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Machine learning (ML) has demonstrated promise in predicting mortality; however, understanding spatial variation in risk factor contributions to mortality rate requires explainability. We applied explainable artificial intelligence (XAI) on a stack-ensemble machine learning model framework to explore and visualize the spatial distribution of the contributions of known risk factors to lung and bronchus cancer (LBC) mortality rates in the conterminous United States. We used five base-learners-generalized linear model (GLM), random forest (RF), Gradient boosting machine (GBM), extreme Gradient boosting machine (XGBoost), and Deep Neural Network (DNN) for developing stack-ensemble models. Then we applied several model-agnostic approaches to interpret and visualize the stack ensemble model's output in global and local scales (at the county level). The stack ensemble generally performs better than all the base learners and three spatial regression models. A permutation-based feature importance technique ranked smoking prevalence as the most important predictor, followed by poverty and elevation. However, the impact of these risk factors on LBC mortality rates varies spatially. This is the first study to use ensemble machine learning with explainable algorithms to explore and visualize the spatial heterogeneity of the relationships between LBC mortality and risk factors in the contiguous USA., (© 2021. The Author(s).)

Competing Interests: Disclosure: There is no conflict of interest or other disclosures.

Background: Endotracheal and endobronchial metastases (EEM) is a rare manifestation in primary lung cancer. It has not yet been reported in Chinese literatures. The aim of this study was to summarize and analyze the clinical feature of lung cancer with EEM., Methods: We retrospectively reviewed 6 patients who presented with EEM of lung cancer from Peking University Third Hospital from January 2015 to December 2018. With "endotracheal metastases, endobronchial metastases, lung cancer" as the keywords, 13 cases were retrieved from PubMed database until February 2020. The clinical, radiologic and bronchoscopic data were collected., Results: Six patients were selected from 967 patients with lung cancer, and all were diagnosed with lung cancer and EEM simultaneously. There were 4 cases of squamous cell carcinoma, 1 case of adenocarcinoma, and 1 case of small cell lung cancer. One patient had stage IIIb and 5 patients had stage IV. There were 5 cases of central lung cancer and 1 case of peripheral lung cancer. EEM on bronchoscope examination presented as endoluminal nodular or polypoid lesion in 5 patients, and abnormal white bulge in 1 patient. 5 cases metastasized to the contralateral bronchus, 1 case to the ipsilateral bronchus and 1 case to the trachea. The median overall survival was 7.5 months. Totally 13 cases of lung cancer with EEM were retrieved from PubMed database. 12 cases were diagnosed during the follow up after lung cancer resection. There were 8 cases of squamous cell carcinoma and 9 cases of central type. Endotracheal or endobronchial nodules showed in 10 cases and eccentric wall thickening in 2 cases were seen on chest computed tomography (CT), which corresponding to the nodular or polypoid lesion bronchoscopically. 5 cases metastasized to the contralateral bronchus, 10 cases to the trachea and 1 case to the ipsilateral bronchus., Conclusions: EEM is a rare metastasis of lung cancer, which can occur at the initial diagnosis of lung cancer or after surgical resection. It is often seen in the patients of squamous cell carcinoma with central type in advanced stage. The prognosis is poor.

Smoking is the leading cause of preventable death worldwide, it is responsible for 90% of bronchopulmonary cancers and is the main cause of chronic bronchitis and emphysema, two disorders which contribute to chronic obstructive pulmonary disease (COPD). We here report the case of a 58-year old not weaned chronic tabagic patient with a 2-month history of diffuse abdominal pain evolving in a context of alteration of the general state. Clinical examination showed generally poor health. Pleuropulmonary examination objectified reduction of vesicular breath sounds in the right hemithorax and diffuse abdominal susceptibility and massive left subclavicular lymphadenopathy. Thoraco-abdominal CT scan showed pleural, intra-abdominal and retroperitoneal tissue infiltration and diffuse bilateral lung emphysema (Figure). Bronchial fibroscopy objectified bud obstructing the orifice of the apical bronchus of the right upper lobar bronchus. Anatomopathologic study of bronchial biopsy and lymph node biopsy showed non-differentiated carcinoma. Evolution was marked by patient's death after two weeks. This study aims to highlight fatal outcome due to these two complications due to tobacco use in the same patient in order to emphasize the importance of prevention awareness of the damages of tobacco use and on smoking cessation.

