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Folia Histochemica Et Cytobiologica 2023Incidentally discovered lung nodules can be worrisome for both the patient and their physicians. Although 95% of solitary lung nodules are benign, it is important to... (Review)
Review
INTRODUCTION
Incidentally discovered lung nodules can be worrisome for both the patient and their physicians. Although 95% of solitary lung nodules are benign, it is important to distinguish which nodules have high clinical suspicion for malignancy. Existing clinical guidelines do not apply to patients with signs and symptoms related to the lesion and with an increased baseline risk of lung cancer or metastasis. This paper highlights the vital role of pathohistological analysis and immunohistochemistry in the definitive diagnosis of such incidentally discovered lung nodules.
MATERIAL AND METHODS
The three cases presented were selected based on their similar clinical presentations. A review of the literature was performed using the online database PubMed, for articles published in the period between January of 1973 to February of 2023 using the following medical subject headlines: "primary alveolar adenoma," "alveolar adenoma," "primary pulmonary meningioma," "pulmonary meningioma," and "pulmonary benign metastasizing leiomyoma." Results (Case Series). The case series consists of three incidentally discovered lung nodule(s). Although they presented with high clinical suspicion for malignancy, detailed workup confirmed the diagnosis of three rare benign lung tumours: primary alveolar adenoma, primary pulmonary meningioma, and benign metastasizing leiomyoma.
CONCLUSIONS
Clinical suspicion for malignancy in the presented cases arose from previous and current medical history of malignancy, family history of malignancy, and/or specific radiographic findings. This paper highlights the need for a multidisciplinary approach in the management of incidentally discovered pulmonary nodules. Excisional biopsy and pathohistological analysis remain the gold standard in confirming the presence of a pathologic process and determining the nature of the disease. Common features of the diagnostic algorithm utilized among the three cases include multi-slice computerized tomography, excisional biopsy via atypical wedge resection (if the nodule is peripherally located), and lastly, pathomorphological analysis using haematoxylin and eosin staining and immunohistochemistry.
Topics: Humans; Meningioma; Lung Neoplasms; Leiomyoma; Biopsy; Meningeal Neoplasms
PubMed: 37435900
DOI: 10.5603/FHC.a2023.0011 -
Cell Death & Disease Feb 2022The BRAF gene is frequently mutated in cancer. The most common genetic mutation is a single nucleotide transition which gives rise to a constitutively active BRAF kinase...
The BRAF gene is frequently mutated in cancer. The most common genetic mutation is a single nucleotide transition which gives rise to a constitutively active BRAF kinase (BRAF) which in turn sustains continuous cell proliferation. The study of BRAF murine models has been mainly focused on the role of BRAF in tumor development but little is known on the early molecular impact of BRAF expression in vivo. Here, we study the immediate effects of acute ubiquitous BRAF activation in vivo. We find that BRAF elicits a rapid DNA damage response in the liver, spleen, lungs but not in thyroids. This DNA damage response does not occur at telomeres and is accompanied by activation of the senescence marker p21 only in lungs but not in liver or spleen. Moreover, in lungs, BRAF provokes an acute inflammatory state with a tissue-specific recruitment of neutrophils in the alveolar parenchyma and macrophages in bronchi/bronchioles, as well as bronchial/bronchiolar epithelium transdifferentiation and development of adenomas. Furthermore, whereas in non-tumor alveolar type II (ATIIs) pneumocytes, acute BRAF induction elicits rapid p53-independent p21 activation, adenoma ATIIs express p53 without resulting in p21 gene activation. Conversely, albeit in Club cells BRAF-mediated proliferative cue is more exacerbated compared to that occurring in ATIIs, such oncogenic stimulus culminates with p21-mediated cell cycle arrest and apoptosis. Our findings indicate that acute BRAF expression drives an immediate induction of DNA damage response in vivo. More importantly, it also results in rapid differential responses of cell cycle and senescence-associated proteins in lung epithelia, thus revealing the early molecular changes emerging in BRAF-challenged cells during tumorigenesis in vivo.
