Changes In Bronchial Epithelium Research Articles

Precursor lesions of lung tumors

Lung cancer is the leading cause of cancer deaths globally with many new cases diagnosed each year. Recent studies have shown that an accumulation of various genetic abnormalities results in progressive morphologic changes in bronchial epithelium. Such changes are part of the continuum from precursor lesions to invasive lung cancers. Improvement in diagnostic modalities has made the detection of such preneoplastic lesions possible and resection at this stage confer excellent prognosis. The World Health Organization (WHO) has recognized atypical adenomatous hyperplasia/ adenocarcinoma in situ, squamous dysplasia/ squamous cell carcinoma in situ, and diffuse idiopathic pulmonary neuroendocrine cell hyperplasia as the precursor lesions of adenocarcinoma, squamous cell carcinoma, and carcinoid tumors respectively. This review summarizes the key features of these preneoplastic lesions based on the current understanding and knowledge.

IS MARIJUANA SAFE? A CASE OF A NON-SMALL CELL LUNG CARCINOMA IN A SOLE MARIJUANA SMOKER

SESSION TITLE: Medical Student/Resident Lung Cancer Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: Marijuana is the most commonly used illicit drug worldwide. Marijuana smoking shares almost the same carcinogens and irritants as tobacco smoking. Several case studies to date have documented premalignant changes in bronchial epithelium in marijuana smokers that lead to cancer. We present a case of a NSCLC in a patient who only smoked marijuana for 40 years. CASE PRESENTATION: A 67-year-old male with past medical history of hypertension and hyperlipidemia presents with a month history of cough, congestion and intermittent hemoptysis. He had been smoking marijuana joints for about 40 years but denied any tobacco smoking. Physical examination revealed prolonged expiratory breath sounds. CT chest with contrast showed spiculated left perihilar mass measuring 6.9 x 4.01 x 3.8 cm extending into the left upper lobe (LUL) causing mild narrowing. PET/CT scan showed hypermetabolic 6 cm LUL lung mass with SUV of 22. EBUS with a transbronchial biopsy of the LUL of the lung was positive for poorly differentiated adenocarcinoma. Lymph node and adrenal gland biopsies were negative for malignancy. Ultimate staging was cT3N0M0. Genomic testing showed no expression of PDL 1 and was negative for ROS 1 rearrangement. Patient was started on neoadjuvant chemotherapy with Alimta and Carboplatin for locally advanced disease. DISCUSSION: Around 3.9% of the global population age 15 to 64 years smokes marijuana. Marijuana smoke contains about 50% more benzopyrene and nearly 75% more benzanthracene than tobacco smoke, in addition to other carcinogens and co-carcinogens including phenols, vinyl chlorides, nitrosamines, and reactive oxygen species. Moreover, differences in the technique of smoking marijuana including deeper inhalation, lack of filter, much longer breath holding time and lower rod filtration result in a fourfold increase in deposition of the tar in the lung. Few experimental studies also suggested tetrahydrocannabinol (THC) promotes tumor growth by inhibiting antitumor immunity by a cannabinoid 2 receptor mediated pathway. In a chronic cannabis smoker, sputum cytomorphological analysis showed metaplastic cells, macrophages, pigmented macrophages and columnar cells. Endobronchial biopsies from habitual marijuana-only smokers reveal squamous cell metaplasia and cellular atypia which are precursors for malignancies. Immunohistology of bronchial tissue was also remarkable for overexpression of the nuclear proliferation antigen Ki-67, and of epidermal growth factor receptors. CONCLUSIONS: A definite association between lung cancer and smoking marijuana has been still limited by selection bias, small sample size and failure to adjust for tobacco smoking. Given the increased popularity of marijuana use in young adults and also for medicinal purposes, more prospective studies need to be performed to establish the association of marijuana with serious adverse events including lung Ca. Reference #1: Tashkin, D. P. (2013, June). Effects of marijuana smoking on the lung. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23802821/ Reference #2: Zhang, L. R., Morgenstern, H., Greenland, S., Chang, S.-C., Lazarus, P., Teare, M. D., … Hung, R. J. (2015, February 15). Cannabis smoking and lung cancer risk: Pooled analysis in the International Lung Cancer Consortium. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4262725/ Reference #3: Aldington, S., Harwood, M., Cox, B., Weatherall, M., Beckert, L., Hansell, A., … Cannabis and Respiratory Disease Research Group. (2008, February). Cannabis use and risk of lung cancer: a case-control study. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2516340/ DISCLOSURES: No relevant relationships by Santhosh Bayambe, source=Web Response no disclosure on file for Kristine Fless; No relevant relationships by Aditi Saha, source=Web Response No relevant relationships by Paarth Shah, source=Web Response No relevant relationships by Sohaib Tariq, source=Web Response

