Histological Types Of Lung Cancer Research Articles

Patterns of Extrathoracic Metastases in Different Histological Types of Lung Cancer.

Lung cancer is the leading cause of cancer-related deaths mainly attributable to metastasis, especially extrathoracic metastasis. This large-cohort research is aimed to explore metastatic profiles in different histological types of lung cancer, as well as to assess clinicopathological and survival significance of diverse metastatic lesions. Lung cancer cases were extracted and enrolled from the Surveillance, Epidemiology, and End Results (SEER) database. χ2-tests were conducted to make comparisons of metastatic distribution among different histological types and odds ratios were calculated to analyze co-occurrence relationships between different metastatic lesions. Kaplan–Meier methods were performed to analyze survival outcomes according to different metastatic sites and Cox regression models were conducted to identify independent prognostic factors. In total, we included 159,241 lung cancer cases with detailed metastatic status and complete follow-up information. In order to understand their metastatic patterns, we elucidated the following points in this research: (1) Comparing the frequencies of different metastatic lesions in different histological types. The frequency of bone metastasis was highest in adenocarcinoma, squamous cell carcinoma, LCLC and NSCLC/NOS, while liver was the most common metastatic site in SCLC. (2) Elaborating the tendency of combined metastases. Bi-site metastases occurred more common than tri-site and tetra-site metastases. And several metastatic sites, such as bone and liver, intended to co-metastasize preferentially. (3) Clarifying the prognostic significance of single-site and bi-site metastases. All single-site metastases were independent prognostic factors and co-metastases ended up with even worse survival outcomes. Thus, our findings would be beneficial for research design and clinical practice.

A gene expression-based immune signature for lung adenocarcinoma prognosis.

Lung adenocarcinoma (LUAD) has become the most frequent histologic type of lung cancer in the past several decades. Recent successes with immune checkpoint blockade therapy have demonstrated that the manipulation of the immune system is a very potent treatment for LUAD. This study aims to explore the role of immune-related genes in the development of LUAD and establish a signature that can predict overall survival for LUAD patients. To identify the differential expression genes (DEGs) between normal and tumor tissues, we developed an analysis strategy to combine an independent-sample design and a paired-sample design using RNA-seq transcriptomic profiling data of The Cancer Genome Atlas LUAD samples. Further, we selected prognostic markers from DEGs and evaluated their prognostic value in a prediction model. We identified and validated PD1, PDL1 and CTLA4 genes as prognostic markers, which are well-known immune checkpoints, and revealed two new potential prognostic immune checkpoints for LUAD, HHLA2 (logFC = 2.55, FDR = 1.89 × 10-6) and VTCN1 (logFC = -2.86, FDR = 1.72 × 10-11). Furthermore, we identified an 18-gene LUAD prognostic biomarker panel and observed that the classified high-risk group presented a significantly shorter overall survival time (HR = 3.57, p value = 4.07 × 10-10). The prediction model was validated in five independent high-throughput gene expression datasets. The identified DEG features may serve as potential biomarkers for prognosis prediction of LUAD patients and immunotherapy. Based on that assumption, we identified a gene expression-based immune signature for lung adenocarcinoma prognosis.

Younger patients operated for lung cancer have a better prognosis.

BackgroundThe incidence of lung cancer in the population of patients younger than 50 years of age is relatively low. The aim of this study was to compare the clinical outcomes of patients with early lung cancer onset (ELCO, onset before the age of 50) and late lung cancer onset (LLCO, onset after the age of 50).MethodsWe have retrospectively analyzed the prospectively collected data of 1,518 patients with lung cancer treated in a Thoracic Surgery Department in the years 2007–2015. Including carcinoid tumors for the analysis may blur ELCO and LLCO population comparison; therefore we have made three analyses. We have compared overall survival (OS) in unmatched (86 patients with ELCO and 1,432 patients with LLCO) and matched the populations (with the use of propensity-score matched analysis).ResultsIn comparison of unmatched patients, five-year survival in patients with ELCO was 71.9% compared to 58.7% in LLCO patients (P=0.008). In comparison of matched populations (comparing sex, pTNM, type of operation, pathological diagnosis and Charlson Comorbidity Index) five-year survival in patients with ELCO was 77.6% comparing to 61.5% in LLCO patients P<0.001). After exclusion of rare histological types of lung cancer and advanced stages no significant difference in survival rates was discovered comparing ELCO patients with LLCO patients, although there was still a trend towards better survival in ELCO patients (P=0.086).ConclusionsPatients with ELCO have higher five-year survival after surgical treatment compared to patients with LLCO.