We describe two patients with hepatitis C and a diagnosis of pulmonary extranodal marginal zone B cell lymphoma. Both patients demonstrated a chronic nonproductive cough without hemoptysis. Diagnosis was obtained after a computed tomographic chest scan and flexible bronchoscopic biopsy. We discuss the staging and prognosis of this disease, its correlation with hepatitis C, and potential benefits of treating the associated hepatitis C., (Copyright © 2016 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Pleural plaques (fibrosis of the parietal pleura) are sometimes seen following light exposure. Their prevalence may reach 70% in heavily exposed populations. Fibrosis of the visceral pleura is much less common and it is not specifically related to asbestos. The incidence of asbestosis (pulmonary fibrosis induced by asbestos exposure) is diminishing in France. According to the data of the National Programme for the Surveillance of Mesothelioma, the annual number of cases of pleural mesothelioma varied from 646 to 800 for the period 1998-2003. Primary lung cancer due to asbestos does not have specific clinical, radiological or anatomical-pathological features. The number of cases attributable to asbestos has been estimated as between 2086 and 4172 for 1999. A report of the National Academy of Medicine, the Academy of Sciences and the International Centre of Cancer Research has calculated the incidence of primary lung cancer due to asbestos in 2000 as 969 for men and 133 for women. The risk of primary lung cancer is increased in populations exposed to asbestos even in the absence of radiological signs of pulmonary fibrosis. For an identical total exposure, asbestosis increases the risk of primary lung cancer. On the basis of radiological studies, pleural plaques are associated with an increased risk of lung cancer and mesothelioma. For identical levels of total asbestos exposure, it has not been established that the presence of pleural plaques increases the risk of developing thoracic cancer., (Copyright © 2012 SPLF. Published by Elsevier Masson SAS. All rights reserved.)

In this report, we present two cases of bronchial foreign body granulomas caused by the suture ties used in bronchial surgery for esophageal cancer. Both of them was hospitalized as "tumor transfer or an invasion", but pathological examination of the neoplasms indicated an inflammatory granuloma showing reaction to the foreign body. These two cases give us an attention that the neoplasms in tracheal or bronchial was not only the invasion or transfer of the primary tumor, but also the possibility of granuloma development due to the surgical sutures.

Introduction: The aim of this study was to describe associations between lung tumor location and smoking as well as selected occupational exposures. In the context of lung cancer screening by computed tomography scan, tumor location may have an interest. Computed tomography scan is known to better detect more peripheral tumors., Methods: Lung cancer cases diagnosed in two French University hospitals between 1997 and 2009 were included. Tumors visible on white-light bronchoscopy were defined as central. Occupational exposures were assessed by the same expert. Data were analyzed by case-case comparisons using unconditional logistic regressions., Results: A total of 1701 cases were included, comprising mainly men (86.3%), current smokers (52.8%), or former smokers (42.8%). Main histological subtypes of cancer were adenocarcinomas (33.8%) and squamous cell carcinomas (32.6%). The tumor location was found to be central in 61% of cases, and never smokers and women had more often peripheral tumors. Exposure to asbestos was significantly associated with central location with dose-response relationship (odds ratio [OR] for peripheral tumors = 0.45, 95% confidence interval [CI] 0.29-0.70) for the highest level of exposure. Exposure to silica dust was significantly associated with peripheral tumor (OR for peripheral tumors = 3.28, 95%CI 1.50-7.17) for the highest level of exposure. Exposure to welding fumes was associated with central location (OR for peripheral tumors = 0.51, 95% CI 0.26-0.96) for the first level of exposure)., Conclusions: Smoking characteristics and occupational exposures have to be considered to define more accurately high-risk populations suitable for lung cancer screening or early detection programs.