Topics: Adenoma; Animals; Carcinogenesis; Cell Line, Tumor; Cyclin-Dependent Kinase Inhibitor p21; Disease Models, Animal; Mice; Mutation; Oncogenes; Proto-Oncogene Proteins B-raf; Tumor Suppressor Protein p53
PubMed: 35145078
DOI: 10.1038/s41419-022-04597-z -
Journal of Veterinary Diagnostic... Jan 2021Herein we describe a rare case of systemic infection with concurrent pleural mesothelioma in a stray cat that was found dead and submitted for autopsy. Gross pathology...
Herein we describe a rare case of systemic infection with concurrent pleural mesothelioma in a stray cat that was found dead and submitted for autopsy. Gross pathology changes consisted of thoracic clear yellow fluid admixed with suspended fibrin strands; clear-to-tan, variably sized, <3 mm diameter pulmonary nodules; and enlargement of the submandibular, retropharyngeal, and prescapular lymph nodes. Histologic changes consisted of extensive areas of suppurative inflammation and necrosis with mineralization that partially effaced the pulmonary parenchyma and lymph nodes. Random, distinct necrotic foci were present throughout the hepatic parenchyma. Extending from the pleura, within perinecrotic alveolar spaces, and infiltrating the submandibular, retropharyngeal, and prescapular lymph nodes were dense sheets of neoplastic epithelioid cells with moderate pleomorphism and occasional karyomegaly and multinucleation. Neoplastic cells exhibited immunolabeling for pancytokeratin AE1/AE3 and vimentin, consistent with pleural mesothelioma. Aerobic bacterial culture of lung yielded heavy growth of . Immunohistochemistry (IHC) for revealed clusters of bacteria in the lung, lymph node, and liver. Pathologic changes were consistent with systemic listeriosis, confirmed by bacterial culture and IHC, and concurrent pleural mesothelioma.
Topics: Animals; Cat Diseases; Cats; Diagnosis, Differential; Female; Listeria monocytogenes; Listeriosis; Mesothelioma; Pleural Neoplasms
PubMed: 33054600
DOI: 10.1177/1040638720966321 -
Journal of Cardiothoracic Surgery Oct 2023Alveolar adenoma is a rare benign tumour, usually presenting as a peripherally located solid mass, sometimes mimicking malignancy.
BACKGROUND
Alveolar adenoma is a rare benign tumour, usually presenting as a peripherally located solid mass, sometimes mimicking malignancy.
CASE PRESENTATION
A 37-year-old woman presented with chronic intermittent vague chest discomfort. The chest x-ray showed a simple cyst in the left lower lung field, and serial computed tomography (CT) over the following 2-year period showed rapid growth of the cyst, from 3.5 to 9.0 cm in diameter. The CT scan suggested bronchiolar communication, which was suspected to be the cause of growth, via check-valve mechanism. Thoracoscopic surgery was performed, and we found a thin-walled cyst in the lingular segment. Wedge resection was performed and the pathology was an unexpected alveolar adenoma which had grown on the terminal bronchiole, causing the alveolus to rupture and the cyst to grow. In 48 months of follow-up, there was no evidence of recurrence and the patient's symptoms resolved.
CONCLUSIONS
Rapidly growing pulmonary cysts can lead to complications including rupture with pneumothorax and haemothorax, and surgery is always indicated. Abnormally rapid growth may indicate an underlying pathology such as alveolar adenoma. Surgical resection is the treatment of choice and there have been no reported cases of recurrence. Here we present a rare form of alveolar adenoma, which was a form of rapidly growing pulmonary cyst.
Topics: Female; Humans; Adult; Lung Neoplasms; Lung Diseases; Lung; Cysts; Rupture; Adenoma
PubMed: 37907949
DOI: 10.1186/s13019-023-02409-9 -
Turkish Thoracic Journal Jul 2019Alveolar adenoma is one of the rarely seen benign tumors of the lung, to date, one or two series have been reported. In this study, four rare alveolar adenoma cases were...
Alveolar adenoma is one of the rarely seen benign tumors of the lung, to date, one or two series have been reported. In this study, four rare alveolar adenoma cases were presented, thereby contributing to the existing scarce data.
PubMed: 30986170
DOI: 10.5152/TurkThoracJ.2018.18015 -
Medicine International 2024Alveolar adenoma is a rare and benign pulmonary tumor, which originates from type II pneumocytes and is often incidentally identified on radiographic images. Alveolar...
