Lung Cancer in Never Smokers: Delving into Epidemiology, Genomic and Immune Landscape, Prognosis, Treatment, and Screening DOI
Ayse Ece Cali Daylan, Emily Miao, Kevin Tang

и другие.

Lung, Год журнала: 2023, Номер 201(6), С. 521 - 529

Опубликована: Ноя. 16, 2023

Язык: Английский

Lung adenocarcinoma promotion by air pollutants DOI
William Hill, Emilia L. Lim, Clare E. Weeden

и другие.

Nature, Год журнала: 2023, Номер 616(7955), С. 159 - 167

Опубликована: Апрель 5, 2023

Язык: Английский

Процитировано

412

Mapping clustered mutations in cancer reveals APOBEC3 mutagenesis of ecDNA DOI Creative Commons
Erik N. Bergstrom, Jens Luebeck, Mia Petljak

и другие.

Nature, Год журнала: 2022, Номер 602(7897), С. 510 - 517

Опубликована: Фев. 9, 2022

Clustered somatic mutations are common in cancer genomes and previous analyses reveal several types of clustered single-base substitutions, which include doublet- multi-base substitutions

Язык: Английский

Процитировано

117

Lung cancer in patients who have never smoked — an emerging disease DOI
Jaclyn LoPiccolo, Alexander Gusev, David C. Christiani

и другие.

Nature Reviews Clinical Oncology, Год журнала: 2024, Номер 21(2), С. 121 - 146

Опубликована: Янв. 9, 2024

Язык: Английский

Процитировано

67

Mechanisms Contributing to the Comorbidity of COPD and Lung Cancer DOI Open Access
Aisling Forder,

Rebecca Zhuang,

Vanessa G. P. Souza

и другие.

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(3), С. 2859 - 2859

Опубликована: Фев. 2, 2023

Lung cancer and chronic obstructive pulmonary disease (COPD) often co-occur, individuals with COPD are at a higher risk of developing lung cancer. While the underlying mechanism for this is not well understood, its major contributing factors have been proposed to include genomic, immune, microenvironment dysregulation. Here, we review evidence significant studies that explore mechanisms heightened in people COPD. Genetic epigenetic changes, as aberrant expression non-coding RNAs, predispose epithelium carcinogenesis by altering cancer- immune-related genes. Oxidative stress generated tobacco smoking plays role reducing genomic integrity, promoting epithelial-mesenchymal-transition, generating inflammatory environment. This leads abnormal immune responses promote development, though all smokers develop Sex differences metabolism smoke females accumulating damage from oxidative poses development Dysregulation microbiome contributes inflammation, which observed known facilitate initiation various tumor types. Further, there need better characterize identify proportion who high We evaluate possible novel individualized screening strategies, including biomarkers identified genetic exhaled breath condensate analysis. also discuss use corticosteroids statins chemopreventive agents prevent It crucial optimize current methods early detection management order improve health outcomes large affected population.

Язык: Английский

Процитировано

47

Lung cancer associated with combustion particles and fine particulate matter (PM2.5) - The roles of polycyclic aromatic hydrocarbons (PAHs) and the aryl hydrocarbon receptor (AhR) DOI Creative Commons
Jørn A. Holme, Jan Vondráček, Miroslav Machala

и другие.

Biochemical Pharmacology, Год журнала: 2023, Номер 216, С. 115801 - 115801

Опубликована: Сен. 9, 2023

Air pollution is the leading cause of lung cancer after tobacco smoking, contributing to 20% all deaths. Increased risk associated with living near trafficked roads, occupational exposure diesel exhaust, indoor coal combustion and cigarette suggest that components in ambient fine particulate matter (PM2.5), such as polycyclic aromatic hydrocarbons (PAHs), may be central drivers cancer. Activation aryl hydrocarbon receptor (AhR) induces expression xenobiotic-metabolizing enzymes (XMEs) increase PAH metabolism, formation reactive metabolites, oxidative stress, DNA damage mutagenesis. Lung tissues from smokers workers exposed high PM levels contain mutagenic signatures derived PAHs. However, recent findings air PM2.5 primarily development through tumor promotion cells harboring naturally acquired oncogenic mutations, thus lacking typical PAH-induced mutations. On this background, we discuss role AhR PAHs caused by focusing on promoting properties including immune system, cell proliferation survival, microenvironment, cell-to-cell communication, growth metastasis. We dichotomy patterns observed between smoking outdoor represent two ends a dose–response continuum exposure, where peripheral appears driving factor at relatively low-dose exposures PM2.5, whereas genotoxicity airways becomes increasingly more important higher encountered exposure.

Язык: Английский

Процитировано

46

Non-small-cell lung cancer DOI
Lizza E.L. Hendriks, Jordi Remón, C. Faivre‐Finn

и другие.