Introduction: The expression of cyclooxygenase 2 (COX-2) is usually increased in inflammation and cancer. This study examines the expression of COX-2 in the lung of chronic obstructive pulmonary disease (COPD) patients with lung cancer., Methods: We studied 44 male patients with bronchial cancer (27 squamous carcinoma and 17 adenocarcinoma). Samples were obtained from the pulmonary parenchyma, from the bronchial mucosa adjacent to the tumor and from the tumor itself. Lung tissue specimens from 14 patients with pneumothorax were used as control. The mRNA and the COX-1 and COX-2 proteins were assessed by RT-PCR and Western blot, respectively., Results: COX-1 and COX-2 mRNA levels were significantly higher in the lung parenchyma of COPD patients than in the control subjects. COX-2 mRNA levels were also higher in the lung parenchyma than in both tumor and airway tissue samples procured from COPD patients. There were no differences in the COX-2 mRNA levels between squamous carcinoma and adenocarcinoma. In contrast, COX-2 protein levels were significantly higher in tumors than in lung parenchyma and airways. COX-2 protein levels were higher in adenocarcinoma compared with squamous carcinoma., Conclusion: This study shows that in COPD, the pathway of cyclooxygenase is activated and associated with an increase in the expression of COX-2 in lung tumors. These observations suggest that COX-2 is possibly involved in the association between COPD and cancer., (Copyright © 2011 SEPAR. Published by Elsevier Espana. All rights reserved.)

Advances in endoscopic technology have improved the detection of precancerous bronchial lesions associated with the occurence of proximal squamous cell lung cancer (SCC) in high-risk individuals for broncho-pulmonary neoplasm. The debates and controversies regarding the control and treatment of intraepitelial bronchial lesions is due to the fact that the regression rate of all preneoplastic bronchial lesions is 54%. But the progression to carcinoma in situ or to cancer is significantly higher for severe dysplasia, than for preneoplastic lesions showing lower-grade dysplasia, such as squamous metaplasia and mild or moderate dysplasia. The progression rate to carcinoma in situ or cancer with squamous cells varies between 19% and 46% for patients with severe dysplasia. The diagnosis and resection of pulmonary cancer in incipient stages increases spectacularly the survival rates of the resected patients, by comparison to the non-operated patients.

We report a rare case of radiation-induced sarcoma (RIS) that arose in the right bronchial stump, 8 years after right pneumonectomy followed by adjuvant chemotherapy and thoracic radiotherapy for a localized small-cell lung cancer. The patient was treated in 2002 with 6 MV X-ray irradiation in a total dose of 60 Gy. Eight years after the end of radiotherapy, he presented with an undifferentiated high-grade pleomorphic sarcoma. Although an increased rate of soft tissue sarcoma has been reported after radiotherapy for some solid cancers or lymphomas, to our knowledge, this is the first report of RIS related to small-cell lung cancer.

In the case of radon exposure, the spatial distribution of deposited radioactive particles is highly inhomogeneous in the central airways. The object of this research is to investigate the consequences of this heterogeneity regarding cellular burdens in the bronchial epithelium and to study the possible biological effects at tissue level. Applying computational fluid and particle dynamics techniques, the deposition distribution of inhaled radon daughters has been determined in a bronchial airway model for 23 min of work in the New Mexico uranium mine corresponding to 0.0129 WLM exposure. A numerical epithelium model based on experimental data has been utilised in order to quantify cellular hits and doses. Finally, a carcinogenesis model considering cell death-induced cell-cycle shortening has been applied to assess the biological responses. Present computations reveal that cellular dose may reach 1.5 Gy, which is several orders of magnitude higher than tissue dose. The results are in agreement with the histological finding that the uneven deposition distribution of radon progenies may lead to inhomogeneous spatial distribution of tumours in the bronchial airways. In addition, at the macroscopic level, the relationship between cancer risk and radiation burden seems to be non-linear.

Epigenetic silencing of tumor suppressor genes commonly occurs in human cancers via increasing DNA methylation and repressive histone modifications at gene promoters. However, little is known about how pathogenic environmental factors contribute to cancer development by affecting epigenetic regulatory mechanisms. Previously, we reported that both hypoxia and nickel (an environmental carcinogen) increased global histone H3 lysine 9 methylation in cells through inhibiting a novel class of iron- and α-ketoglutarate-dependent histone demethylases. Here, we investigated whether inhibition of histone demethylase JMJD1A by hypoxia and nickel could lead to repression/silencing of JMJD1A-targeted gene(s). By using Affymetrix GeneChip and ChIP-on-chip technologies, we identified Spry2 gene, a key regulator of receptor tyrosine kinase/extracellular signal-regulated kinase (ERK) signaling, as one of the JMJD1A-targeted genes in human bronchial epithelial BEAS-2B cells. Both hypoxia and nickel exposure increased the level of H3K9me2 at the Spry2 promoter by inhibiting JMJD1A, which probably led to a decreased expression of Spry2 in BEAS-2B cells. Repression of Spry2 potentiated the nickel-induced ERK phosphorylation, and forced expression of Spry2 in BEAS-2B cells decreased the nickel-induced ERK phosphorylation and significantly suppressed nickel-induced anchorage-independent growth. Taken together, our results suggest that histone demethylases could be targets of environmental carcinogens and their inhibition may lead to altered gene expression and eventually carcinogenesis.

