Comorbidity of lung cancer and chronic obstructive pulmonary disease: correlation and optimization of treatment strategies

Introduction

Lung cancer (LC) and chronic obstructive pulmonary disease (COPD) are major global health challenges due to their high incidence and mortality rates (1-3). COPD significantly increases the risk of LC, with up to 70% of LC patients exhibiting concurrent COPD (3). This comorbidity leads to poorer prognoses and increased mortality, necessitating a deeper understanding of shared mechanisms and therapeutic strategies (4-6). LC share common risk factors, including smoking, aging, and environmental exposures, and are characterized by chronic inflammation, oxidative stress, immune dysregulation, and genetic susceptibility. The complex interplay between these factors contributes to tumorigenesis and disease progression. Recent research highlights the need for integrated diagnostic and treatment approaches that consider both LC and COPD to improve patient outcomes (7). This review explores the epidemiology, risk factors, underlying mechanisms, and personalized treatment strategies for LC-COPD comorbidity, emphasizing the importance of early detection, targeted interventions, and multidisciplinary care.

Epidemiological characteristics

Incidence and prevalence rates

LC is one of the most common and deadliest malignancies worldwide (1). While the incidence and mortality of lung cancer have decreased in several high-income countries, many low- and middle-income countries continue to experience increasing lung cancer burden associated with higher smoking prevalence (8,9). In China, due to the production and consumption of tobacco, the incidence and mortality rates of LC have continued to rise in recent years, posing a significant clinical challenge for respiratory specialists Further, global epidemiological data indicate that the prevalence of COPD in individuals over 40 years old is 10.3% [95% confidence interval (CI): 8.2–12.8%], with some regions reporting rates as high as 19.7%, and approximately 3 million deaths are attributed to COPD annually worldwide (10-13). Despite a general decline in the global age-standardized incidence rate (ASIR) of COPD over the past 30 years, population growth and regional disparities have contributed to an increase in absolute case numbers, with COPD disease burden and mortality remaining significantly high worldwide (14-16). The association between smoking, COPD, and lung cancer is complex and multidimensional, encompassing epidemiological patterns, molecular mechanisms, and clinical management considerations. Although progress has been made globally in tobacco control and disease prevention, the burden of COPD and lung cancer remains substantial (17,18). The comorbidity of these two diseases represents a substantial challenge for the healthcare system.

Prevalence of COPD in patients with LC

There is a significant clinical association between COPD and LC. A 12-year follow-up study reported that more than one-third of the COPD patients eventually developed LC (19). Among LC patients, the prevalence of COPD ranges from 30% to 70%, and the COPD-related mortality rate is 261.5 per 100,000 people, which is double that of the general population (19,20). COPD is the second leading non-cancer cause of death in LC patients, and the annual mortality rate continues to rise (21). Notably, among LC-COPD patients, those with predominant emphysema are more likely to develop squamous cell carcinoma (SCC) and demonstrate poorer clinical outcomes compared to those with other COPD phenotypes (22-24).

Prevalence of LC in patients with COPD

The prevalence of LC in COPD patients ranges from 5% to 9.1% (19). A landmark study by Divo et al. found that among 1,664 COPD patients, 9.1% developed LC, and 21% died from cancer, most often LC (5). An important study from New Zealand of 5,446 LC patients, 95% of whom had their diagnosis confirmed by histological or cytological samples, showed that the prevalence of Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage 2 COPD was as high as 50%, and the prevalence was even higher in patients with small cell lung cancer (SCLC) and SCC (25). Additionally, a comprehensive observational study using the United Kingdom General Practice Research Database involving 18,077 patients indicated that COPD increases the risk of LC four- to five-fold (26). LC accounts for 33% of all COPD-related deaths, and nearly 40% of COPD patients die within a year of their LC diagnosis (4).

