• Epstein-Barr virus (EBV)
• Lung cancer
• adolescents and young adults (AYA)
• human papilloma virus (HPV)
• viral infection

• Infectious lung diseases
• Malignant lung diseases
• Obstructive lung diseases
• Pulmonary diseases
• Restrictive lung diseases
• Sarcoidosis

• Carnitine genes
• SLC
• lung adenocarcinoma (LUAD)
• lung cancer (LC)
• lung squamous cell carcinoma (LUSC)

• Humans
• Early Detection of Cancer/methods
• Lung Neoplasms/diagnosis
• Lung Neoplasms/epidemiology
• Lung Neoplasms/prevention & control
• Mass Screening/methods
• Missouri/epidemiology
• Risk Factors

• Biomarker
• Mass spectrometry
• Metabolic profile
• Non-small cell lung cancer
• Tobacco smoking

• Humans
• Lung Neoplasms/blood
• Lung Neoplasms/metabolism
• Metabolomics/methods
• Biomarkers, Tumor/blood
• Male
• Female
• Middle Aged
• Smoking/blood
• Smoking/adverse effects
• Aged
• Sphingosine/analogs & derivatives
• Sphingosine/blood
• Sphingosine/metabolism
• Lysophospholipids/blood
• Lysophospholipids/metabolism
• Metabolome
• Pulmonary Disease, Chronic Obstructive/metabolism
• Pulmonary Disease, Chronic Obstructive/blood
• Chromatography, Liquid/methods
• Succinic Acid/blood
• Succinic Acid/metabolism
• Glutamic Acid/blood
• Glutamic Acid/metabolism

• 2017/01/X/NZ7/02064 National Science Centre, Poland

• acute myeloid leukemia
• immune infiltration
• m7G
• prognostic biomarkers
• prognostic risk-score model

• Non-small cell lung cancer
• miRNA delivery systems
• miRNA-based therapy
• miRNAs

• Bronchogenic carcinoma
• Castellón
• Incidence
• Lung cáncer
• Sex
• Spain
• Survival

• Male
• Humans
• Female
• Middle Aged
• Aged
• Lung Neoplasms/epidemiology
• Lung Neoplasms/diagnosis
• Spain/epidemiology
• Incidence
• Carcinoma, Bronchogenic/epidemiology
• Carcinoma, Bronchogenic/diagnosis
• Retrospective Studies

• Meta analysis
• Non-small cell lung cancer
• Pembrolizumab
• Predictor

• Cholesterol
• Cisplatin
• HMGCR
• Lung cancer
• SIAH1

• 81301800 National Science Foundation Committee of China

• Cancer predisposition
• Cancer treatment
• Germline pathogenic variants
• Hereditary cancer syndromes
• Next-generation sequencing

• air pollution
• early detection
• epidemiology
• incidence
• lung cancer
• particulate matters
• prevention
• risk-factors
• screening
• smoking

• Male
• Female
• Humans
• Lebanon/epidemiology
• Risk Factors
• Lung Neoplasms/epidemiology
• Smoking
• Incidence
• Neoplasms, Second Primary

Lung cancer is the second most common and the most lethal malignancy worldwide. It is estimated that lung cancer in never smokers (LCINS) accounts for 10-25% of cases, and its incidence is increasing according to recent data, although the reasons remain unclear. If considered alone, LCINS is the 7th most common cause of cancer death. These tumors occur more commonly in younger patients and females. LCINS tend to have a better prognosis, possibly due to a higher chance of bearing an actionable driver mutation, making them amenable to targeted therapy. Notwithstanding, these tumors respond poorly to immune checkpoint inhibitors (ICI). There are several putative explanations for the poor response to immunotherapy: low immunogenicity due to low tumor mutation burden and hence low MANA (mutation-associated neo-antigen) load, constitutive PD-L1 expression in response to driver mutated protein signaling, high expression of immunosuppressive factors by tumors cells (like CD39 and TGF-beta), non-permissive immune TME (tumor microenvironment), abnormal metabolism of amino acids and glucose, and impaired TLS (Tertiary Lymphoid Structures) organization. Finally, there is an increasing concern of offering ICI as first line therapy to these patients owing to several reports of severe toxicity when TKIs (tyrosine kinase inhibitors) are administered sequentially after ICI. Understanding the biology behind the immune response against these tumors is crucial to the development of better therapeutic strategies.