Background: Israeli Jews of European origin have high incidence rates of all cancers, and many of them were exposed to severe famine and stress during World War II. We assessed cancer incidence in Israeli Jewish survivors of World War II., Methods: Cancer rates were compared in a cohort of 315 544 Israeli Jews who were born in Europe and immigrated to Israel before or during World War II (nonexposed group, n = 57 496) or after World War II and up to 1989 (the exposed group, ie, those potentially exposed to the Holocaust, n = 258 048). Because no individual data were available on actual Holocaust exposure, we based exposure on the immigration date for European-born Israeli Jews and decided against use of the term "Holocaust survivors," implying a known, direct individual Holocaust exposure. Cancer incidences were obtained from the Israel National Cancer Registry. Relative risk (RR) estimates and 95% confidence intervals (95% CIs) were calculated for all cancer sites and for specific cancer sites, stratified by sex and birth cohort, and adjusted for time period., Results: The nonexposed group contributed 908 436 person-years of follow-up, with 13 237 cancer diagnoses (crude rate per 100 000 person-years = 1457.1). The exposed group contributed 4 011 264 person-years of follow-up, with 56 060 cancer diagnoses (crude rate per 100 000 person-years = 1397.6). Exposure, compared with nonexposure, was associated with a statistically significantly increased risk for all-site cancer for all birth cohorts and for both sexes. The strongest associations between exposure and all-site cancer risk were observed in the youngest birth cohort of 1940-1945 (for men, RR = 3.50, 95% CI = 2.17 to 5.65; for women, RR = 2.33, 95% CI = 1.69 to 3.21). Excess risk was pronounced for breast cancer in the 1940-1945 birth cohort (RR = 2.44, 95% CI = 1.46 to 4.06) and for colorectal cancer in the 1935-1939 cohort (for men, RR = 1.75, 95% CI = 1.19 to 2.59; for women, RR = 1.93, 95% CI = 1.25 to 3.00)., Conclusions: Incidence of all cancers, particularly breast and colorectal cancer, was higher among Israeli Jews who were potentially exposed to the Holocaust than among those who were not.

Objectives: To study the difficulties faced by general practitioners to detect and report asbestos-related cancers, focusing on the influence of patients' tobacco use, physicians' training and role perception., Method: Telephone survey conducted among 486 general practitioners and pulmonologists randomly selected in the French region of Provence-Alpes-Côte d'Azur, with: 1) a standardized questionnaire on their behaviors, attitudes and practices in the field of occupational health; 2) a clinical case (case vignette) about a lung cancer patient with occupational asbestos exposure. Two alternative versions of the clinical case varying only in the patient's smoking status were presented randomly to two subgroups of general practitioners and pulmonologists. The primary variable examined was the physician recommendation that the patient described in the vignette file an occupational disease claim., Results: The response rate was 64.4% among general practitioners and 62.5% among pulmonologists. In multiple logistic regressions, the recommendation to file an occupational disease claim was significantly associated with specialty (OR = 4,46; 95% CI: 2.38-8.37 for pulmonologists versus general practitioners), patient's smoking status (OR = 3.15; 95% CI: 2.11-4.70, for non-smokers versus smokers), physician's workload (OR =1,8; 95% CI:1.17-2.88, for physicians examining less than 25 patients per day versus those examining more than 25) and role perception (OR = 2.00; 95% CI:1.22-3.27, for those who considered completing occupational disease medical certificates to be part of their role versus those who did not)., Conclusion: For a certain number of physicians, tobacco use often over-shadows the role of environmental carcinogens in the development of cancers. Those responsible for initial and continuing medical education should give occupational health higher priority in their programs. Tools designed to help physicians detecting and managing occupational diseases should be developed and disseminated.

