PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Lung Cancer”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2025

Panorama of Chromosomal Instability in Lung Cancer.

Lung cancer is a highly heterogeneous disease primarily driven by tobacco smoking. About 20% of lung cancers occur among patients who have never smoked (LCINS) with differences in patient ancestry, sex, tumor histology, and clinical features. Our understanding of chromosomal instability in lung cancer, especially LCINS, is still limited. Here, we perform a comprehensive study of 182,429 somatic structural variations (SVs) detected in 1,209 whole-genome sequenced lung cancers, of which 864 LCINS. SVs are more abundant in tumors from patients who have smoked (LCSS); however, they are more complex and play more important roles in tumorigenesis in LCINS. EGFR mutations and KRAS mutations profoundly and independently shape the SV landscape. EGFR-mutant tumors have higher SV burden and more cancer-driving SVs. In contrast, KRAS mutations are associated with lower SV burden and less driver SVs. We decompose 16 SV signatures for both complex and simple SVs that likely represent divergent molecular mechanisms. The SV breakpoints have distinct distributions across the genome depending on the signatures due to mutagenic mechanisms and positive selection. Many established cancer-driving genes are recurrently rearranged by multiple SV signatures suggesting functional convergence of these genome instability mechanisms.

Journal Article↗
PubMed1978

Atmospheric pollution and lung cancer.

Lung cancer is consistently more common in urban areas than in rural. The excess cannot be accounted for by specific occupational hazards but some of it might be due to the presence of carcinogens in urban air. The excess cannot be wholly due to such agents, because the excess in nonsmokers is small and variable. Cigarette consumption has also been greater in urban areas, but it is difficult to estimate how much of the excess it can account for. Occupational studies confirm that pollutants present in town air are capable of causing lung cancer in man and suggest that the pollutants and cigarette smoke act synergistically. The trends in the mortality from lung cancer in young and middle-aged men in England and Wales provide uncertain evidence but support the belief that atmospheric pollution has contributed to the production of the disease. In the absence of cigarette smoking, the combined effect of all atmospheric carcinogens is not responsible for more than about 5 cases of lung cancer per 100,000 persons per year in European populations.

Air Pollutants↗
PubMed1975

The association of economic status with the occurrence of lung cancer.

Lung cancer in men was shown to be inversely associated with economic class by analysis of 1959-61 mortality rates from Buffalo, New York. Using five economis strata, white men below and above age 55 in the poorest group had rates 2.6 and 3.8 times higher than those in the richest. For women, the trend was not significant. The question that was investigated was whether, for males, an economic-class trend for smoking existed which paralleled that for lung cancer. Individuals from a Buffalo sample survey were classified according to cigarette smoking habits. Age was found highly associated with both smoking and economic class. In data from white males stratified for age, no significant association was observed between smoking and econimic class. In women, the upper economic groups smoked more, particularly those above age 55. Thus, a strong inverse economic class gradient for lung cancer in men, observed by other investigators among women, cannot be explained by class-related cigarette smoking patterns alone. The possible interaction of cigarette-smoking with other potential etiologic factors that may be associated with economic class is discussed.

Adult↗
PubMed2026

Development and validation of a plasma miRNA-CEA biomarker panel for early detection of lung cancer.

Lung cancer remains a leading cause of cancer-related mortality worldwide, underscoring the critical need for early detection to improve patient outcomes. This study aimed to develop and validate a plasma microRNA biomarker panel for the early detection of non-small cell lung cancer in a Japanese cohort. We enrolled 525 participants, comprising 261 LC cases and 264 non-LC controls, divided into optimization and validation cohorts. A 12-miRNA panel was optimized and further combined with CEA to enhance diagnostic performance. The miRNA-alone model demonstrated robust performance in both the optimization (AUC = 77.0%) and validation cohorts (AUC = 77.9%). Integration with CEA significantly improved accuracy, achieving AUCs of 86.2% in optimization and 84.9% in validation, with particularly high performance in late-stage cancers (AUC = 94.4%) and squamous cell carcinoma (AUC = 90.7%). Sensitivity and specificity thresholds were evaluated, enabling model customization for diverse clinical scenarios. These findings highlight the potential of the miRNA-CEA panel as a minimally invasive tool for early LC detection, especially in non-smoking populations.

