P2.16: Atypical Adenomatous Hyperplasia (AAH) in a Patient With a Primary Carcinoid Lung Tumor: Case-Report (original) (raw)
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Pulmonary Atypical Adenomatous Hyperplasia: Diagnostic and Therapeutic Implications
Cureus
Lung cancer still remains one of the most common cancers throughout the world, especially in smokers. Adenocarcinoma is now the predominant histological type in many western countries. The etiology of adenocarcinoma is unknown, but evidence suggests that atypical adenomatous hyperplasia (AAH) may act as a precursor lesion. Here we present two case reports of patients diagnosed with AAH on biopsy, highlighting 1) available treatment strategies and 2) AAH's progression to adenocarcinoma. A review of AAH is warranted as little literature is currently available regarding its treatment strategies, especially in light of its role as a precursor to adenocarcinoma. In this review, we will address the following topics: 1. What is the pathophysiology of AAH? 2. What is the natural history of AAH and its risk of malignant transformation? 3. When is surgery recommended? 4. What is the role of stereotactic body radiotherapy (SBRT) in the rare patient who refuses surgery?
CT Findings of Atypical Adenomatous Hyperplasia in the Lung
Korean Journal of Radiology, 2006
The aim of this study was to analyze the computed tomographic (CT) findings of atypical adenomatous hyperplasia (AAH) in the lung. Materials and Methods: The CT findings of AAHs in eight patients were retrospectively reviewed. The CT findings of each AAH lesion were evaluated for multiplicity, location, shape, size and internal density of the lesion, the interface between the normal lung and the lesion, the internal features within the lesion and any change of the lesion on the follow-up CT scans (range: 33 to 540 days; average: 145.3 days). Results: The eight patients consisted of three men and five women (age range: 43 71 years). Six of eight patients were asymptomatic. Four of them (50%) had synchronous malignancies in the lung: adenocarcinoma of the lung (n = 3), and metastatic squamous cell carcinoma from the uterus (n = 1). We could identify and evaluate eleven AAH nodules in seven patients on the CT scans. Three patients had multiple AAHs. Seven of the 11 lesions (64%) were located in the upper lobe. All the AAHs showed a well-defined oval or round shape and pure ground-glass opacity (GGO) without any solid component (size: 3.9 3 mm to 19 17 mm; internal attenuation: 467 to 785 HU). All the AAHs showed no change of their size and internal density on the follow-up CT scans. Conclusion: Atypical adenomatous hyperplasia is often associated with malignancy. This tumor is shown on CT as persistent well-defined oval or round nodular GGOs without solid components, and it does not change on the follow-up CT.
Lung Cancer, 2003
Background: Adenomatous hyperplasia of the peripheral lung has been suggested to be a preneoplastic lesion leading to peripherally localized lung carcinomas. The paucity of data about cellular and vascular characteristics of this lesion in comparison to normal lung prompted this investigation. Material and methods : We describe results of two investigations comprising 75 cases and 70 cases, respectively, with atypical adenomatous hyperplasia (AAH) of the lung, respectively: (a) a prospective study part with thorough analysis of surgical lung specimens (lobes and lungs) for light microscopical detection of the lesion; and (b) a retrospective study part with immuno-and lectin histochemical analysis of AAH and non-neoplastic lung parenchyma monitoring expression of growth-related markers and changes in vascularization patterns. Sections of the individual cases were examined by an imageanalyzing system including automated measurement of staining intensities and structure analysis. Results : The prospective study part revealed an incidence of AAH in 2/31 cases with squamous cell carcinoma and in 5/32 cases with adenocarcinomas. No relation to pT-or pN stages was detectable, high grade AAHs were seen to be close to the tumor lesions (B/2 cm distance) and those with low grade at greater distances. Statistically significantly increased levels of expression of anti-apoptotic bcl-2, macrophage migration inhibitory factor (MIF) capable to suppress p53 activities, heparin-binding lectin, interleukin-2, galectin-1 and of binding sites for
Pathologica
Alveolar adenoma is a rare tumour of the lung. It is typically found in asymptomatic adults as a peripheral or subplerual nodule on imaging examination. Microscopically, the tumour is composed of admixture of epithelial and mesenchymal component in variable sized cystic or alveolar structures. The tumour shows a benign nature. There have been no reported recurrences or metastases. Malignant transformation of alveolar adenoma and coexisting with lung carcinoma have been rarely described. In this article, we report a case of an alveolar adenoma and coexisting atypical adenomatous hyperplasia. This case, contributing to the limited numbers of cases described to date, illustrates the importance of awareness on the possibility of alveolar adenoma being associated with lung carcinoma and its precursor lesions especially when diagnosed by small biopsy specimens.