The inhibitor of apoptosis protein survivin is selectively expressed in tumor cells. The tobacco component nicotine increases the transcription of the survivin gene in non-small cell lung cancer cells. However, the role of survivin expression induced by tobacco component is not clear during lung carcinogenesis. We investigated the effects of the tobacco components nicotine and its related carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on survivin expression in normal human bronchial epithelial (NHBE) cells and examined the role of survivin in the malignant transformation of normal human bronchial epithelial (HBE) cells induced by these components. We found that survivin messenger RNA (mRNA) expression was detected in 41% (7 of 17) of bronchial brush specimens from heavy smokers. Nicotine and NNK increased survivin mRNA and protein expression levels in primary cultured NHBE cells and immortalized HBE cells. Bronchial epithelium in mice administered NNK also showed increased staining for survivin. Nicotine and NNK stimulated the Akt-mammalian target of rapamycin (mTOR) pathway in NHBE cells, leading to increased de novo synthesis of survivin protein. Induced survivin expression increased the survival potential of the cells, which was blocked by transfection with survivin-specific small interfering RNA (siRNA). siRNA-induced down-regulation of survivin expression also suppressed the tumorigenic potential of premalignant and malignant HBE cells exposed to the tobacco components. These findings suggest that NNK and nicotine induce survivin protein synthesis in NHBE cells by activating the Akt-mTOR pathway and thus blockade of the pathway effectively inhibits the tobacco-induced malignant transformation of HBE cells.

Fanconi anemia (FA) is characterized by pancytopenia, congenital malformations, and susceptibility to malignancies. We describe a 31-year-old man with FA, who had undergone bone marrow transplantation and whole body irradiation at the age 17 years for FA. Fourteen years later, he presented with squamous cell carcinoma of the bronchus intermedius in the right lung. The tumor was located next to the main pulmonary artery and between the superior and inferior pulmonary veins. Two cycles of neoadjuvant therapy were given in an attempt to decrease tumor size and avoid a potential right pneumonectomy. Treatment consisted of a 21-day cycle with carboplatin (area under the curve 3) given on day 1 and gemcitabine (1250 mg/m) on day 1 and 8. Because FA cells are hypersensitive to DNA crosslinking agents, we reduced the carboplatin dose to minimize treatment-related toxicity. The tumor regressed sufficiently to permit performance of a right middle and lower lobectomy. In our case, neoadjuvant therapy with gemcitabine and low-dose carboplatin exhibited antitumor activity with manageable side-effects, suggesting that this chemotherapy regimen can be safely and effectively used in the treatment of NSCLC in FA patients who have achieved hematopoietic reconstitution after bone marrow transplantation.

The serum levels of non-enzymatic antioxidants were studied in patients with chronic nonspecific lung diseases with first-to-third-degree dysplasia of the bronchial epithelium (BE) before and after therapeutic correction. The development of BE dysplastic changes was ascertained to cause a considerable reduction in the content of antioxidant vitamin A. During the therapy contributing to reversal of BE dysplastic alterations, there was an increase in the serum levels of vitamin A and uric acid in patients with simple chronic bronchitis with both first- and second-degree dysplasia. If no therapeutic effect occurred, the systemic level of the antioxidants remained unchanged.

In the past several years an increased number of lung tumors has been reported in laboratory studies of rats and mice after lifetime exposure to mainstream cigarette smoke. Proliferative epithelial lesions are present in the lungs of both species and are apparent antecedent lesions to benign and malignant tumors. Both species have alveolar epithelia hyperplasia, alveolar adenomas, and alveolar carcinomas. The incidence of all three are more in the rats. In addition, mice also have bronchiolar epithelial hyperplasia and bronchial papillomas not found in rats. Rats have a low incidence of squamous cyst that is not found in mice. Lung tumors in rats and mice are found at the end of the life span and rarely metastasize. The characteristics of the lung tumors, and the proliferative changes associated with the tumors, are important in helping understand the mechanisms of lung cancer induction. These studies in rats and mice allow new approaches to the study of cigarette smoke-induced changes in the lung.