Ways of enhancement of the surgical treatment efficacy in treatment of patients, suffering pulmonary tumors

Objective. Efficacy of endoscopic bronchosanation for prophylaxis of preoperative and postoperative complications in patients with pulmonary tumors.
 Маterials and methods. There was studied the efficacy of endoscopic photodynamic therapy in accordance to procedure, elaborated by the authors, including injection of the water solution of a methylene blue dye in concentration 0.04% into tracheobronchial tree, irradiated by laser with the wave length 0.63 mcm, independently and in conjunction with a standard anti-inflammatory therapy as preoperative preparation of tracheobronchial tree in patients, suffering pulmonary cancer. In the investigation 181 patients were included, suffering pulmonary cancer Stages II-III, morphologically confirmed, and with coexistent endobronchitis.
 Results. In accordance to analysis of the pathogenic microflora titer and character in lumen of bronchial tree after preoperative preparation there was established, that while application of independent endoscopic bronchosanation in 55 (87%) observations the pathogenic microflora was absent. While combination of photodynamical bronchosanation in accordance to standard therapy a pathogenic microflora was not revealed in 52 patients. While conduction of a standard preparation without application of a laser therapy microflora was not revealed only in 44.8% observations. Together with the bronchial mucosa metaplasia in some investigated patients the dysplastic changes of bronchial epithelium of various severity degree were registered. Independent endoscopic bronchosanation have leaded to trustworthy lowering of a general rate of the bronchial epithelial dysplasia in the patients tо 36.1%, together with standard anti-inflammatory therapy - tо 42.4%.
 Conclusion. Application of endoscopic photodynamic bronchosanation in accordance to the proposed procedure in preoperative period in the patients with objective to correct a concomitant endobronchitis, as independent option or together with standard anti-inflammatory therapy, leads to reduction of the endobronchial complications rate after operative treatment for pulmonary cancer, comparing with a control group. Еndoscopic bronchosanation is accompanied by significant lowering of severity of endoscopic signs of coexistent endobronchitits and improvement of mucociliary transport. In accordance to microbiological tests in 87 - 88% of patients a complete sanation of bronchial tree and elimination of main histological criteria of inflammation were noted, while in 67.2 - 100% patients – restoration of normal structure of the bronchial tree mucosa.

Spectrum of chronic lung allograft pathology in a mouse minor-mismatched orthotopic lung transplant model.

Chronic lung allograft dysfunction (CLAD) is a fatal condition that limits survival after lung transplantation (LTx). The pathological hallmark of CLAD is obliterative bronchiolitis (OB). A subset of patients present with a more aggressive CLAD phenotype, called restrictive allograft syndrome (RAS), characterized by lung parenchymal fibrosis (PF). The mouse orthotopic single LTx model has proven relevant to the mechanistic study of allograft injury. The minor-alloantigen-mismatched strain combination using C57BL/10(B10) donors and C57BL/6(B6) recipients reportedly leads to OB. Recognizing that OB severity is a spectrum that may coexist with other pathologies, including PF, we aimed to characterize and quantify pathologic features of CLAD in this model. Left LTx was performed in the following combinations: B10→B6, B6→B10, B6→B6. Four weeks posttransplant, blinded pathologic semi-quantitative assessment showed that OB was present in 66% of B10→B6 and 30% of B6→B10 grafts. Most mice with OB also had PF with a pattern of pleuroparenchymal fibroelastosis, reminiscent of human RAS-related pathology. Grading of pathologic changes demonstrated variable severity of airway fibrosis, PF, acute rejection, vascular fibrosis, and epithelial changes, similar to those seen in human CLAD. These assessments can make the murine LTx model a more useful tool for further mechanistic studies of CLAD pathogenesis.

