to progress to nonmucinous bronchioloalveolar carcinomas.

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Natural history of pure ground-glass opacity after long-term follow-up of more than 2 years

Cited by 151 publications

References 13 publications

Pulmonary subsolid nodules: what radiologists need to know about the imaging features and management strategy

Pulmonary subsolid nodules: what radiologists need to know about the imaging features and management strategy

Incidental, subsolid pulmonary nodules at CT: etiology and management

Epidermal growth factor receptor gene mutations in atypical adenomatous hyperplasias of the lung

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