• Female
• Humans
• Immunologic Factors/therapeutic use
• Immunotherapy
• Lung Neoplasms/drug therapy
• Smokers
• Tumor Microenvironment/genetics

• DDR genes
• Family history of cancer
• Immune checkpoint inhibitors
• Immunotherapy
• NSCLC
• Pembrolizumab

• Carcinoma, Non-Small-Cell Lung/genetics
• Carcinoma, Non-Small-Cell Lung/therapy
• DNA Damage
• Female
• Humans
• Immune Checkpoint Inhibitors/therapeutic use
• Immunotherapy
• Lung Neoplasms/genetics
• Lung Neoplasms/therapy
• Male
• Treatment Outcome

• Department of Health
• PS3416 Wellcome Trust

Background: Emerging evidence has proven that ferroptosis plays an important role in the development of acute myeloid leukemia (AML), whereas the exact role of ferroptosis-associated genes in AML patients’ prognosis remained unclear.

Materials and Methods: Gene expression profiles and corresponding clinical information of AML cases were obtained from the TCGA (TCGA-LAML), GEO (GSE71014), and TARGET databases (TARGET-AML). Patients in the TCGA cohort were well-grouped into two clusters based on ferroptosis-related genes, and differentially expressed genes were screened between the two clusters. Univariate Cox and LASSO regression analyses were applied to select prognosis-related genes for the construction of a prognostic risk-scoring model. Survival analysis was analyzed by Kaplan–Meier and receiver operator characteristic curves. Furthermore, we explored the correlation of the prognostic risk-scoring model with immune infiltration and chemotherapy response. Risk gene expression level was detected by quantitative reverse transcription polymerase chain reaction.

Results: Eighteen signature genes, including ZSCAN4, ASTN1, CCL23, DLL3, EFNB3, FAM155B, FOXL1, HMX2, HRASLS, LGALS1, LHX6, MXRA5, PCDHB12, PRINS, TMEM56, TWIST1, ZFPM2, and ZNF560, were developed to construct a prognostic risk-scoring model. AML patients could be grouped into high- and low-risk groups, and low-risk patients showed better survival than high-risk patients. Area under the curve values of 1, 3, and 5 years were 0.81, 0.827, and 0.786 in the training set, respectively, indicating a good predictive efficacy. In addition, age and risk score were the independent prognostic factors after univariate and multivariate Cox regression analyses. A nomogram containing clinical factors and prognostic risk-scoring model was constructed to better estimate individual survival. Further analyses demonstrated that risk score was associated with the immune infiltration and response to chemotherapy. Our experiment data revealed that LGALS1 and TMEM56 showed notably decreased expression in AML samples than that of the normal samples.

Conclusion: Our study shows that the prognostic risk-scoring model and key risk gene may provide potential prognostic biomarkers and therapeutic option for AML patients.

• National Natural Science Foundation of China
• High-Level Hospital Construction Project of Guangdong Provincial People’s Hospital
• Natural Science Foundation of Guangdong Province
• Science and Technology Planning Project of Guangdong Province

Lung cancer is the most common malignancy, being a serious threat of human lives. The incidence and mortality of lung cancer has been increasing rapidly in the past decades. Although the development of new therapeutic modes, such as target therapy, the overall survival rate of lung cancer remains low. It is urgent to advance the understanding of molecular oncology and find novel biomarkers and targets for the early diagnosis, treatment, and prognostic prediction of lung cancer. Long non-coding RNAs (lncRNAs) are non-protein coding RNA transcripts that are more than 200 nucleotides in length. LncRNAs exert diverse biological functions by regulating gene expressions at transcriptional, translational, and post-translational levels. In the past decade, it has been shown that lncRNAs are extensively involved in the pathogenesis of various diseases, including lung cancer. In this review, we highlighted the lncRNAs characterized in lung cancer and discussed their translational potential in lung cancer clinics.

• LncRNAs
• MALAT1
• and HOTAIR
• lung cancer
• tumor biomarkers

• ADAURA trial
• Adjuvant EGFR-TKI treatment
• Bioluminescence imaging
• Orthotopic mouse lung cancer model
• Tail vein injection

Emerging evidence has suggested that inherited factors are also involved in lung cancer development. However, most studies focused on well-elucidated cancer predisposition genes, the majority of which are tumor suppressor genes. The profile of germline mutations in oncogenic driver genes remains unrevealed, which might also provide potential clinical implications for lung cancer management.