Pulmonary microRNA profiles identify involvement of Creb1 and Sec14l3 in bronchial epithelial changes in allergic asthma

Asthma is highly prevalent, but current therapies cannot influence the chronic course of the disease. It is thus important to understand underlying early molecular events. In this study, we aimed to use microRNAs (miRNAs) - which are critical regulators of signaling cascades - to identify so far uncharacterized asthma pathogenesis pathways. Therefore, deregulation of miRNAs was assessed in whole lungs from mice with ovalbumin (OVA)-induced allergic airway inflammation (AAI). In silico predicted target genes were confirmed in reporter assays and in house-dust-mite (HDM) induced AAI and primary human bronchial epithelial cells (NHBE) cultured at the air-liquid interface. We identified and validated the transcription factor cAMP-responsive element binding protein (Creb1) and its transcriptional co-activators (Crtc1-3) as targets of miR-17, miR-144, and miR-21. Sec14-like 3 (Sec14l3) - a putative target of Creb1 - was down-regulated in both asthma models and in NHBE cells upon IL13 treatment, while it’s expression correlated with ciliated cell development and decreased along with increasing goblet cell metaplasia. Finally, we propose that Creb1/Crtc1-3 and Sec14l3 could be important for early responses of the bronchial epithelium to Th2-stimuli. This study shows that miRNA profiles can be used to identify novel targets that would be overlooked in mRNA based strategies.

PRE-NEOPLASTIC AND NEOPLASTIC CHANGES IN BRONCHIAL EPITHELIUM OF PATIENTS WITH SQUAMOUS CELL LUNG CANCER AND LUNG ADENOCARCINOMA

The data on modern views on the problem of pre-cancerous changes (epithelial hyperplasia, squamous metaplasia, preneoplasia (dysplasia I) and neoplasia (dysplasia II-III) when squamous cell cancer and adenocarcinoma of the lung are summarizes in the present review. Atypical adenomatous hyperplasia, which is considered precancerous process for adenocarcinoma of the lung, due to the rare occurrence in the review is not considered. The attention is focused on the classification of morphological characteristics of precancerous changes in respiratory epithelium. The analysis of frequency and reversibility of preand neoplastic changes in bronchial epithelium. We discuss the connection between the nature of the changes of respiratory epithelium in the bronchi, developing simultaneously with squamous cell cancer or adenocarcinoma of the lung, with tumour progression.

Primary malignant achromic melanoma of the lung.

Currently, less than thirty cases of primary malignant melanoma of the lung have been reported in the literature. Thus, strict criteria for diagnosis have been published and include: malignant melanoma associated with bronchial epithelial changes; a solitary lung tumor; no prior history of skin, mucous membrane, intestinal or ocular melanoma; and absence of any other detectable tumor at the time of diagnosis. In this article we present a case of melanoma of the lung without evidence of extra-pulmonary disease.

Mitigating Effects of Captopril and Losartan on Lung Histopathology in a Rat Model of Fat Embolism

Fat embolization (FE) is an often overlooked and poorly understood complication of skeletal trauma and some orthopedic procedures. Fat embolism can lead to major pulmonary damage associated with fat embolism syndrome (FES). A model of FE in unanesthetized rats, using intravenous injection of the neutral fat triolein, was used to study the potential therapeutic effect on lung histopathology of altering the production of, or response to, endogenous angiotensin (Ang) II. Either captopril, an Ang I converting enzyme inhibitor, or losartan, an Ang II type 1 receptor blocker, was injected 1 hour after FE by triolein injection. After euthanasia at 48 hours, histopathologic evaluation was used to compare the drug-treated animals with control animals that received only triolein. Histology of the lungs of rats treated only with triolein revealed severe, diffuse pathology. Alveolar septa showed severe, diffuse inflammation. Bronchial lumina showed severe mucosal epithelial loss. The media of the pulmonary small arteries and arterioles was thicker, and the lumen patency was reduced 60% to 70%. Trichrome staining confirmed the abundant presence of collagen in the media and adventitia, as well as collagen infiltrating the bronchial musculature. Both captopril and losartan treatments reduced the inflammatory, vasoconstrictor, and profibrotic effects present at 48 hours (p<0.001). With treatment, the vascular lumen remained patent, and the fat droplets were reduced in size and number. There was a reduction in the number of infiltrating leukocytes, macrophages, myofibroblasts, and eosinophils, along with a significant decrease in hemorrhage and collagen deposition (p<0.001). Pathologic changes in bronchial epithelium were also diminished. The results suggest that the use of drugs that act on the renin-Ang system might provide an effective and targeted therapy for fat embolism syndrome.