Growing attention to the comorbidity of LC and COPD

The prognosis of patients with LC-COPD is particularly concerning. Compared to patients with LC without COPD, those with LC-COPD have significantly reduced overall survival (OS). Moreover, LC-COPD patients also have lower OS than those with COPD but without LC (27). This is especially evident in elderly non-small cell lung cancer (NSCLC) patients, such that those with COPD have significantly lower survival rates than those without COPD (28,29). Studies indicate that advanced NSCLC patients with COPD who receive COPD treatment have a significantly extended OS (of 16.8 months), while those who do not receive COPD treatment have a shorter OS (of only 8.2 months) (29-31). Research has confirmed that standardized COPD treatment combined with LC therapy improves the prognosis of LC-COPD patients, underscoring the importance of addressing COPD as a comorbidity in lung cancer management (32,33). Despite its clinical significance, COPD remains both underdiagnosed and undertreated in patients with LC. The 2024 GOLD report revealed high prevalence of undiagnosed COPD among patients undergoing LC screening, with only 7.1% of patients receiving accurate and comprehensive diagnoses and only 28–35% undergoing standardized treatment (34). Awareness of the clinical significance of this comorbidity is growing; the 2021 GOLD guidelines first included information on COPD concurrent with LC, which was reemphasized in the 2024 GOLD guidelines. Additionally, in August 2023, the Chinese Medical Association’s LC and COPD Working Group issued an international expert consensus (35).

Risk factors and mechanisms

Environmental and behavioral factors, such as long-term smoking and aging, are major risk factors for both LC and COPD. Better understanding of these common risk factors could aid in identifying high-risk populations and provide a scientific basis for targeted interventions and preventive measures.

Risk factors

Smoking

Smoking is the primary shared risk factor for both COPD and LC, associated with approximately 70% of COPD and 50% of LC cases (1,36,37). Prolonged exposure to tobacco smoke leads to excessive inflammatory responses in the airways of COPD patients, with repeated cycles of tissue damage and repair ultimately causing irreversible airway narrowing and fibrosis—key features of airway remodeling in COPD. Smokers are at markedly higher risk of developing SCC of the lung than non-squamous NSCLC subtypes: among current smokers, the odds ratio is 18.8 for SCC versus 7.9 for adenocarcinoma compared with never-smokers (38). Tobacco smokers’ respiratory epithelium contains multifocal premalignant lesions throughout the bronchial tree—a phenomenon known as “field cancerization”—with shared genetic and epigenetic alterations detectable even in histologically normal-appearing mucosa (39). Tobacco smoke contains specific carcinogens, such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), and pro-inflammatory components like lipopolysaccharide (LPS), which play critical roles in inducing chronic pulmonary inflammatory responses and driving malignant cellular transformation (40,41). These agents act through epigenetic alterations and direct DNA damage, which promotes persistent genomic instability and creates a microenvironment conducive to the malignant transformation of pulmonary epithelial cells (42,43). Chronic inflammation induced by tobacco smoke also plays a critical role in lung carcinogenesis by promoting genetic mutations, oxidative stress, and an immunosuppressive tumor microenvironment that facilitates cancer development (44). The numerous irritant and carcinogenic compounds in tobacco not only harm active smokers but also harm passive smokers. Additionally, smoking intensity (i.e., the number of cigarettes smoked per day) and the age at which smoking begins are positively correlated with the risk of LC, and secondhand smoke exposure significantly increases the risk of LC (45,46). As a result, cumulative smoking duration and intensity directly affect the likelihood of developing both COPD and LC (47,48). Given that smoking is the primary shared risk factor for these conditions, smoking cessation interventions are crucial public health strategies to prevent COPD comorbid with LC. However, despite its well-known risks, smoking remains prevalent in many countries. Thus, personalized smoking cessation plans and more effective public policies need to be implemented to reduce smoking rates.

Age and gender since old MEN with COPD have higher risk of LC

Age is a significant risk factor for both COPD and LC. COPD primarily occurs in smokers over the age of 40 years, while LC incidence increases with age, with an average age of onset of 66 years (49). In patients with coexisting COPD, the risk of LC is notably higher in older men (aged ≥75 years) (50). Age-related dysfunction of lung progenitor cells impairs lung repair and regeneration, further increasing susceptibility to these diseases (51). Interestingly, an epidemiological study reveals a paradoxical decline in LC prevalence among extremely elderly populations (≥85 years) (52). Experimental models demonstrate that aging represses lung tumor initiation and alters the functional impact of tumor suppressor genes such as phosphatase and Tensin Homolog deleted on chromosome 10, which coordinates phosphatidylinositol 3-kinase/AK strain transforming (PI3K/AKT) signaling dynamics in the aging lung microenvironment. This dual effect of aging—promoting carcinogenesis through DNA damage accumulation while paradoxically suppressing tumor progression via microenvironmental reprogramming—highlights the complexity of age-related oncogenesis (53). Further longitudinal studies are needed to clarify the mechanisms by which aging influences LC-COPD morbidity.