Virchows Archiv, 1997
We used immunohistochemistry and electron microscopy to evaluate the differentiation of cells comprising atypical adenomatous hyperplasia (AAH; n = 26), early bronchioloalveolar lung carcinoma (BAC; n = 11), and overt BAC (n = 16), which are assumed to constitute a continuous spectrum of developmental steps of BAC. Surfactant apoprotein (SAP), a marker for type 2 alveolar cells, was expressed in cells from all the lesions of AAH, early BAC, and overt BAC. However, the proportion of SAP-positive cells decreased and their distribution became more heterogeneous with advancing lesion grade. Urine protein 1, which is identical to the Clara cell-specific 10 kDa protein, was expressed in 70% of overt BAC, whereas only 20% of early BAC showed weak reactivity and none of AAH lesions showed any reactivity at all. Ultrastructurally, type 2 alveolar cell differentiation was predominant among cells from AAH and early BAC. Our results suggest that precursor cells of BAC differentiate predominantly towards type 2 alveolar cells. Cells comprising overt BAC retain this differentiation phenotype, but to a reduced extent. In contrast, concomitantly with progression, cells with Clara cell differentiation emerge and their proportion increases. Such phenotypic changes may reflect metaplasia occurring in tumour cells during the development of BAC.
Coexistence of Atypical Adenomatous Hyperplasia and Hamartoma of the Lung
Atypical adenomatous hyperplasia is considered to be a preliminary lesion for pulmonary adenocarcinoma while lung hamartomas (mesenchymomas) are non-neoplastic, tumor-like malformations. A patient underwent transthoracic fine-needle aspiration biopsy for a pulmonary mass and then lingulectomy following a diagnosis of adenocarcinoma. The surgical specimen was solid and 25 mm in diameter. Microscopic investigation revealed that the mass was a hamartoma with an atypical adenomatous hyperplasia focus at the periphery. We believe that the cells leading the cancer diagnosis had come from the atypical adenomatous hyperplasia focus around the hamartoma. We presented this case as atypical adenomatous hyperplasia contains atypical epithelium and can be diagnosed as a malignancy on fine needle aspiration biopsy and the coexistence of atypical adenomatous hyperplasia and hamartoma has not been reported previously.
Epidermal growth factor receptor gene amplification in atypical adenomatous hyperplasia of the lung
2010
Atypical adenomatous hyperplasia (AAH) is postulated to be the earliest morphologic precursor lesion in lung carcinogenesis. The epidermal growth factor receptor (EGFR), one of the members of the Erb-2 family of receptors, is commonly expressed in non-small cell lung carcinoma (NSCLC). A subset of the patients with NSCLC has molecular abnormalities in the EGFR gene, including missense mutations and deletions and/or abnormal gene copy numbers, and the relative importance of each of these for patient outcome is an area of great interest. Recent reports show that EGFR mutations are rare or absent in AAH and are rare in bronchioloalveolar carcinoma (BAC). However, the EGFR gene copy number status in AAH is unknown. In this study, we examined the EGFR gene copy number status in lung adenocarcinomas, synchronous AAH, and BAC in surgical pathology resection specimens. EGFR gene copy number was analyzed by chromogenic in situ hybridization (CISH) using formalin fixed paraffin embedded tissue sections and EGFR probes as recommended by the manufacturer. A known positive case of high-grade glioma was used as a positive control. The results indicate that four of eight adenocarcinomas (50%) had more than five EGFR signals per nucleus, suggesting a gain in copy number. Interestingly, in four of nine cases of AAH (44.4%) more than three EGFR signals per nucleus were noted, with scattered cells showing up to 6 signals per nucleus. In addition, in five of 12 cases of BAC (42%), more than three EGFR signals per nucleus were noted. In the remaining cases two to three intranuclear dot-like peroxidase positive signals were present consistent with non-amplification of the gene. Our study reveals an abnormal EGFR gene copy gain in several cases of AAH. In our cohort, the rate of EGFR gene copy abnormalities in AAH appears similar to BAC and lower than in lung adenocarcinomas. These findings suggest that although EGFR gene copy abnormalities may be an early event in lung carcinogenesis, they are associated with tumor progression to invasive cancer and highlight the complexity of tumor morphogenesis.
Primary adenoid cystic carcinoma of the lung
Cancer, 2007
BACKGROUND. Primary pulmonary adenoid cystic carcinomas (ACCs) are rare lung neoplasms that are challenging to completely resect and can exhibit poor survival. Adjuvant therapy is often ineffective and identification of a targeted novel therapy would be useful. The objective of the current study was to evaluate KIT expression and KIT-activating mutations.