Biologic risk model development for recurrent and second primary tumors (SPTs) in patients (pts) with early stage non-small cell lung cancer (ES NSCLC).

e17503 Background: Pts with ES NSCLC are at significant risk for recurrence or SPTs. Identifying higher risk pts is key to personalizing therapy. Goals of the Vanguard trial are to assess smoking-related disease-free survival and to develop a risk model, utilizing a large cohort of archived ES NSCLC specimens, to predict the risk of recurrence or SPTs in this high risk group. Methods: Pts on the phase II prospective Vanguard study had definitively treated ES NSCLC or head and neck cancer and were current/former smokers. Pts had bronchoscopies with biopsies at 6 predefined sites at enrollment, 12, 24, and 36 months (mos). Serum was collected every 6 mos for 3 yrs. ES NSCLC pt specimens identified in our tumor bank were used to explore promising biomarkers; pathological and clinical data was collected for all pts. Results: 54 pts (46 eligible) were enrolled in the Vanguard trial between 12/04 and 2/09. Median age 61 yrs (42-81); 26 (57%) were male. 42 pts had NSCLC; stage I 32 (76%), II 8 (19%), IIIA 2 (5%). 9 pts (21%) have recurred and 3 pts (7%) have SPTs so far. 37 pts (80%) have completed bronchoscopy at 12 mo, 21 pts (46%) at 24 mos, 10 pts (22%) at 36 mos. 27 pts remain on study. Analyses are planned on biopsy specimens to characterize molecular changes in bronchial epithelium over time. Tumor specimens from 521 pts with ES NSCLC from 2002-2005 were also collected with outcome data. Tissue microarrays have been constructed from archived tumor specimens and numerous biomarkers were tested, including members of IGF, EGF, and apoptotic pathways. On multivariate analyses, several markers correlate with overall survival, including pAMPK (p=0.002), MCM6 (p=0.014), and CXCR2 (p=0.003). Conclusions: This is a unique pt cohort with prospectively collected bronchial specimens over a 3 yr follow-up period. Also, we have assembled a large matched population of over 500 archived ES NSCLC specimens. Molecular testing performed in archived specimens will be validated in the Vanguard pts, which will allow for analysis of progressive molecular changes in bronchial epithelium over time. With these results, we will establish a risk model for development of recurrence or SPTs in ES NSCLC pts. (DoD W81XWH-04-1-0142) No significant financial relationships to disclose.

Autofluorescence Bronchoscopy to Detect Bronchial Epithelial Changes Associated With Cigarette Smoking Among Asymptomatic Volunteers: A Single Center Prospective Pilot Study

Autofluorescence Bronchoscopy to Detect Bronchial Epithelial Changes Associated With Cigarette Smoking Among Asymptomatic Volunteers: A Single Center Prospective Pilot Study

Increased expression of high mobility group A proteins in lung cancer

High mobility group A (HMGA) proteins play an important role in the regulation of transcription, differentiation, and neoplastic transformation. In this work, the expression of HMGA 1 and 2 in 152 lung carcinomas of mainly non-small-cell histological type has been studied by immunohistochemistry in order to evaluate their feasibility as lung cancer markers. In 17 lung cancer cases, the related bronchial epithelial changes were also studied for HMGA1 and 2 expression. RNA expression of HMGA1a and b isoforms and of HMGA2 was determined by real-time semi-quantitative RT-PCR in 23 lung carcinomas. High expression of HMGA1 and HMGA2 at both mRNA and protein levels was detected in lung carcinomas, compared with normal lung tissue. Nuclear immunostaining for HMGA1 and 2 proteins also occurred in hyperplastic, metaplastic, and dysplastic bronchial epithelium. Increased nuclear expression of HMGA1 and 2 correlated with poor survival (for adenocarcinomas, HMGA1, p=0.006; HMGA2, p=0.05). While the expression of HMGA2 was significantly associated with cell proliferation (p=0.008), HMGA1 expression did not show any association with proliferation or apoptotic index. Sequencing of HMGA2 transcripts from tumours with very high expression showed a normal full-length transcript. As HMGA proteins were expressed in about 90% of lung carcinomas and their expression was inversely associated with survival, they may provide useful markers for lung cancer diagnosis and prognosis.