Dieulafoy's disease of the lung is very rare. We present 2 cases, which are, to our knowledge, the 9th and 10th cases reported in the literature. Haemoptysis is the leading symptom of Dieulafoy's lesion of the lung. In spite of its rareness, the lesion is relevant to the bronchoscopist because a biopsy of the unobtrusive but characteristic bronchial manifestation can precipitate profuse arterial bleeding with a fatal outcome. The bleeding can occur immediately after the biopsy and/or after an interval of up to 12 days. Angiographic images document that this vascular malformation is based on a left-to-right shunt, with a bronchial artery draining into a pulmonary artery. Endobronchial ultrasound may be helpful in detecting the vascular nature of the lesion.

Tobacco carcinogens induce Akt activation and lung carcinogenesis. We previously demonstrated that deguelin, a natural plant product, specifically inhibits the proliferation of premalignant and malignant human bronchial epithelial cells by blocking Akt activation. To evaluate the ability of deguelin to block tobacco carcinogen-induced lung tumorigenesis, we evaluated the in vivo effects of deguelin on Akt activation and lung tumorigenesis in transgenic mice in which Akt expression was induced by tamoxifen and in 4-(methylnitrosoamino)-1-(3-pyridyl)-1-butanone (NNK)/benzo(a)pyrene (BaP)-treated A/J mice. Deguelin suppressed Akt activation in vivo, as measured by immunohistochemistry and immunoblotting, and statistically significantly reduced NNK/BaP-induced lung tumor multiplicity, volume, and load in A/J mice, as monitored by microcomputed tomography image analysis, with no detectable toxicity. These results indicate that deguelin warrants consideration as a chemopreventive agent for early-stage lung carcinogenesis in a clinical lung cancer chemoprevention trial.

Primary pulmonary cryptococcosis is difficult to diagnose because the symptoms and radiologic findings are non-specific. Further, pulmonary cryptococcal infections are extremely rare in individuals with normal immunity. This case report describes a case of primary pulmonary cryptococcosis in an immunocompetent individual who presented with left upper lobe collapse due to endobronchial occlusion.

Bronchopulmonary carcinoma is the first cause of death by cancer in males, its principal cause being tobacco consumption. Nonetheless, different studies have attributed a certain, by no means negligible percent of its aetiology to the occupational exposure to agents considered carcinogenic such as asbestos, with which half of the cases of occupational lung cancer are related. Given the low survival rate of this pathology, preventive measures directed at identifying carcinogenic agents and reducing exposure to them are extremely important. Given that the clinical presentation does not differ from tobacco-related carcinoma, a high level of suspicion, based on a meticulous occupational history, is fundamental to its diagnosis. Due to the synergic effect of tobacco, measures aimed at reducing its consumption continue to be extremely important in the exposed population.

High-energy (HZE) heavy ions, when compared to low-LET radiation, are highly effective in inducing gene mutation, chromosomal aberrations and neoplastic transformation. However, the underlying molecular mechanisms are not clearly understood. We have recently shown that the down-regulation of Betaig-h3 expression is causally linked to the tumorigenic phenotype of papillomavirus-immortalized human bronchial epithelial (BEP2D) cells treated with high-LET alpha-particle radiation. Using the BEP2D cell culture system, a radiation-induced transformation model has been established by a single 60-cGy dose of (56)Fe heavy-ion radiation. To determine whether the Betaig-h3 gene is involved in (56)Fe ion-induced tumorigenesis, the expression levels of the Betaig-h3 gene in tumorigenic cell lines and the ability of in vivo tumor suppression through the reintroduction of the Betaig-h3 gene in tumorigenic cells were determined. We found that the expression level of this gene is markedly decreased in three tumorigenic cell lines ((56)FeT1-T3) compared with parental BEP2D cells. Ectopic expression of its cDNA in the (56)FeT2 tumorigenic cells significantly suppressed their tumorigenicity. Although biologically active TGFB1 is elevated in two of three tumorigenic cell lines, all these cell lines are resistant to the induction of Betaig-h3 expression by incubating the transformed cells with exogenous TGFB1 relative to control cells. Our data strongly suggest that down-regulation of Betaig-h3 expression results from the defect in the TGFB1 signaling pathway and plays a pivotal role in the tumorigenic process induced by (56)Fe heavy-ion radiation.