Environmental exposure factors

Air pollution and occupational exposures (e.g., among coal miners and construction workers) are also significant shared risk factors for COPD and LC (54,55). Long-term exposure to polluted air can lead to excessive activation of macrophages, which subsequently release large amounts of pro-inflammatory cytokines, such as interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and IL-1β. These cytokines trigger chronic inflammatory responses (56), thereby increasing the risk of both COPD and LC (56-58). Particulate matter (PM), particularly PM2.5, has been linked to an increased risk of EGFR-mutant lung adenocarcinoma (LUAD), with higher PM2.5 concentrations correlating with the residential locations of affected patients (56). In murine models, PM exposure promoted tumor formation in both EGFR- and KRAS-driven LUAD, increased progenitor-like alveolar type II epithelial cells, and triggered macrophage infiltration with cytokine release (IL-1, granulocyte-macrophage colony-stimulating factor, C-C motif chemokine ligand 6, IL-33), suggesting a role in alveolar regeneration (56,57). Additionally, a clinical study found that former smokers with COPD exhibited heightened inflammatory responses to diesel exhaust, indicating increased susceptibility to air pollution-induced lung injury (58). Socioeconomic factors also have a notable impact on the incidence and prognosis of COPD and LC (56,59,60). Prevalence rates for these diseases are significantly higher in low-income populations than higher-income populations, with worse prognoses likely due to limited access to healthcare resources, lower levels of health education, and fewer healthy lifestyle practices (61,62). Additional risk factors include a long history of smoking, an age over 45 years, concurrent emphysema, severe airway obstruction, high-risk occupational exposure, male gender, and a lower body mass index (BMI) (63,64). A multicenter study found that these characteristics are more prevalent among COPD patients with LC, especially among older adults, men, individuals with a low BMI, those with a history of smoking, and those with SCC (50). Recognizing these shared risk factors could help to identify high-risk populations and support the implementation of personalized screening strategies, ultimately improving early detection and interception (64).

Mechanisms

The above-mentioned factors increase the risk of disease occurrence. In-depth research indicates that the comorbidity of COPD and LC results from the interaction of multiple mechanisms.

The role of oxidative stress in COPD and LC

Oxidative stress is considered a key shared pathophysiological mechanism in both COPD and LC. Smoking-induced reactive oxygen species (ROS) directly damage DNA, leading to carcinogenic mutations (e.g., tumor protein 53, Kirsten rat sarcoma viral oncogene homolog), while simultaneously inducing apoptosis of alveolar epithelial cells, a hallmark feature of COPD (65-68). This process activates pathways involving nuclear factor-kappa B (NF-κB) and p38 mitogen-activated protein kinase, which induce the release of inflammatory cells and pro-inflammatory factors, creating a vicious cycle of inflammation and oxidative stress (69,70). Consequently, oxidative stress is a major driving force behind airway remodeling in COPD and LC progression. It not only damages the airway epithelium, triggering airway remodeling and fibrosis, but also supports carcinogenesis through mechanisms like DNA damage and gene mutations (71,72).

The impact of chronic inflammation on COPD and LC

Chronic inflammation also plays a central role in the comorbidity of COPD and LC. COPD patients exhibit a significant increase in inflammatory cells, particularly alveolar macrophages, neutrophils, and T lymphocytes, which release large amounts of pro-inflammatory (e.g., IL-6, TNF-α) and growth factors [e.g., vascular endothelial growth factor, transforming growth factor-β (TGF-β)] (73). These factors not only disrupt the structure of lung tissue but also promote the proliferation and survival of tumor cells by activating signaling pathways such as NF-κB and signal transducer and activator of transcription 3 (36,74,75). In this setting, processes such as cell proliferation, angiogenesis, and epithelial cell transformation are enhanced, making chronic inflammation a fundamental promoter of tumor development. Chronic inflammation also increases the likelihood of DNA damage while suppressing the host’s immune system. Study has shown that pro-inflammatory cytokines such as IL-6 are closely associated with the development of LC; IL-6 promotes tumor cell growth by inhibiting the host’s anti-tumor immunity (76). Additionally, certain tumor cells secrete anti-inflammatory cytokines (e.g., IL-4 and IL-10), further driving and sustaining a pro-tumor inflammatory cycle (56,77). Research also indicates that alterations in the pulmonary microbiome intensify the inflammatory response, potentially influencing tumor-related gene expression through the regulation of bacterial metabolites, thus enhancing the inflammatory cycle in the tumor microenvironment (78-80). Furthermore, study have found that the tumor-promoting effects of PM2.5 disappear in immunodeficient mouse models, suggesting that macrophages and other components are indispensable in the process of chronic inflammation (56). The mechanisms of chronic inflammation further highlight the shared pathogenic basis between COPD and LC, while changes in the lung microbiome exacerbate this pathological process. Future research should seek to explore anti-inflammatory therapies and microbiome modulation as interventions to reduce the cancer development risk in COPD patients. In an inflammatory environment, the functions of immune cells, such as macrophages and T cells, are suppressed, leading to a decline in immune surveillance capabilities.