Role of Type I IFNs in Pulmonary Complications of Pneumocystis murina Infection

Despite the advent of highly active antiretroviral therapy, pulmonary complications in AIDS are a common clinical problem. Pneumocystis jiroveci infection causes a life-threatening pneumonia, especially in individuals with CD4 T cell deficiencies as occurs in AIDS. Although Pneumocystis sp. is an extracellular fungal pathogen, CD8 T cells are the predominant lymphocyte recruited to the lung in CD4-deficient humans and mice during Pneumocystis pneumonia, and we have found that these CD8 T cells are responsible for subsequent lung damage in CD4 T cell-depleted mice. Comparing CD4 T cell-depleted IFN-alpha receptor knockout (KO) mice to wild-type mice, we found that this CD8 T cell recruitment and lung damage is type I IFN (IFN-alphabeta) dependent. However, in both CD4 competent, wild-type and IFN-alpha receptor (IFNAR) KO mice, Pneumocystis infection leads to an eosinophilic granulocyte influx with bronchial epithelial changes as seen in asthma. This response is delayed in IFNAR KO mice, as is pathogen clearance. Although the inflammation is transient in wild-type animals and resolves upon Pneumocystis clearance, it is more severe and persists through day 35 postinfection in IFNAR KO mice, leading to fibrosis. In addition, IFNAR KO, but not wild-type, mice mount a Pneumocystis-specific IgE response, an indicator of allergic sensitization. Thus, in the absence of IFNAR signaling and CD4 T cells, Pneumocystis-mediated lung damage does not occur, whereas in CD4-competent animals, the absence of IFNAR signaling results in an exacerbated Th2 response, asthma-like symptoms, and fibrosis. Therefore, both CD4 T cell- and type I IFN-mediated mechanisms can determine pulmonary complications from Pneumocystis infection.

Preinvasive Bronchial Lesions: Surveillance or Intervention?

Preinvasive lesions are prevalent in the bronchial epithelium of smokers and are believed to be precursors of squamous cell carcinoma. 1 Auerbach O Stout AP Hammond EC et al. Changes in bronchial epithelium in relation to cigarette smoking and lung cancer. N Engl J Med. 1961; 265: 253-267 Crossref PubMed Scopus (423) Google Scholar These lesions are not easily detected with standard white light bronchoscopy, and so their natural history remains incompletely understood. However, their detection has been enhanced significantly over the past decade with the development of fluorescence bronchoscopy. 2 Lam S Kennedy T Unger M et al. Localization of bronchial intraepithelial neoplastic lesions by fluorescence bronchoscopy. Chest. 1998; 113: 696-702 Abstract Full Text Full Text PDF PubMed Scopus (536) Google Scholar We are undertaking a detailed longitudinal study of patients with preinvasive bronchial epithelial lesions in order to define their natural history. In contrast to the practice of most other centers, 3 Bota S Auliac JB Paris C et al. Follow-up of bronchial precancerous lesions and carcinoma in situ using fluorescence endoscopy. Am J Respir Crit Care Med. 2001; 164: 1688-1693 Crossref PubMed Scopus (179) Google Scholar we have elected to keep lesions of all grades of severity under surveillance, including carcinoma in situ, but to intervene at the earliest signs of progression to invasive disease.

The evolution of lung cancer screening.

In the 1970s, four trials failed to demonstrate any mortality reduction using a combination of chest X-ray (CXR) and/or sputum cytology. The recent early lung cancer action project (ELCAP) demonstrated that modern screening is capable of detecting Stage I lung cancers. Bronchial epithelial changes leading up to cancers are now being understood to include histologic changes and genetic alterations. Emerging molecular markers detected in sputum and serum show promise in the future of lung cancer screening.

RESPONSE: Re: Sex-Related Differences in Bronchial Epithelial Changes Associated With Tobacco Smoking

RESPONSE: Re: Sex-Related Differences in Bronchial Epithelial Changes Associated With Tobacco Smoking

Phonation bronchoscopy

Fluorescence bronchoscopy is one of the methods of the early detection of lung cancer that involves the large airways. The method is based on the detection of the altered autofluorescence of malignantly transformed tissue, and confirmed by biopsy and histopathologic examination. Fluorescence bronchoscopy was performed in 18 patients, mean age of 51.2 years (male n = 12, female n = 6) due to the suspected lung cancer. Fluorescence bronchoscopy was performed using the Xillix LIFE-Lung System, Vancouver, Canada. After conventional white-light bronchoscopy, the tracheobronchial tree was illuminated by blue light (442 nm) using helium-cadmium laser, and the results of autofluorescence were classified into three classes. Normal mucosa was of green fluorescence (Class I), abnormal mucosa was red or dark brown fluorescence (Class II and II), which was the indication for performing biopsy. Normal endoscopy findings were established in 15 patients by conventional bronchoscopy. In the same group, by fluorescence bronchoscopy, Class I of fluorescence (normal finding) was found in 9 patients, while Class II changes occurred in 6 patients. Histopathologic analysis of bronchial mucosa with Class II changes was performed detecting planocellular carcinoma in situ in one patient. Tumor-like changes were detected in 3 patients by conventional bronchoscopy, and were determined as Class III changes by fluorescence bronchoscopy. By the biopsy of these chages carcinoma was documented in 2 patients while in one patient metaplasia of epithelium and granulation tissue around aspirated foreign body was detected. Fluorescence bronchoscopy is one of the methods for detecting metaplasia, carcinoma in situ and cancerous changes of bronchial epithelium in the large airways. However, the high rate of falsely positive findings represents a limitation of this method.