A Non-invasive Method to Diagnose Lung Adenocarcinoma.

Purpose: To find out the CT radiomics features of differentiating lung adenocarcinoma from another lung cancer histological type.Methods: This was a historical cohort study, three independent lung cancer cohorts included. One cohort was used to evaluate the stability of radiomics features, one cohort was used to feature selection, and the last was used to construct and evaluate classification models. The research is divided into four steps: region of interest segmentation, feature extraction, feature selection, and model building and validation. The feature selection methods included the intraclass correlation coefficient, ReliefF coefficient, and Partition-Membership filter. The performance metrics of the classification model included accuracy (Acc), precision (Pre), area under curve (AUC), and kappa statistics.Results: The 10 features (First order shape features: Sphericity and Compacity, Gray-Level Run Length Matrix: Short-Run Emphasis, Low Gray-level Run Emphasis, and High Gray-level Run Emphasis, Gray Level Co-occurrence Matrix: Homogeneity, Energy, Contrast, Correlation, and Dissimilarity) showed the most stable and classification capability. The 6 classifiers, Logistic regression classifier (LR), Sequence Minimum Optimization algorithm, Random Forest, KStar, Naive Bayes and Random Committee, have great performance both on the train and the test sets, and especially LR has the best performance on the test set (Acc = 98.72, Pre = 0.988, AUC = 1, and kappa = 0.974).Conclusion: Lung adenocarcinoma can be identified based on CT radiomics features. We can diagnose lung adenocarcinoma with CT non-invasively.

YIPF2 promotes chemotherapeutic agent-mediated apoptosis via enhancing TNFRSF10B recycling to plasma membrane in non-small cell lung cancer cells

Non-small cell lung cancer (NSCLC) is the most common histological type of lung cancer, and the identification of the apoptotic process of NSCLC is vital for its treatment. Usually, both the expression level and the cell surface level of TNFRSF10B (TNF Receptor superfamily member 10B) will increase after treatment with some chemotherapeutic agents, which plays a critical role in the apoptosis induction. However, the exact molecular mechanism underlying TNFRSF10B regulation remains largely elusive. Here, we found that TNFRSF10B, along with a vesicular trafficking regulator protein, YIPF2, were upregulated after treatment with pemetrexed (PEM) in NSCLC cells. Besides, YIPF2 increased the surface level of TNFRF10B, while YIPF2 knockdown inhibited the upregulation of TNFRSF10B and its recycling to plasma membrane. In addition, RAB8 decreased the cell surface TNFRSF10B by promoting its removing from plasma membrane to cytoplasm. Furthermore, we found that YIPF2, RAB8 and TNFRSF10B proteins interacted physically with each other. YIPF2 could further inhibit the physical interaction between TNFRSF10B and RAB8, thereby suppressing the removing of TNFRSF10B from plasma membrane to cytoplasm mediated by RAB8 and maintaining its high level on cell surface. Finally, using bioinformatics database, the YIPF2-TNFRSF10B axis was confirmed to be associated with the malignant progression of lung cancer. Taken together, we show that YIPF2 promotes chemotherapeutic agent-mediated apoptosis via enhancing TNFRSF10B recycling to plasma membrane in NSCLC cells. These findings may be beneficial for the development of potential prognostic markers of NSCLC and may provide effective treatment strategy.

Histopathological Type of Lung Cancer and Underlying Driver Mutations in Patients with Chronic Obstructive Pulmonary Disease (COPD) versus Patients with Asthma and COPD Overlap: A Single-Center Retrospective Study.