Alveolar adenoma is a rare and benign pulmonary tumor, which originates from type II pneumocytes and is often incidentally identified on radiographic images. Alveolar adenoma presents as a peripleural, solitary and cystic nodule in the lung and may mimic other types of lung tumors, thus rendering its differential diagnosis difficult. Alveolar adenoma is diagnosed based on histopathological and immunohistochemical analyses. The present study describes the case of a 50-year-old male patient with alveolar adenoma. He visited a local doctor ~3 years prior due to left chest pain. A chest computed tomography scan revealed a cystic lesion in segment 8 of the left lung. A nodular shadow appeared in the cyst and gradually increased in size; the patient was thus referred to the authors' hospital. The nodule was well-defined, solitary and solid; thus, lung cancer or aspergilloma were suspected. Thoracoscopic wedge resection was performed as diagnostic therapy. The frozen sections were non-diagnostic, and a pathological examination revealed an alveolar adenoma with no evidence of malignancy and a negative culture. The patient had a good post-operative course, with no sign of recurrence at the follow-up evaluation 46 months later. On the whole, alveolar adenoma is a rare, benign pulmonary tumor that is difficult to diagnose pre-operatively.
PubMed: 38476983
DOI: 10.3892/mi.2024.140 -
Turk Patoloji Dergisi 2022Alveolar adenoma is a rare lung benign tumour originating from type II pneumocytes. It presents as a well-defined nodule. In some cases, it is difficult to differentiate...
Alveolar adenoma is a rare lung benign tumour originating from type II pneumocytes. It presents as a well-defined nodule. In some cases, it is difficult to differentiate from lung cancer. Few cases of this tumour have been reported. We describe here a case of alveolar adenoma in a 63-year-old man discovered incidentally on chest X-ray. The lesion was reported as lepidic adenocarcinoma in bronchoscopic biopsy. The patient underwent a thoracoscopic left lower lobectomy. The histopathological and immunohistochemical examinations resulted in a diagnosis of alveolar adenoma. We report this case to describe its morphological and immunohistochemical characteristics and to emphasize its diagnostic difficulties.
Topics: Adenoma; Biopsy; Diagnosis, Differential; Humans; Incidental Findings; Lung Neoplasms; Male; Middle Aged; Radiography
PubMed: 34514578
DOI: 10.5146/tjpath.2021.01547 -
Particle and Fibre Toxicology Apr 2022Considering the expanding industrial applications of carbon nanotubes (CNTs), safety assessment of these materials is far less than needed. Very few long-term in vivo...
BACKGROUND
Considering the expanding industrial applications of carbon nanotubes (CNTs), safety assessment of these materials is far less than needed. Very few long-term in vivo studies have been carried out. This is the first 2-year in vivo study to assess the effects of double walled carbon nanotubes (DWCNTs) in the lung and pleura of rats after pulmonary exposure.
METHODS
Rats were divided into six groups: untreated, Vehicle, 3 DWCNT groups (0.12 mg/rat, 0.25 mg/rat and 0.5 mg/rat), and MWCNT-7 (0.5 mg/rat). The test materials were administrated by intratracheal-intrapulmonary spraying (TIPS) every other day for 15 days. Rats were observed without further treatment until sacrifice.
RESULTS
DWCNT were biopersistent in the rat lung and induced marked pulmonary inflammation with a significant increase in macrophage count and levels of the chemotactic cytokines CCL2 and CCL3. In addition, the 0.5 mg DWCNT treated rats had significantly higher pulmonary collagen deposition compared to the vehicle controls. The development of carcinomas in the lungs of rats treated with 0.5 mg DWCNT (4/24) was not quite statistically higher (p = 0.0502) than the vehicle control group (0/25), however, the overall incidence of lung tumor development, bronchiolo-alveolar adenoma and bronchiolo-alveolar carcinoma combined, in the lungs of rats treated with 0.5 mg DWCNT (7/24) was statistically higher (p < 0.05) than the vehicle control group (1/25). Notably, two of the rats treated with DWCNT, one in the 0.25 mg group and one in the 0.5 mg group, developed pleural mesotheliomas. However, both of these lesions developed in the visceral pleura, and unlike the rats administered MWCNT-7, rats administered DWCNT did not have elevated levels of HMGB1 in their pleural lavage fluids. This indicates that the mechanism by which the mesotheliomas that developed in the DWCNT treated rats is not relevant to humans.