Humans↗
PubMed1976

Occupational differences in rates of lung cancer.

Lung cancer rates in Los Angeles County were reviewed for different occupations and industries. Employment groups found to be at excess risk who have not been previously implicated included roofers, dental lab technicians, decorators, nonautomotive mechanics, photoengravers, clothing ironers, electricians, bar and restaurant managers, janitors: and workers in the radio-TV brooad-casting, dairy, leather, food and drink, bakery, and auto repair industries. Mo lung cancer in Los Angeles County had exposure to asbestos, polycyclic aromatic hydrocarbon compounds (PAH), or both.

Adult↗
PubMed2026

Circulating tumor-associated autoantibody signatures for diagnosis and prognosis in small-cell lung cancer and lung adenocarcinoma.

BACKGROUND: Tumour-associated autoantibodies (TAAbs) are promising biomarkers for cancer detection, but their induction and clinical relevance in lung cancer remain unclear. METHODS: Serum samples from 695 individuals were analysed for TAAb profiling by protein-array screening and two-stage ELISA validation. Diagnostic models were constructed with identified TAAbs and compared with conventional tumour markers. Potential mechanisms, clinical and prognostic features of TAAb seropositivity were analysed and its presence in prediagnostic sera was evaluated to assess the potential for early detection. RESULTS: Six TAAbs for small cell lung cancer (SCLC) and four for lung adenocarcinoma (LUAD) were identified, demonstrating excellent diagnostic performance (AUC > 0.8) and outperforming ProGRP and CEA. TAAb induction correlated with antigen overexpression, somatic mutations and HLA class II amino acid polymorphisms. TAAb panel seropositivity was associated with older age and advanced stage in both subtypes, and predicted poor survival in SCLC but a favourable outcome in advanced LUAD. In prediagnostic sera, the TAAb concentration increased progressively, with detectability up to 2 years before clinical diagnosis. CONCLUSIONS: Distinct TAAb panels were identified for SCLC and LUAD, serving as accurate diagnostic markers that enable early detection and as indicators of prognosis in different clinical contexts.

Humans↗
PubMed1979

Placental type of membrane-bound arylamidase (Shiba isoenzyme) found in human cancerous lung.

A placental type of membrane-bound arylamidase (Shiba isoenzyme) was found in the tissue of adenocarcinoma of the lung. Cancerous lung membrane-bound arylamidase had the same electrophoretic mobility, isoelectric point (pH 4.2), and susceptibility to SDS inactivation as placental membrane-bound arylamidase. Cancerous lung membrane-bound arylamidase had molecular weight and kinetic properties similar to normal lung membrane-bound arylamidase, but differed from the normal lung membrane-bound arylamidase with respect to electrophoretic mobility, isoelectric point, heat stability and inactivation by SDS.

Aminopeptidases↗
PubMed1975

[Smoking habits and epidemiology of lung cancer in Austria. III. Changes in lung cancer mortality in men].

It has been possible to show that the international trend of a reduced mortality rate in lung cancer of men can also be demonstrated in the Austrian population. By means of cohort-analysis this trend has been attributed mainly to a reduced mortality in younger male population. The improvement in the quality of cigarettes, namely the reduction in the amount of carcinogens and its relation to the reduction of lung cancer death rates will be discussed. At the present time, it is impossible to decide whether or not this reduced mortality rate will remain constant in the future or whether these results may be interpreted as expressing an increased period of latency in pulmonary carcinoma.

Austria↗
PubMed2026

Beyond mutations: epigenetic and fragmentomic landscapes of cfDNA in lung cancer.