Chronic obstructive pulmonary disease (COPD) increases the risk of lung cancer. The relationships between COPD and Asthma COPD Overlap (ACO), and between the histopathological types of lung cancer and driver mutations remain unclear and need further study. The aim of this retrospective study was to examine the relationships between the histopathological type, frequency of epidermal growth factor receptor (EGFR) driver mutations, and anaplastic lymphoma receptor tyrosine kinase (ALK) rearrangements in the lung cancers of patients with COPD and ACO. Patients with pure COPD (n=198) or ACO (n=318) who were admitted to our hospital were reviewed retrospectively. Lung cancers were identified in 43 (21.7%) patients with pure COPD and 54 (17.0%) patients with ACO. The following lung cancers types were observed: patients with pure COPD had 19 (44.2%) adenocarcinomas, 13 (30.2%) squamous cell lung carcinomas (SCC), 8 (18.6%) small cell lung carcinomas (SCLC); patients with ACO had 23 (42.6%) adenocarcinomas, 23 (42.6%) SCC, 2 (3.70%) SCLC. SCLC was significantly more prevalent in patients with pure COPD (p<0.05) than in those with ACO. Differences between the numbers of other histological types of lung cancer and the numbers of driver mutations in the 2 groups of patients were not significant. The differences in the rate of lung cancer and prevalence of EGFR driver mutations between the patients with pure COPD and those with ACO were not significant.

Non-invasive prediction of lung cancer histological types through exhaled breath analysis by UV-irradiated electronic nose and GC/QTOF/MS

Lung cancer (LC) is one of the most lethal diseases from the last decades. Accurate diagnosis of LC histology could lead to the prescription of personalized medical treatment to the affected subjects, which could reduce the mortality rate. We present here an experimental study performed in the pulmonology units of three hospitals from Morocco to non-invasively detect LC and predict LC histology via the analysis of the volatile organic compounds (VOCs) emitted through breathing. Gas chromatography coupled to a quadrupole time-of-flight mass spectrometer (GC/QTOF/MS) employed to detect the breath VOCs, revealed 30 discriminative VOCs in the breath of healthy subjects and LC patients; among them, 4 unique breath VOCs were found for the first time in the breath of LC patients, and could be used as new biomarkers for future LC diagnosis. Besides, an electronic nose (e-nose) system using a novel sensing technique in breath analysis, based on UV-irradiation of the gas sensors, was employed to characterize the overall composition of the collected breath samples, providing a satisfactory discrimination between the breath patterns of LC patients and healthy subjects. Importantly, the e-nose could further discriminate with high accuracy between the two types of LC (non-small cell LC and small cell LC), as well as between two of the major subtypes of non-small cell LC, namely squamous cell carcinoma (SCC) and adenocarcinoma (ADC). The reported results prove that breath analysis with chemical gas sensors and analytical techniques can provided an accurate mean for the non-invasive diagnosis of LC and LC histology.

ARL4C is associated with initiation and progression of lung adenocarcinoma and represents a therapeutic target.

Lung adenocarcinoma is the most common histological type of lung cancer and is classified into adenocarcinoma in situ (AIS), minimally invasive adenocarcinoma (MIA) and invasive adenocarcinoma (IA). Atypical adenomatous hyperplasia (AAH) lesions are possible precursors to adenocarcinoma. However, the mechanism underlying the stepwise continuum of lung adenocarcinoma is unclear. In this study, the involvement of ADP‐ribosylation factor (ARF)‐like (ARL) 4C (ARL4C), a member of the small GTP‐binding protein family, in the progression of lung adenocarcinoma and the possibility of ARL4C as a molecular target for lung cancer therapy were explored. ARL4C was frequently expressed in AAH and ARL4C expression in immortalized human small airway epithelial cells promoted cell proliferation and suppressed cell death. In addition, ARL4C was expressed with increased frequency in AIS, MIA and IA in a stage‐dependent manner, and the expression was correlated with histologic grade, fluorine‐18 fluorodeoxyglucose uptake and poor prognosis. An anti–sense oligonucleotide (ASO) against ARL4C (ARL4C ASO‐1316) inhibited RAS‐related C3 botulinum toxin substrate activity and nuclear import of Yes‐associated protein and transcriptional coactivator with PDZ‐binding motif, and suppressed in vitro proliferation and migration of lung cancer cells with KRAS or epidermal growth factor receptor (EGFR) mutations. In addition, transbronchial administration of ARL4C ASO‐1316 suppressed orthotopic tumor formation induced by these cancer cells. Thus, ARL4C is involved in the initiation of the premalignant stage and is associated with the stepwise continuum of lung adenocarcinoma. ARL4C ASO‐1316 would be useful for lung adenocarcinoma patients expressing ARL4C regardless of the KRAS or EGFR mutation.