The mechanisms of abnormal immune responses in COPD and LC

The altered activity of immune cells exacerbates oxidative stress, leading to detrimental lung remodeling and increasing susceptibility to LC progression (81,82). For example, T helper 17 (Th17) cells secrete inflammatory factors like IL-17, while regulatory T (Treg) cells induce an immunosuppressive environment by inhibiting anti-tumor immunity; the imbalance between the Th17 and Treg cells may promote the development of LC (81,82). In COPD patients, the overexpression of immune checkpoint molecules [e.g., programmed cell death protein 1 (PD-1)] and T cell immunoglobulins results in T cell exhaustion, limiting the immune clearance of tumor cells (83). Study has shown that COPD patients may experience enhanced immune responses when treated with immune checkpoint inhibitors (83). These findings suggest that changes in the immune cell composition and function may serve as biomarkers and potential therapeutic targets in COPD with LC. Abnormal immune responses provide novel insights into the mechanisms underlying the COPD and LC comorbidity. Future research into the roles of different immune cell subpopulations and the regulation of their signaling pathways may help in the design of more targeted immunotherapies, ultimately improving the outcomes of comorbid patients.

The synergistic effect of chronic inflammation and oxidative stress

Oxidative stress and chronic inflammation mutually reinforce each other in the progression of COPD and LC, creating a vicious cycle. ROS not only cause direct cellular damage but also induce the release of various pro-inflammatory factors, such as TNF-α, IL-6, and IL-8, by activating the NF-κB pathway (69,84). The activation of NF-κB further exacerbates local inflammatory responses, leading to continuous damage to the airways and lung tissue, thereby creating an ideal environment for the early carcinogenesis of LC (69,85). Further, prolonged chronic inflammation increases the likelihood of immunosuppression and DNA damage, further promoting tumor initiation and spread (86). The synergistic effect of oxidative stress and chronic inflammation reveals a key mechanism underlying the comorbidity of COPD and LC. Targeting this cycle could help to improve the prognosis of comorbid patients and reduce the incidence of LC.

The link between cellular senescence and COPD and LC

Cellular senescence promotes the progression of COPD through multiple mechanisms, such as oxidative stress, telomere shortening, and DNA damage repair deficiencies, and is closely linked to the development of LC (87,88). The accumulation of senescent cells in the lungs leads to the secretion of inflammatory factors and chemokines, creating a pro-tumorigenic microenvironment that increases the risk of cancer (89). Telomere shortening is notably prominent in COPD patients and is significantly associated with the onset of both COPD and LC (90). Telomere shortening can activate signaling pathways, such as Wnt and TGF-β, further promoting epithelial-mesenchymal transition in epithelial cells, thereby increasing the risk of LC (89,90). Further research is needed to evaluate whether targeting cellular senescence in lung cells could serve as a viable strategy for preventing an LC development in patients with COPD. Additionally, senescence biomarkers may hold potential for monitoring disease progression.