A 22-year-old male presented with multiple bilateral nodular shadows in the lungs by chest radiograph. He had been asymptomatic and showed no significant abnormal findings in laboratory examinations. He underwent a diagnostic partial lobectomy, and was diagnosed as having primary pulmonary mucosa-associated lymphoid tissue (MALT) lymphoma; i.e. bronchus-associated lymphoid tissue (BALT) lymphoma/BALToma. Neither t(11;18)(q21;q21) chromosomal translocation nor API2-MALT1 chimeric transcript was found at diagnosis. Epstein-Barr virus (EBV) was also not detected in lymphoma cells. He had been a nonsmoker, and had also never shown any associated autoimmune disorders, chronic inflammatory lung diseases or human immunodeficiency virus (HIV) infection. However, he had suffered from moderate atopic dermatitis on his arms from childhood. It appears necessary to clarify whether atopy might play a role in the pathogenesis of API2-MALT1(-) BALT lymphoma for HIV(-) young patients who do not exhibit any other antecedent chronic antigenic stimulations.

Since low dose effects of alpha particles are produced by cellular hits in a relatively small fraction of exposed cells, the present study focuses on alpha particle interactions in bronchial epithelial cells following exposure to inhaled radon progeny. A computer code was developed for the calculation of microdosimetric spectra, dose and hit probabilities for alpha particles emitted from uniform and non-uniform source distributions in cylindrical and Y-shaped bronchial airway geometries. Activity accumulations at the dividing spur of bronchial airway bifurcations produce hot spots of cellular hits, indicating that a small fraction of cells located at such sites may receive substantially higher doses. While presently available data on in vitro transformation frequencies suggest that the relative biological effectiveness for alpha particles ranges from about 3 to 10, the effect of inhomogeneous activity distributions of radon progeny may slightly increase the radiation weighting factor relative to a uniform distribution. Thus a radiation weighting factor of about 10 may be more realistic than the current value of 20, at least for lung cancer risk following inhalation of short-lived radon progeny.

Due to environmental asbestos exposure, asbestos related lung diseases are common in Eskisehir district of Anatolia. In this study we aimed both to determine the epidemiological findings of the patients diagnosed as bronchial carcinoma and to discuss the features, which were probably related to asbestos exposure, presented by the patients. From May 1997 to December 2000, 301 cases were included in the study. Of the patients, 97 (32.2%) had epidermoid cell type, 84 (27.9%) had small cell, 39 (13%) had adenocarcinoma, 4 (1.3%) had large cell. Adenocarcinomas were more frequent in women. There were not significant differences among the cell types from the point of view of the age distributions. Adenocarcinomas were more frequently located in lower lobes of the lungs (36.9%) and more frequently showed peripheral locations (45.9%) than other cell types (20.6% for epidermoid and 14.6% for small cell). Pleural effusion was more detected in adenocarcinomas (48.7% to 17.3% in epidermoid, 18.3% in small cell). The duration of smoking was shortest in adenocarcinomas, mean 32.4 years; the same duration was 56.2 years for epidermoid carcinomas. Of the patients, 54% had asbestos exposure. Adenocarcinomas were more frequently detected in the patients who exposed to asbestos but did not smoke. Our findings support that asbestos exposure may increase adenocancer frequency. The epidemiological and clinical features of adenocancer cases exposed to asbestos environmentally were not different than those of adenocancer cases exposed to asbestos occupationally.

A 34-year-old woman who had been keeping five budgerigars in her home was admitted with cough and progressive exertional dyspnea that had continued for three months. Chest CT scan demonstrated diffuse centrilobular nodular opacities throughout both lung fields. Flexible bronchoscopy revealed polypoid lesions with diameters of 2-3 mm located at the right B1/B2 spur. B3a/B3b spur and middle/lower bronchus spur. Their surfaces were glossy and smooth but slightly lobulated. The histological findings were consistent with inflammatory polyps containing lymphoid follicles in a dense infiltrate of lymphocytes. A positive environmental provocation test and precipitating antibodies confirmed the diagnosis of hypersensitivity pneumonitis (HP) caused by budgerigars (bird fanciers' lung). To our knowledge, there is no previous report of HP accompanied with endobronchial polyps, but this rare case shows the involvement of large airways in HP.