INTRODUCTION: Lung cancer is the most frequently diagnosed cancer worldwide and the leading cause of cancer-related mortality. Cell-free DNA (cfDNA) has emerged as a powerful biomarker in cancer detection. Early diagnostics efforts often leverage cancer-associated mutations present in cfDNA, but beyond such mutation-based assays, recent advances have shed light on other non-mutational features. The analysis of cfDNA epigenetic profiles and fragmentation patterns, known as 'fragmentomics,' has revealed a wealth of data to explore in noninvasive lung cancer diagnosis. AREAS COVERED: This review will explore this new narrative, summarizing the current understanding and use of cfDNA epigenetic modifications and fragmentomic patterns, while integrating findings to illustrate their vast potential in early-stage detection and therapeutics. By considering a range of epigenetic and fragmentomic features, cfDNA methylation (5mC, 5hmC), histone modifications, size profiles, and end signatures, this review highlights how the multidimensional integration of such signals shows promise in refining early-stage lung cancer and guiding therapeutic decisions. EXPERT OPINION: cfDNA epigenetic and fragmentomic analyses represent a transformative frontier in lung cancer diagnostics and monitoring. While these approaches demonstrate significant potential, most studies are limited by modest cohort sizes and reports of survival benefits, underscoring the need for large-scale validation and deeper mechanistic understanding.

Humans↗
PubMed1978

Roentogenographic chest screening in the detection and survival of patients with lung cancer. Cooperative Study Group for Early Detection of Lung Cancer in the German Democratic Republic.

In the German Democratic Republic (GDR), annual mass roentgenographic screening of the chest was introduced twenty years ago. To ascertain its value in the detection of lung cancer, data were collected about treatment results at the country's main chest clinics. The study cover 13,283 operations and 10,838 resections, accounting for nearly 90% of all patients with lung cancer treated surgically in the GDR from 1949-1974. From 1965 to 1968, the five-year survival was more favorable in patients who were screened than in those who were diagnosed after clinical symptoms had appeared (36% for the former, 29% for the latter). For improvement of overall results, we recommend differentiated regular chest roentgenographic screening of men 40 to 70 years of age, individualized on the basis of tobacco usage, and full exploitation of all diagnostic and surgical tools now available.

Adult↗
PubMed1977

Epidemiological review of lung cancer in man.

Lung cancer is primarily a 20th century phenomenon; its epidemiology is reviewed and the usefulness of epidemiological studies in providing clues to etiology is evaluated. Internationally, lung cancer accounts for up to 13% of all deaths in age groups above 45 years. It is a disease characterized by large international variations in incidence; in addition, urban-rural differences occur in many countries. Male:female ratios are high, 4 to 5; but after a rise during the first half of the century, these ratios are now declining in a number of countries. Neither racial distribution nor migrant studies indicate that genetic factors play any important role in the etiology of lung cancer. The only possible indication of their playing such a role is the high incidence of lung cancer among Chinese, primarily Cantonese, women. A genetic determination of individual susceptibility has been suggested, but racial differences remain to be demonstrated. The increase in lung cancer that started during the first decades of the 20th century in Europe and North America is consistent with the introduction of a carcinogen into the environment at the turn of the century. Both spatial and temporal trends of lung cancer support the hypothesis that cigarette smoking is the major etiological factor. This is further supported by numerous specific investigations of the problem. A decrease in lung cancer incidence in certain age groups in a number of countries may reflect changing smoking habits and the diminishing tar content of modern cigarettes, thus indicating ways of prevention. Current knowledge of general air pollution seems to ascribe it a secondary role as an etiological factor. The risk of lung cancer is greater in certain occupations, often because of an interaction between industrial air pollution and smoking. It may be concluded that lung cancer is largely a problem of modern society and that the epidemiological results are consistent with an etiological role of preventable environmental factors.

Adult↗
PubMedDate not supplied

Scanning electron microscopy in the study of lung cancer. New technique of comparative studies on the same lung cancer cells by light microscopy and scanning electron microscopy.

A new technique for observing the same lung cancer cells by light microscope and SEM was developed. By this technique it was clarified that the surface ultrastructures of epidermoid carcinoma, adenocarcinoma and oat-cell carcinoma cells are different from each other. Those of adenocarcinoma and mesothelial cells were quite different. This technique might be of use, adding new information into the ordinary cytologic diagnosis of cancer cells.