The Russian Radiobiological Human Tissue Repository: characteristics of biological specimens donated by nuclear workers with lung cancer

Purpose: Characteristics of biological specimens donated by nuclear workers with lung cancer.Materials and methods: Biological specimens were identified at the Radiobiological Human Tissue Repository (RHTR). It was established at the Southern Urals Biophysics Institute in Russia and has been developed and supported within the bilateral US-Russian Agreement on International Cooperation for Minimization of the Effects of Prolonged Radiation Exposure. Biological specimens were collected from workers of the Russian nuclear production facility Mayak PA who were exposed to gamma radiation and/or alpha particles. To determine a histologic type of lung cancer, immunohistochemistry was used.Results and conclusions: Today biological specimens donated by 343 registrants with lung cancer are available at the RHTR. Among them, 255 donors (74%) are Mayak PA workers hired at the main facilities (reactors, plutonium production, and radiochemical plants) in 1948–1982. These workers donated about 6024 specimens of lung tissues (tumor and tumor-free) stored mostly as formalin-fixed paraffin-embedded tissue blocks (31%) and histology slides (64%); in addition, they donated 1800 specimens of blood/blood components, buccal epithelium cells, and sputum. Among histologic types identified for these lung cancer cases, adenocarcinoma and small cell carcinoma were prevalent. Information about individual doses from external and internal radiation exposure, data on quantitative smoking characteristics and diseases are available for all workers with lung cancer. Complete information on radiation exposure, health status and non-radiation factors annotated to RHTR registrants and the high quality of the available biological specimens are a unique resource for studying biological mechanisms of radiation-induced lung cancer.

Residential Radon and Histological Types of Lung Cancer: A Meta-Analysis of Case‒Control Studies.

Epidemiological studies on residential radon exposure and the risk of histological types of lung cancer have yielded inconsistent results. We conducted a meta-analysis on this topic and updated previous related meta-analyses. We searched the databases of Cochrane Library, Embase, PubMed, Web of Science and Chinese National Knowledge Infrastructure for papers published up to 13 November 2018. The pooled odds ratio (OR) and 95% confidence interval (CI) were calculated using fixed and random effects models. Subgroup and dose‒response analyses were also conducted. This study was registered with PROSPERO (No. CRD42019127761). A total of 28 studies, which included 13,748 lung cancer cases and 23,112 controls, were used for this meta-analysis. The pooled OR indicated that the highest residential radon exposure was significantly associated with an increased risk of lung cancer (OR = 1.48, 95% CI = 1.26–1.73). All histological types of lung cancer were associated with residential radon. Strongest association with small-cell lung carcinoma (OR = 2.03, 95% CI = 1.52–2.71) was found, followed by adenocarcinoma (OR = 1.58, 95% CI = 1.31–1.91), other histological types (OR = 1.54, 95% CI = 1.11–2.15) and squamous cell carcinoma (OR = 1.43, 95% CI = 1.18–1.74). With increasing residential radon levels per 100 Bq/m3, the risk of lung cancer, small-cell lung carcinoma and adenocarcinoma increased by 11%, 19% and 13%, respectively. This meta-analysis provides new evidence for a potential relationship between residential radon and all histological types of lung cancer.

Gli promotes tumor progression through regulating epithelial-mesenchymal transition in non\u2013small-cell lung cancer