The objective of this study was to determine the factors associated with central airway versus peripheral bronchial location of lung cancer. All patients diagnosed with lung cancer from 1997 through 2000 in the Respiratory Disease Department of Rouen University Hospital were prospectively interviewed about their smoking and occupational history using a standardized questionnaire. All patients underwent white-light bronchial endoscopy using a 4.5 mm flexible endoscope. Tumors were classified as central when they were accessible and visible using this technique. Out of 217 cases of lung cancer included in this study, 155 (71%) were central. Histological type of lung cancer was strongly associated with bronchial location as central location was observed in 48, 82 and 92% of Adenocarcinoma (AC), Squamous Cell (SqC), and Small Cell Carcinoma (SCC), respectively (P<0.0001). Among non asbestos-exposed patients, location varied little with smoking status, with central location frequency ranging from 74 to 80%. In contrast, lung cancer was recorded central in 41% of long-term (> or =10 years) ex-smokers, 67% of short-term (<10 years) ex-smokers and 75% of current smokers (P=0.04) among patients exposed to asbestos, suggesting an interaction between duration of smoking cessation and occupational asbestos exposure with respect to lung cancer location. These findings were confirmed after adjustment for sex, age and histologic type in multivariate analysis. These results suggest that individually-tailored multimodality screening strategies relying on various combinations of low-dose CT scan, sputum analysis and fluorescence endoscopy according to each patient's profile may be more effective than standard strategies based on a single approach for all patients.

Besides tobacco exposure, factors associated with the development of pre-invasive bronchial lesions are not known. Autofluorescence bronchoscopy was used to assess the prevalence of severe dysplasia and carcinoma in situ (SD/CIS) of the proximal bronchial tree in relation to occupational or nonoccupational carcinogen exposure. Among the 241 individuals in this study, the overall prevalence of at least one SD/CIS was 9% (21 subjects). Multivariable analysis revealed significant and independent associations between presence of SD/CIS and: 1) active smoking, relative to former smokers; 2) presence of synchronous invasive lung cancer; 3) duration of asbestos exposure and; 4) exposure to other occupational carcinogens. The independent associations of synchronous lung cancer with severe dysplasia and carcinoma, after adjusting for both occupational and nonoccupational carcinogen exposures, suggest other mechanisms than a field cancerisation may be involved in the carcinogenesis of these pre-invasive lesions. Moreover, active smokers, patients with recently resected invasive lung cancer and workers occupationally exposed to bronchial carcinogens may represent a population of choice for early cancer endoscopic detection programmes in view of their high severe dysplasia and carcinoma prevalence.

Background: Several recent studies discuss bronchoscopic techniques for treating endobronchial lipoma, an extremely rare benign tumor., Objectives: To describe the epidemiology of endobronchial lipoma and to propose appropriate therapeutic policies for treating this tumor., Methods: We reviewed 64 cases of endobronchial lipoma: 33 cases previously reported in 30 different articles, and 31 case reports presented at thoracic meetings in Japan., Results: Of the 64 patients included in this study (50 male and 14 female; mean age, 60 years), 40 patients had endobronchial lipoma in the right lung and 23 patients had it in the left lung. The overwhelming majority of the tumors (n = 61) were found in the first three subdivisions of the tracheobronchial tree. Forty-eight patients (75%) were symptomatic, and their symptoms included cough, sputum, hemoptysis, elevated temperature, and dyspnea. Additionally, abnormal radiographic findings were reported for 51 patients (80%): 18 patients had atelectasis, 14 patients had infiltration or consolidation, 6 patients showed volume loss of the lung, and mass shadow was identified in 9 patients, and another abnormality including pleural effusion was found in 4 patients. Forty patients underwent surgical resection: 4 pneumonectomies, 24 lobectomies, 8 bilobectomies, and 4 resections by bronchotomy. Bronchoscopic resection was carried out in 17 cases: 7 cases by Nd-YAG laser, 5 cases by electrosurgical snaring forceps, and another 5 cases with a combined therapy using both procedures., Conclusions: Bronchoscopic resection should be considered as the first choice of treatment for endobronchial lipoma; however, surgical therapy is indicated for patients who show the possibility of a complicated malignant tumor, who have destructive peripheral lung disease, who have extrabronchial growth, or who may have technical difficulties during the bronchoscopic procedure.