Adenocarcinoma↗
PubMed1978

[Lung cancer in different chronic lung diseases].

The studies performed have indicated that nearly in 50% of cases lung cancer is associated with different chronic lesions of the lung: chronic purulent bronchitis, tuberculosis, chronic pneumonia, pulmonary emphysema and diffuse pneumosclerosis, and these provide favourable conditions for epithelial metaplasia of the bronchi, bronchioli and alveoli with subsequent cell atypism and development of lung cancer.

Chronic Disease↗
PubMed1979

[Oxygen effect in the therapy of lung cancer].

Nine lung cancer patients were subjected preoperatively to radiotherapy under hypoxia with inhaling of GHM-10 (gas hypoxic mixture). The patients were followed up during 7--12 months. The results obtained evidence the rationality of further studies in this direction, that is of special importance due to introducing of reconstructive--plastic operations on the trachea and bronchi into oncological practice. Thus, there will be a possibility to preserve, in some cases, a porton of the lung. Since the functional status of the lung after surgical and radiation treatment is of primary importance for the duration of patients' survival, the lung tissue protection from side-effects of radiation in irradiating lung tumors may offer good perspectives.

Adenocarcinoma↗
PubMed1976

New horizons in lung cancer diagnosis.

Lung cancer is rarely diagnosed and treated while still localized. Sputum cytology allows detection of radiologically occult tumors but conventional endoscopic procedures frequently prove inadequate for localization. It is the purpose of this report to outline the endoscopic observations and methods we have developed in successfully localizing 17 consecutive, radiologically occult carcinomas discovered in the sputum of 15 patients. A detailed examination of the upper respiratory tract demonstrated occult tumors in two patients. A segment by segment fiberbronchoscopic study under anesthesia allows multiple brushings and meticulous handling of specimens. Lesion localization is provided as well as identification of synchronous second primary tumors. Biopsies at the lobar spur and carina assist in determining the proximal extent of carcinoma in situ at potential surgical margins. Newer methods should enhance our recognition of inapparent carcinoma in situ allowing more efficient and more accurate tumor localization and a better appreciation of its extent.

Bronchi↗
PubMed2026

Integrating molecular subtypes, genomics and functional dependencies to identify context-specific therapeutic vulnerabilities in small cell lung cancer.

Small cell lung cancer is one of the most aggressive malignancies, characterized by rapid tumor growth, early metastatic spread and extremely poor survival. Although most patients initially respond to platinum-based chemotherapy, relapse is almost inevitable and treatment options at recurrence remain limited. The recent introduction of immune checkpoint inhibitors has provided only modest clinical benefit, largely due to the fact that these tumors are immunologically cold. These limitations highlight the urgent need to better understand the molecular features of small cell lung cancer in order to identify more effective therapeutic strategies. In this review, we summarize current knowledge of the molecular landscape of small cell lung cancer, with particular emphasis on transcriptome-based classifications that have identified four major molecular subtypes defined by distinct transcriptional regulators and gene expression programs. We discuss how these classifications have improved the biological understanding of the disease and stimulated efforts to develop subtype-specific therapeutic strategies. At the same time, we highlight important limitations of this framework, including the remarkable transcriptional plasticity of tumor cells, which allows dynamic transitions between subtypes and may contribute to therapeutic resistance. To address these challenges, we examine additional molecular features that may represent more stable vulnerabilities, including recurrent genomic alterations, such as the widespread loss of tumor suppressor genes or oncogene amplifications through extrachromosomal DNA. We also discuss emerging approaches aimed at identifying novel context-specific cancer dependencies, including genome-scale functional screens in vitro and in vivo and genetic restraint analyses. Finally, we consider the growing potential of liquid biopsy strategies, which exploit the high level of circulating tumor DNA in patients with this disease to detect clinically relevant genomic alterations and monitor tumor evolution. Overall, this review highlights both the opportunities and challenges associated with molecular stratification in small cell lung cancer. The integration of transcriptional classifications with genomic and functional approaches may help identify more robust therapeutic vulnerabilities and guide the development of more effective treatments for this highly aggressive disease.

Cancer vulnerabilities↗