The role of genetic susceptibility and epigenetic alterations in COPD and LC

Genetic factors significantly influence the susceptibility of individuals to both COPD and LC (91). Epigenetic changes, such as specific gene mutations, promoter hypermethylation, and global DNA hypomethylation, may contribute to the development of NSCLC. NSCLC patients often exhibit global hypomethylation, particularly in the demethylation of oncogene promoter regions, leading to abnormal gene expression and an increased likelihood of tumorigenesis (92). Additionally, phenotypic and endotypic characteristics in COPD patients are closely associated with the progression of LC (93). COPD and lung cancer exhibit significant associations at the genetic and epigenetic regulatory levels, with epigenetic mechanisms acting as a bridge in their shared genetic susceptibility. Phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha mutations in the PI3K/AKT/mechanistic target of rapamycin pathway are significantly enriched in patients with concurrent COPD and NSCLC, with notable overlap in inflammatory pathways (such as NF-κB) and oxidative stress responses, suggesting their potential role in the comorbidity mechanism of these two diseases. Multiple genome-wide association study (GWAS) studies have revealed shared genetic susceptibility loci between COPD and LC (94,95). Multiple GWAS studies have revealed shared genetic susceptibility loci between COPD and LC. For instance, the CHRNA5-CHRNA3-CHRNB4 gene cluster in chromosome region 15q25.1, associated with smoking behavior and nicotine dependence, is also linked to increased risk of both COPD and lung cancer (96). Additionally, the family with sequence similarity 13, member A gene in chromosome region 4q31 has been identified as relevant to both COPD and LC risk (97). Mendelian randomization analyses examining the relationship between COPD and lung cancer risk have found that COPD may increase LC risk through genetic mechanisms (98). Dysregulation of histone acetyltransferases (HATs) and histone deacetylases (HDACs) has been reported in both COPD and lung cancer, affecting the expression of inflammation and tumor-related genes (99-101). The evidence above suggests that these two conditions share carcinogenic mechanisms through inflammatory and oxidative stress pathways within the gene-epigenetic interaction network.

Management for LC-COPD

Effective management of LC-COPD requires a comprehensive approach that addresses their shared pathogenesis and interactions, emphasizing prompt diagnosis, individualized treatment, and multidisciplinary care. A co-treatment strategy integrating disease monitoring, symptom control, and tailored interventions is essential to improving outcomes and slowing disease progression.

Diagnosis and monitoring

Lung function tests facilitate early airflow limitation detection, improving COPD diagnosis in LC patients. Thus, post-cancer diagnosis, assessments of airway patency and diffusion can be used to evaluate the severity and influence of COPD on LC. Studies have shown that the prevalence of coexisting COPD among patients with lung cancer can be as high as 30–70% (6,7). Airway obstruction, characterized by expiratory airflow limitation, is a hallmark pathological feature of COPD. The assessment of airway obstruction—such as through the forced expiratory volume in 1 second (FEV₁)/forced vital capacity ratio measured in pulmonary function tests—can directly reflect the severity of COPD. Due to the strong association between COPD and an increased risk of LC, it is recommended that high-risk COPD patients undergo annual low-dose computed tomography (CT) scans to detect early cancer progression (102,103).

Bronchodilator-based drug management

Bronchodilators are essential in the treatment of COPD and should be aligned with LC therapy to improve airway patency and symptom control (104). Long-acting beta-agonists (LABAs) and long-acting muscarinic antagonists (LAMAs), individually or combined, are recommended based on COPD severity. A retrospective study showed that perioperative combination therapy with LABAs and LAMAs in LC patients significantly improved postoperative lung function, reduced complications, and extended both progression-free survival and OS in patients with moderate to severe airflow limitation (105). Combining bronchodilators with inhaled corticosteroids can enhance the respiratory function and quality of life of stable-phase LC-COPD patients (35). However, despite the significant clinical benefits of bronchodilators in treating COPD and lung cancer, potential cardiovascular risks warrant careful consideration. Several studies indicate that long-term use of LABAs and LAMAs may increase the risk of cardiovascular adverse events, particularly in patients with pre-existing cardiovascular disease (106,107). Therefore, when developing treatment regimens, clinicians should comprehensively evaluate each patient’s specific condition and weigh the benefits against potential risks. Future research should further explore optimal application strategies across different patient populations, as well as methods to maximize therapeutic efficacy while minimizing potential risks through combination with other medications such as inhaled corticosteroids.