IntroductionLung cancer is the leading causes of cancer-related deaths globally. The most frequent histologic type of lung cancer is non–small-cell lung cancer (NSCLC). NSCLC often undergo epithelial-mesenchymal transition (EMT). The components that control this process are thus promising therapeutic targets.Materials and methodsGli/EMT protein expression levels were examined by western blot in paired NSCLC patient tissues and NSCLC cell lines. Functional analyses were performed to investigate SHH/Gli signaling and EMT in NSCLC cell lines. MTS cell viability, luciferase reporter, and western blot assays were performed to analyze pathway activity, while wound healing and transwell assays were executed to measure cell migration and invasion.ResultsHigher Gli1 expressions were detected in tumor samples than in paired normal tissues. Differential expression of EMT biomarkers and activation of p-AKT were observed in tumor tissues. N-Shh stimulation of cells significantly increased reporter activity in NSCLC cell lines, while Gli-i treatment of transfected cells showed less relative reporter activity. When subjected to both Gli-i and N-Shh treatment, NSCLC cell lines continued to demonstrate decreased Gli transcriptional activity. Gli inhibition is associated with decreased expression level of p-AKT, N-cadherin and Vimentin. Knockdown of both Gli1 and Gli2 showed decreased EMT, migrative and invasive ability. Cells stimulated by N-Shh demonstrated greater mobility. In addition, AKT-i treated cells also demonstrated inhibited EMT activity.ConclusionsThis study provides evidence for aberrant upregulation of the Gli signaling pathway and a strong association between expression of Gli versus AKT and EMT markers in NSCLC.

Membrane Location of Syntaxin-Binding Protein 1 Is Correlated with Poor Prognosis of Lung Adenocarcinoma.

Lung cancer is the leading cause of cancer-related death, and adenocarcinoma is the most common histological type of lung cancer. Syntaxin-binding protein 1 (STXBP1) is essential for exocytosis of secretory vesicles. Since exocytosis is the basic cellular process of cells, we investigated STXBP1 expression and clinical significance in lung adenocarcinoma. We performed quantitative real-time polymerase chain reaction in 20 pairs of lung adenocarcinoma and paired normal tissues, and demonstrated that the relative expression levels of STXBP1 mRNA in lung adenocarcinoma was significantly higher than those in normal lung tissues. We then carried out immunohistochemistry (IHC) to determine the expression profile of STXBP1 in 276 lung adenocarcinoma specimens, and categorized patients into subgroups with low or high STXBP1 expression, based on the IHC score. Moreover, STXBP1 expression phenotypes were categorized as membrane, cytoplasm, and mixed expression (both membrane and cytoplasm) expression. High STXBP1 protein accounted for 58.0% of all the 276 cases (160/276), and membrane, cytoplasm or mixed STXBP1 accounted for 28.75%, 25.63% and 45.63% in the 160 cases of high STXBP1 expression. The clinical significances of these phenotypes were evaluated by analyzing their correlation with clinicopathological factors, as well as their prognostic values. Consequently, the whole STXBP1 expression or membranal STXBP1 expression were correlated with poor prognosis and were independent prognostic factors of lung adenocarcinoma. The whole and membranal STXBP1 expression are independent prognostic factors of lung adenocarcinoma. STXBP1 detection is capable to help screen patients who may have poor prognosis and strengthen the adjuvant therapy more precisely.

Centromere protein F and Forkhead box M1 correlation with prognosis of non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) is the most common histological type of lung cancer. Altered expression of centromere protein F (CENPF), a transient kinetochore protein, has been found in a variety of human cancers. However, its clinical significance in NSCLC remains unknown. In the present study the results of quantitative PCR and western blot analyses demonstrated that CENPF and Forkhead box M1 (FOXM1) were significantly higher in NSCLC tissues than in the non-cancerous controls at both transcriptional and translational levels. Immunohistochemical staining results showed 58.7% (44/75) and 64.0% (48/75) of NSCLC tissues displayed high expression of CENPF and FOXM1, respectively. CENPF protein expression showed a positive correlation with tumor size (P=0.0179), vital status (P=0.0008) and FOXM1 expression (P=0.0013) in NSCLC. Poor overall survival was correlated with high levels of CENPF and FOXM1 in NSCLC patients as evaluated by Kaplan-Meier and log rank test. Multivariate analyses showed that CENPF expression was an independent prognostic factor for NSCLC. In conclusion, our study provides evidence of the prognostic function of CENPF in NSCLC.