Sequencing data from 36,813 unselected lung cancer patients who underwent somatic mutation profiling were retrospectively reviewed. All recruited patients had matched white blood cell samples sequenced in parallel using a capture-based panel including eight key lung cancer driver genes (epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), MET proto-oncogene, receptor tyrosine kinase (MET), Kirsten rat sarcoma viral oncogene homolog (KRAS), Erb-B2 receptor tyrosine kinase 2(ERBB2), ROS proto-oncogene 1, receptor tyrosine kinase (ROS1), ret proto-oncogene (RET), and B-Raf proto-oncogene, serine/threonine kinase (BRAF)). Likely pathogenic/pathogenic (LP/P) variants were called according to the classification criteria of the American College of Medical Genetics and Genomics. Variants of uncertain significance (VUS) located in the kinase domains of driver genes and occurring recurrently (n ≥3) were also included for further analyses.

Seven different LP/P variants in EGFR, MET, or RET were identified in 0.03% of lung cancer patients (n = 14) and 25 different VUS in the kinase domains of seven driver genes (except KRAS) were found with a prevalence of 0.3% (n = 117).Collectively, germline mutations were most frequently seen in ROS1 (n = 31, 0.084%), followed by MET (n = 23, 0.062%), EGFR (n = 22, 0.06%), ALK (n = 22, 0.06%) and RET (n = 17, 0.046%). LP/P variants and VUS fell the most commonly in EGFR (n = 10, 72%) and ROS1 (n = 31, 26%), respectively. Of the 10 patients with EGFR LP/P germline mutation, 70% also acquired somatic EGFR driver mutation exon21 p.L858R or exon19 deletion at baseline; while the three patients with pathogenic germline RET mutation displayed distinct baseline somatic profiles of rare EGFR mutation or KRAS exon2 p.G12C. We discovered 11 germline mutations that also occurred somatically, including four LP/P variants and seven VUS.

We present the first study to systemically characterize the germline mutation in oncogenic driver genes in a large cohort of unselected patients with lung cancers.

• germline mutation
• likely pathogenic/pathogenic variant
• lung cancers
• oncogenic gene
• variants of uncertain significance

Lung cancer is the most commonly diagnosed cancer in men worldwide. Studies regarding dietary patterns (DPs) and lung cancer are limited, with results remaining inconclusive, and the association of DPs with lung cancer in smokers is unclear. This study analyzed the associations between DPs, including the Polish-adapted Mediterranean diet (Polish-aMED) score, and lung cancer risk in Polish adult male smokers. This case-control study involved 439 men aged 45–80 years from northeastern Poland, including 187 newly diagnosed lung cancer cases. Dietary data was collected with a 62-item food frequency questionnaire (FFQ-6). Two approaches were applied to identify dietary patterns. The Polish-aMED score was calculated (hypothesis-driven approach) and a principal component analysis (PCA) was used to identify PCA-driven DPs (data-driven approach). A logistic regression analysis was performed to estimate the odds ratio (OR) and 95% confidence interval (95% CI) of the lung cancer risk associated with the adherence to DPs overall as well as for moderate (2.5–11 pack-years) and heavy (>11 pack-years) smokers. Among moderate smokers, the risk of lung cancer was lower by 41% (OR: 0.59; 95% CI: 0.39–0.90; p < 0.05; adjusted model) in the higher adherence to the prudent DP when compared to the lower adherence, and by 66% (OR: 0.34; 95% CI: 0.15–0.76; p < 0.05; adjusted model) in the high adherence (7–9 points) to the Polish-aMED score when compared to the low adherence (0–3 points). No significant association between the westernized traditional DP or the sweet dairy DP and lung cancer was revealed. In conclusion, the current study suggests that pro-healthy dietary patterns, including the Mediterranean pattern, may favour lower risk of lung cancer in moderate smokers, although it was not confirmed in heavy smokers.

• Mediterranean diet
• diet quality score
• dietary patterns
• lung cancer
• men
• prudent diet
• smokers
• smoking

• Aged
• Aged, 80 and over
• Case-Control Studies
• Diet Surveys
• Diet, Healthy/statistics & numerical data
• Diet, Mediterranean/statistics & numerical data
• Feeding Behavior
• Humans
• Logistic Models
• Lung Neoplasms/epidemiology
• Lung Neoplasms/etiology
• Male
• Middle Aged
• Odds Ratio
• Poland/epidemiology
• Principal Component Analysis
• Risk Factors
• Smoking/adverse effects
• Surveys and Questionnaires