CONCLUSIONS
Our results demonstrate that the DWCNT fibers we tested are biopersistent in the rat lung and induce chronic inflammation. Rats treated with 0.5 mg DWCNT developed pleural fibrosis and lung tumors. These findings demonstrate that the possibility that at least some types of DWCNTs are fibrogenic and tumorigenic cannot be ignored.
Topics: Animals; Inhalation Exposure; Lung; Lung Neoplasms; Mesothelioma; Nanotubes, Carbon; Pleura; Rats
PubMed: 35449069
DOI: 10.1186/s12989-022-00469-8 -
PloS One 2021There have been no studies on the effects of polyhexamethylene guanidine phosphate (PHMG) after a long period of exposure in the rodent model. We aimed to evaluate...
Evaluation of the long-term effect of polyhexamethylene guanidine phosphate in a rat lung model using conventional chest computed tomography with histopathologic analysis.
There have been no studies on the effects of polyhexamethylene guanidine phosphate (PHMG) after a long period of exposure in the rodent model. We aimed to evaluate long-term lung damage after PHMG exposure using conventional chest computed tomography (CT) and histopathologic analysis in a rat model. A PHMG solution was intratracheally administrated to 24 male rats. At 8, 26, and 52 weeks after PHMG instillation, conventional chest CT was performed in all rats and both lungs were extracted for histopathologic evaluation. At 52 weeks after PHMG instillation, four carcinomas had developed in three of the eight rats (37.5%). Bronchiolo-alveolar hyperplasia and adenoma were found in rats at 8, 26, and 52 weeks post-instillation. The number of bronchiolo-alveolar hyperplasia significantly increased over time (P-value for trend< 0.001). The severity of lung fibrosis and fibrosis scores significantly increased over time (P-values for trend = 0.002 and 0.023, respectively). Conventional chest CT analysis showed that bronchiectasis and linear density scores suggestive of fibrosis significantly increased over time (P-value for trend < 0.001). Our study revealed that one instillation of PHMG in a rat model resulted in lung carcinomas and progressive and irreversible fibrosis one year later based on conventional chest CT and histopathologic analysis. PHMG may be a lung carcinogen in the rat model.
Topics: Animals; Disease Models, Animal; Guanidines; Humans; Lung; Lung Diseases; Pulmonary Fibrosis; Rats; Thorax; Tomography, X-Ray Computed
PubMed: 34492061
DOI: 10.1371/journal.pone.0256756 -
Journal of Immunology (Baltimore, Md. :... Sep 2019The CD4Cre transgenic model has been widely used for T cell-specific gene manipulation. We report unexpected highly efficient Cre-mediated recombination in alveolar...
The CD4Cre transgenic model has been widely used for T cell-specific gene manipulation. We report unexpected highly efficient Cre-mediated recombination in alveolar macrophages (AMFs), bronchial epithelial cells (BECs), and alveolar epithelial cells (AECs) in this strain of mice. Different from CD4 T cells, AMFs, AECs, and BECs do not express detectable Cre protein, suggesting that Cre protein is either very transiently expressed in these cells or only expressed in their precursors. Mice carrying a conditional constitutively active KRas (caKRas) allele and the CD4Cre transgene contain not only hyperactivated T cells but also develop severe AMF accumulation, AEC and BEC hyperplasia, and adenomas in the lung, leading to early lethality correlated with caKRas expression in these cells. We propose that caKRas-CD4Cre mice represent, to our knowledge, a novel model of proliferative pneumonitis involving macrophages and epithelial cells and that the CD4Cre model may offer unique usefulness for studying gene functions simultaneously in multilineages in the lung. Our observations, additionally, suggest that caution in data interpretation is warranted when using the CD4Cre transgenic model for T cell-specific gene manipulation, particularly when lung pathophysiological status is being examined.
Topics: Alveolar Epithelial Cells; Animals; CD4 Antigens; Hyperplasia; Integrases; Macrophages, Alveolar; Mice; Mice, Inbred C57BL; Pneumonia; Proto-Oncogene Proteins p21(ras); Recombination, Genetic; Transgenes
PubMed: 31315887
DOI: 10.4049/jimmunol.1900566