Dickkopf‐related protein 3 promotes cell adhesion and invasion during progression of lung adenocarcinoma

Dickkopf-related protein 3 (DKK3) is one of the DKK family (DKK1-4), an evolutionally conserved group of secreted glycoproteins characterized by two distinct cysteine-rich domains. DKK3 is considered to be a tumor suppressor gene. However, it has been shown that 30-50% of various cancers are DKK3-positive, suggesting that DKK3 may have an additional function other than tumor suppression. In this study, we focused on lung adenocarcinoma, which is the major histological type of lung cancer. We analyzed the relationship between DKK3 expression and clinicopathological features by immunohistochemistry, using 200 lung adenocarcinoma specimens. We found that 40.5% and 59.5% of cases were DKK3-positive and -negative, respectively, and that positive cases had a greater tendency for progression than negative cases (P < 0.05). Furthermore, in vitro analyses demonstrated that DKK3 suppression affected cell adhesion in three DKK3-expressing lung adenocarcinoma cell lines and that DKK3-knockdown cells were less invasive in comparison to control cells. These results suggest that DKK3 plays a role in the progression of lung adenocarcinoma by promoting cell adhesion and invasion. DKK3 might be a new extracellular cancer therapeutic target, and it seems important to clarify molecular mechanisms underlying the DKK3 functions depending on cell context.

A Case/Control Study: AGBL1 Polymorphism Related to Lung Cancer Risk in Chinese Nonsmoking Females.

ATP/GTP binding protein like 1 (AGBL1) plays a role in controlling the length of polyglutamate side chains. Polymorphism rs4513061 in AGBL1 is suspected to influence the risk of lung cancer. A case/control study was performed involving 556 cases and 563 controls from a hospital participating in donation. The relationship between rs4513061 and the risk of lung cancer and the interaction between rs4513061 and environmental exposure were determined by the chi-square tests, logistic regression analysis, and crossover analysis. The survival analysis was conducted by Cox proportional hazard regression. The results showed that rs4513061 polymorphism is associated with the risk of lung cancer. The stratified analysis suggested the protective effect of rs4513061 to different histological types of lung cancer, including lung adenocarcinoma (AA vs. GG: odds ratio [OR] = 0.505, 95% confidence interval [CI] = 0.337-0.756, p < 0.001), squamous cell lung cancer (AG vs. GG: OR = 0.488, 95% CI = 0.269-0.883, p = 0.018), and small-cell lung cancer (AA vs. GG: OR = 0.421, 95% CI = 0.216-0.819, p = 0.011). Nevertheless, there was no significant interaction between rs4513061 and cooking oil fume. Significant impact was not observed between the rs4513061 polymorphism and survival time of lung cancer. Our study indicated that rs4513061 in AGBL1 decreases the risk of lung cancer in nonsmoking females from northeast China.

MS12.03 LC-SCRM-Japan, a Pan-Japan Genetic Screening of Lung Cancer

Recently many actionable driver oncogenes such as EGFR, ALK, RET, ROS1, BRAF and MET have been identified in non-small cell lung cancer (NSCLC). However, most of these driver oncogenes are rare and found in only about 1-2% of lung adenocarcinomas. To develop new molecular targeted agents for rare alterations, efficient genomic screening is needed to identify patients. A nationwide genomic screening platform (LC-SCRUM-Japan) was established to primarily screen for ALK, RET and ROS1 fusions using RT-PCR and FISH in advanced non-squamous NSCLC without EGFR mutations in February 2013. From March 2015, this project was expanded to an academic-industrial collaboration initiative with broader eligibility criteria and tumor samples were analyzed by next-generation sequencing (NGS multiplex analysis with OncomineTM Cancer Research Panel). In addition, non-squamous NSCLC regardless of EGFR mutation status and other histological type of lung cancer including squamous NSCLC and small cell lung cancer (SCLC) were enrolled. Clinical information of all patients have also been collected to generate a clinical-genomic database that enables detailed outcome analysis of the cohort. Since its inception, more than 200 Japanese hospitals participated in this project and 7739 patients were enrolled into LC-SCRUM-Japan. 776 squamous NSCLCs and 823 SCLCs were enrolled. Through this platform, many patients with rare driver oncogenes were identified for approved targeted therapies or successfully enrolled into various clinical trials that have helped develop new targeted agents. Based on our project, crizotinib and dabrafenib/trametinib were approved for ROS1 fusions and BRAF mutation positive lung cancers in Japan, respectively. From December 2017, liquid screening with Guardant 360 (LC-SCRUM-Liquid) was initiated and a large concordance study between tissue and liquid NGS analysis was performed in 2000 patients. Additionally, to identify novel biomarkers for immune checkpoint inhibitors, an immuno-oncology biomarker study (LC-SCRUM-IBIS) was conducted with 1017 patients enrolled from February 2017 to May 2018. PD-L1 assessment by IHC and whole exon sequencing was performed. The LC-SCRUM platform was recently expanded to hospitals in Taiwan and we will expand the collaboration to China and other Southeast Asia to establish an integrated Asia cancer clinical genomic database. Genomic screening in LC-SCRUM has provided clinical value by identifying patients with actionable mutations and has helped accelerate clinical development of novel agents. To continue to elevate the standard of cancer care and treatment options for patients in Asia, we are establishing a high quality platform of genomic screening technologies and a mechanism of collecting clinical data that will help elevate precision medicine and drug development in Asia.