Efficacy of Two Sputum Collection Techniques in Patients with Air Flow Obstruction

To compare the efficacy of two sputum collection techniques in patients with chronic obstructive pulmonary disease (COPD) in order to diagnose dysplasia or neoplasia. This was a crossover study design comparing induced sputum with sputum collected at home. One hundred seven patients with COPD were enrolled. Fifty-six were randomized to collect induced sputum first followed by sputum collection at home. Fifty-one randomly assigned patients collected the sputum in reverse order. The second sputum collection technique for both random assignments gave the greatest yield of adequate sputum. There was no significant difference in efficacy between the collection of the two sputum collection techniques in the presence of the learning (period) effect. Sputum collection is equally efficacious by the induced method and the home collection method. A learning effect was responsible for the increased yield of sputum abnormalities in the second collection session. Sputum collection at home may facilitate the amount of dysplasic and neoplastic bronchial epithelial changes in heavy smokers with COPD.

Sex-related differences in bronchial epithelial changes associated with tobacco smoking

Sex-related differences in bronchial epithelial changes associated with tobacco smoking

Sex-related differences in bronchial epithelial changes associated with tobacco smoking.

Lung cancer is the most common cause of cancer death in North American women. Because smoking-related changes in the bronchial epithelium and in lung function have not been studied in detail in women, we used fluorescence bronchoscopy-directed biopsy to determine the prevalence of high-grade preinvasive lesions in former and current smokers of both sexes. Spirometry, white-light bronchoscopy, and fluorescence bronchoscopy were performed in 189 women and 212 men older than 40 years of age who had smoked 20 pack-years or more (pack-years = number of packs of cigarettes smoked per day x number of years of smoking). Carcinoma in situ was found in 1.8% of the subjects, severe dysplasia was found in 6.5%, and moderate dysplasia was found in 14% (all preinvasive lesions). Compared with men, women had a lower prevalence of high-grade preinvasive lesions in the observed airways (14% versus 31%; odds ratio = 0.18; 95% confidence interval = 0.04-0.88), and women with preinvasive lesions had fewer such lesions (two-sided P = .048). The prevalence of preinvasive lesions did not change substantially for more than 10 years after cessation of smoking. Lung function was associated with the prevalence of preinvasive lesions, but the association was weaker in women than in men. If the presence of airflow obstruction was defined by an FEV1/FVC (forced expiratory volume in 1 second/forced vital capacity) value of 70% or less, only 56% of the men and 44% of the women with preinvasive lesions had abnormal lung function. In developing strategies for chemoprevention or early detection of lung cancer in high-risk populations, it is important to consider the effect of sex and arbitrarily chosen lung function values on the prevalence of preinvasive airway lesions.

Detection of Bronchial Neoplasia in Uranium Miners by Autofluorescence Endoscopy (SAFE‐1000)

The increase in the detection rate for premalignant changes of bronchial epithelium was studied in 56 symptom-free volunteers from the risk group of Czech uranium miners (mean age 50.69 years, mean WLM 21.06 (1 Working Level Month is equal to the absorption of latent energy of 2.08 × 10–5 J/m3 in one month, i.e. 170 working hours)) by the additional employment of the System of Autofluorescence Endoscopy (SAFE-1000 Pentax) to conventional white-light bronchoscopy, comparing results with those of bronchial biopsy histopathology examination. Histopathology using hematoxylin and eosin staining confirmed intraepithelial neoplasias in 15 areas in 10 persons. White-light bronchoscopy sensitivity was 21.05%, and specificity 93.7% which an autofluorescence bronchoscopy sensitivity was 78.95% and specificity 81.89%.