Tumor treatment adjustment and individualized management

Chemotherapy, targeted therapy, and immunotherapy are the primary treatment modalities for advanced lung cancer. However, for Patients with LC and COPD comorbidity, these treatments may pose higher risks, as LC-COPD patients have a higher risk of adverse effects like QT interval prolongation and dyspnea (35). Therefore, monitoring lung function and opting for gentler treatments are crucial. Alternatives like radioactive seed implantation or ablation (e.g., radiofrequency or microwave) should be considered for patients with inoperable early-stage LC or localized lesions (35). Furthermore, the severity of COPD is a critical factor in determining surgical eligibility for lung cancer patients. Wei et al. have demonstrated that post-lobectomy lung function loss in COPD patients correlates positively with COPD severity, indicating that the degree of impaired lung function directly affects postoperative survival rates and complication risks (108). Particularly for patients with FEV₁ below 50% of predicted values, surgical risks increase significantly (109). Consequently, COPD severity serves not only as an important screening criterion for surgical indications but also as a key predictor of postoperative recovery (110). For lung cancer patients deemed ineligible for surgery due to severe COPD or other comorbidities, non-surgical interventions such as radiation therapy represent important alternatives (111). Studies indicate that stereotactic body radiation therapy achieves local control rates and survival outcomes comparable to surgery in early-stage NSCLC patients, particularly benefiting those with severely compromised lung function (111,112). Perfusion scanning, by evaluating pulmonary blood flow distribution, can reveal lung function heterogeneity and affected regions in COPD patients, offering significant value in assessing postoperative lung function (113,114). Tumors may reduce local blood flow, subsequently affecting postoperative pulmonary function recovery (115). For patients with comorbid lung cancer, perfusion scanning helps identify tumor-related local blood flow alterations, thereby informing surgical planning.

Dynamic assessment and adverse event monitoring

In patients with LC and COPD comorbidity, dynamic assessment and adverse event monitoring during cancer treatment are crucial. These patients face not only challenges from cancer itself but also increased treatment complexity and risk of adverse reactions due to COPD. COPD patients frequently use bronchodilators (such as β2-receptor agonists) and corticosteroids, which may synergistically prolong QT intervals when combined with anticancer drugs (like tyrosine kinase inhibitors), increasing the risk of fatal arrhythmias (35,116,117). Regular electrocardiogram monitoring is necessary, with treatment adjustments based on QTc values. Cancer treatments (chemotherapy/targeted/immunotherapy) may exacerbate pulmonary toxicity in COPD patients (such as interstitial pneumonitis), requiring pulmonary function tests to monitor vital capacity and diffusion function, combined with comprehensive assessment of symptoms (dyspnea, cough) (118,119). High-resolution CT can simultaneously evaluate structural COPD abnormalities (emphysema/fibrosis) and tumor progression, while offering significant advantages in early identification of treatment-related complications (interstitial pneumonitis, pulmonary embolism) and differentiating between immune checkpoint inhibitor-related pneumonitis and infectious pneumonia (120-123).

Lifestyle management and supportive care

LC-COPD patients can seek to manage COPD progression and reduce LC recurrence risk by smoking cessation, exercise, and balanced nutrition (124). Respiratory rehabilitation and long-term oxygen therapy can improve lung function and reduce exacerbation risk (104). For patients with severe COPD symptoms, bronchoscopy lung volume reduction surgery may improve breathing efficiency.

Multidisciplinary team (MDT) collaboration and individualized treatment

Effective LC-COPD management requires collaboration among respiratory, oncology, imaging, and rehabilitation teams to establish personalized MDT treatment plans. Comprehensive patient evaluation fosters integrated treatment strategies, improving outcomes, extending survival, and enhancing quality of life (35).

Conclusion and prospects

COPD and LC share similar risk factors and pathogenesis, and many patients initially seek care due to respiratory symptoms. Therefore, pulmonologists should consider the possibility of LC when diagnosing COPD, and recommend timely screening for high-risk individuals. For COPD patients without an LC diagnosis, proactive management of COPD treatment may be associated with a reduced risk of developing LC, although current evidence is limited. For those with both conditions, personalized treatment plans should not only be guided by cancer type, stage, molecular subtype, and PD-1/programmed death-ligand 1 expression, but also take into account the patient’s respiratory reserve and COPD severity, in order to optimize both oncologic outcomes and lung function. However, the coexistence of COPD and LC presents a complex clinical management challenge, necessitating further research. Currently, the epidemiological data on LC-COPD are limited, which could hinder adequate screening and early diagnosis efforts. Additionally, under-treatment remains a concern; some COPD patients, on being diagnosed with LC, focus primarily on the cancer treatment, and only around 10% receive standard COPD management (34). Some LC-COPD patients forego standard LC treatment due to concerns related to prognosis. Addressing these issues requires an MDT approach in which pulmonologists should play a key role in designing and overseeing personalized treatment plans.

Acknowledgments

None.

Footnote

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2025-480/prf

Funding: This work was supported by National Key R&D Program of China (No. 2021YFC2301101) and Guangzhou Science and Technology Major Clinical Project (No. 2023C-DZ06).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2025-480/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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