GR03.02 Adenocarcinoma

GR03.02 Adenocarcinoma

EP1.18-04 Do Tumor-Related Factors Predict Postoperative Pulmonary Complications in Patients Undergoing Curative Surgery for Lung Cancer?

The purpose of the present study is to identify preoperative risk factors related to pulmonary complications with a focus on tumor-related factors. The authors conducted a retrospective review of the clinical records of all patients operated at the thoracic department of the Lviv State Oncological Regional Treatment and Diagnostic Center in 2010-2011. Tumor-related factors (histological type of lung cancer, tumor localization, TNM classification, past medical history of different cancer types) were analyzed. Postoperative pulmonary morbidity was defined as: respiratory failure, atelectasis, air leak more than 7 days, prolonged intubation (>72hours), pleural effusion, pleural empyema, chylothorax, and pneumothorax. The study included patients meeting the following criteria: age under 70, absence of neoadjuvant chemo- and/or radiotherapy, benign lung lesions, lung metastases, and non-curative lung resection. Logistic regression was performed using IBM SPSS Statistics 22 program. The result was considered statistically significant when p<0.05. 144 patients underwent surgery for primary lung cancer at our institution. Lobectomy was performed in 36.1%, pneumonectomy – in 59%, lung resection – in 4.9% of patients. Histological examination showed that 84 patients had squamous cell carcinoma, 31 patients – adenocarcinoma, 6 patients – large cell carcinoma, 6 patients – small cell carcinoma, 8 patients – NET and 9 patients – other histological types. 12 (8.3%) patients had a medical history of a different type of cancer. The 30-day postoperative mortality rate was 3.47%, postoperative morbidity was 36.8%. The analysis showed that presence of a different type of cancer in past medical history (p<0.05) remained a significant risk factor for respiratory morbidity after lung cancer surgery while the presence of NET reduces the risk of postoperative pulmonary complications (p<0.05). Presence of a different type of cancer in past medical history constitutes a significant risk factor for respiratory postoperative morbidity in lung cancer patients. Patients with NET have a lower risk of postoperative pulmonary complications. We suggest that this result requires confirmation by further research.

P1.13-09 Utility of Artificial Intelligence in Estimation of the Histologic Type of Lung Cancer

P1.13-09 Utility of Artificial Intelligence in Estimation of the Histologic Type of Lung Cancer

Chemotherapy-associated Acute Exacerbation of Interstitial Lung Disease Shortens Survival Especially in Small Cell Lung Cancer

In lung cancer (LC) patients, pre-existing interstitial lung disease (ILD) is a risk of chemotherapy-associated acute exacerbation of ILD (AE-ILD). AE-ILD shows a diverse clinical course varying from fatal respiratory failure to asymptomatic event, and the prognostic impact is still unclear. We retrospectively evaluated the association between the prognosis and AE-ILD in 86 LC patients with pre-existing ILD who were treated with cytotoxic chemotherapy, especially focusing on histological types of LC. Thirty (34.9%) patients had AE-ILD, that was significantly associated with a poor prognosis in LC patients with ILD. When analyzed by histological types, a significant association of AE-ILD with shorter survival was observed only in the small cell LC (SCLC) group, but not in the non-small cell LC group. The development of AE-ILD by cytotoxic chemotherapy is associated with poor prognosis in LC patients with ILD, especially in patients with SCLC.