Nature Reviews Disease Primers, Год журнала: 2024, Номер 10(1)

Опубликована: Сен. 26, 2024

Язык: Английский

Процитировано

37

Low-Dose Computed Tomography (LDCT) Lung Cancer Screening in Asian Female Never-Smokers Is as Efficacious in Detecting Lung Cancer as in Asian Male Ever-Smokers: A Systematic Review and Meta-Analysis DOI Creative Commons
Natthaya Triphuridet, Shannon Zhang, Misako Nagasaka

и другие.

Journal of Thoracic Oncology, Год журнала: 2023, Номер 18(6), С. 698 - 717

Опубликована: Фев. 10, 2023

Lung cancer in never-smokers is the major cause of death globally. We compared efficacy low-dose computed tomography (LDCT) lung screening among versus ever-smokers using systematic review and meta-analysis.LDCT studies that simultaneously included both ever-smoker never-smoker participants published by April 30, 2021, were searched through PubMed Scopus. Primary outcome measure was relative risk (RR) diagnosed ever-smokers.A total 14 (13 from Asia) (141,396 ever-smokers, 109,251 never-smokers, 1961 cases diagnosed). RR between overall 1.21 (95% confidence interval [CI]: 0.89-1.65), 1.37 CI: 1.08-1.75) males, 0.88 0.59-1.31) females. 1.78 1.41-2.24) 1.22 0.89-1.68) for Asian female male respectively, 0.99 0.65-1.50) high-risk (≥30 pack-years). Proportional meta-analysis revealed significantly more cancers at first scan (95.4% [95% 84.9-100.0] 70.9% 54.6-84.9], p = 0.010) stage 1 (88.5% 79.3-95.4] 79.7% 71.1-87.4], 0.071) respectively. 5-year all-cause mortality 0.27 0.1-0.55, < 0.001) 0.13 0.05-0.33, 0.001), respectively.The detected LDCT Asia statistically similar. Overall specific reduced to ever-smokers.

Язык: Английский

Процитировано

33

Gender Differences in Oxidative Stress in Relation to Cancer Susceptibility and Survival DOI Creative Commons
Alessandro Allegra, Santino Caserta, Sara Genovese

и другие.

Antioxidants, Год журнала: 2023, Номер 12(6), С. 1255 - 1255

Опубликована: Июнь 11, 2023

Genetic, developmental, biochemical, and environmental variables interact intricately to produce sex differences. The significance of differences in cancer susceptibility is being clarified by numerous studies. Epidemiological research registries have revealed over the past few years that there are definite variations incidence, progression, survival. However, oxidative stress mitochondrial dysfunction also a significant impact on response treatment neoplastic diseases. Young women may be more protected from than men because most proteins implicated regulation redox state function under control sexual hormones. In this review, we describe how hormones activity antioxidant enzymes mitochondria, as well they affect several molecular pathways underlie gender-related discrepancies been identified better understood, which lead effective precision medicine vital information options for both males females with illnesses.

Язык: Английский

Процитировано

30

Distinct immune microenvironment of lung adenocarcinoma in never-smokers from smokers DOI Creative Commons
Wenxin Luo, Zhen Zeng,

Jin Yang

и другие.

Cell Reports Medicine, Год журнала: 2023, Номер 4(6), С. 101078 - 101078

Опубликована: Июнь 1, 2023

Lung cancer in never-smokers (LCINS) presents clinicopathological and molecular features distinct from that smokers. Tumor microenvironment (TME) plays important roles progression therapeutic response. To decipher the difference TME between never-smoker smoker lung cancers, we conduct single-cell RNA sequencing on 165,753 cells 22 treatment-naive adenocarcinoma (LUAD) patients. We find dysfunction of alveolar induced by cigarette smoking contributes more to aggressiveness LUADs, while immunosuppressive exerts effects LUADs' aggressiveness. Moreover, SPP1hi pro macrophage is identified be another independent source monocyte-derived macrophage. Importantly, higher expression immune checkpoint CD47 lower major histocompatibility complex (MHC)-I LUADs imply may a better immunotherapy target for LCINS. Therefore, this study reveals tumorigenesis provides potential strategy

Язык: Английский

Процитировано

26

Topography of mutational signatures in human cancer DOI Creative Commons
Burçak Otlu, Marcos Díaz‐Gay,

Ian Vermes

и другие.

Cell Reports, Год журнала: 2023, Номер 42(8), С. 112930 - 112930

Опубликована: Авг. 1, 2023

The somatic mutations found in a cancer genome are imprinted by different mutational processes. Each process exhibits characteristic signature, which can be affected the architecture. However, interplay between signatures and topographical genomic features has not been extensively explored. Here, we integrate from 5,120 whole-genome-sequenced tumors 40 types with 516 ENCODE to evaluate effect of nucleosome occupancy, histone modifications, CTCF binding, replication timing, transcription/replication strand asymmetries on cancer-specific accumulation distinct mutagenic Most features, related etiologies being similarly affected. Certain exhibit periodic behaviors or cancer-type-specific enrichments/depletions near revealing further information about processes that them. Our findings, disseminated via COSMIC (Catalog Somatic Mutations Cancer) database, provide comprehensive online resource for exploring interactions across human cancer.

Язык: Английский

Процитировано

25