Elevated carbohydrate antigen (CA) 19-9 can indicate malignancies of the gastrointestinal, pancreatic, and biliary tracts, and be found in a pulmonary sequestration. A 30-year-old man visited Seoul National University Bundang Hospital due to elevated CA 19-9 levels, representing pulmonary sequestration of the bilateral lower lobes, which were connected with each other. We performed left lower lobectomy and division of the systemic arteries. After operation, CA 19-9 levels decreased to normal range, even though a small amount of sequestrated lung remained in the right lower lobe. It is not uncommon that presence of pulmonary sequestration might elevate serum CA 19-9 levels; however, horseshoe type bilateral pulmonary sequestration is very rare.
Adult ; Arteries ; Biliary Tract ; Bronchopulmonary Sequestration* ; Humans ; Lung ; Reference Values ; Seoul

BACKGROUND: A better understanding of the histopathology and molecular biology of lung cancer might improve our capability to predict the outcome for any individual patient. The purpose of this study was to evaluate several histopathologic and molecular markers in order to assess their prognostic value in stage I non-small cell lung cancer. MATERIALS AND METHODS: One hundred ten patients at the Kyungpook National University Hospital were enrolled in the study. Histopathologic factors and molecular markers were selected. RESULTS: Univariate analysis showed that the T stage, differentiation, visceral pleural invasion, and survivin expression were significantly associated with recurrence. Multivariate analysis demonstrated that differentiation and survivin overexpression emerged as independent prognostic factors of recurrence. CONCLUSION: In resected stage I non-small cell lung cancer, poor differentiation and survivin overexpression have been identified as independent predictors of poor disease-free survival.
Carcinoma, Non-Small-Cell Lung ; Disease-Free Survival ; Humans ; Immunohistochemistry ; Lung ; Lung Neoplasms ; Molecular Biology ; Multivariate Analysis ; Prognosis ; Recurrence

Idiopathic non-cirrhotic portal hypertension (INCPH) is a disease with an uncertain etiology consisting of non-cirrhotic portal hypertension and portal pressure increase in the absence of liver cirrhosis. In INCPH, patients exhibit normal liver functions and structures. The factors associated with INCPH include the following: Umbilical/portal pyremia, bacterial diseases, prothrombic states, chronic exposure to arsenic, vinyl chloride monomers, genetic disorders, and autoimmune diseases. Approximately 70% of patients present a history of major variceal bleeding, and treatment relies on the prevention of complications related to portal hypertension. Autoimmune disorders associated with INCPH are mainly systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis. To the best of our knowledge, a case of ankylosing spondylitis (AS) associated with INCPH has not been reported thus far. Therfore, we report our experience of a patient with AS accompanied by INCPH, who showed perisplenic varices with patent spleno-portal axis and hepatic veins along with no evidence of cirrhosis on liver biopsy, and provide a brief literature review.

Idiopathic non-cirrhotic portal hypertension (INCPH) is a disease with an uncertain etiology consisting of non-cirrhotic portal hypertension and portal pressure increase in the absence of liver cirrhosis. In INCPH, patients exhibit normal liver functions and structures. The factors associated with INCPH include the following: Umbilical/portal pyremia, bacterial diseases, prothrombic states, chronic exposure to arsenic, vinyl chloride monomers, genetic disorders, and autoimmune diseases. Approximately 70% of patients present a history of major variceal bleeding, and treatment relies on the prevention of complications related to portal hypertension. Autoimmune disorders associated with INCPH are mainly systemic sclerosis, systemic lupus erythematosus and rheumatoid arthritis. To the best of our knowledge, a case of ankylosing spondylitis (AS) associated with INCPH has not been reported thus far. Therfore, we report our experience of a patient with AS accompanied by INCPH, who showed perisplenic varices with patent spleno-portal axis and hepatic veins along with no evidence of cirrhosis on liver biopsy, and provide a brief literature review.
Arsenic ; Arthritis, Rheumatoid ; Autoimmune Diseases ; Biopsy ; Esophageal and Gastric Varices ; Fibrosis ; Hepatic Veins ; Humans ; Hypertension, Portal ; Liver ; Liver Cirrhosis ; Lupus Erythematosus, Systemic ; Portal Pressure ; Scleroderma, Systemic ; Spondylitis, Ankylosing ; Varicose Veins ; Vinyl Chloride

Purpose: Despite advances in treatment, lung cancer remains the leading cause of cancer mortality. This study aimed to characterise genome-wide tumorigenesis events and to understand the hypothesis of the multistep carcinogenesis of lung adenocarcinoma (LUAD) Materials and Methods: We conducted multiregion whole-exome sequencing of LUAD with synchronous atypical adenomatous hyperplasia (AAH), adenocarcinoma in situ, or minimally invasive adenocarcinoma of 19 samples from three patients to characterize genome-wide tumorigenesis events and validate the hypothesis of the multistep carcinogenesis of LUAD. We identified potential pathogenic mutations preserved in preinvasive lesions and supplemented the finding by allelic variant level from RNA sequencing. Results: Overall, independent mutational profiles were observed per patient and between patients. Some shared mutations including epidermal growth factor receptor (EGFR , p.L858R) were present across synchronous lesions. Conclusion Here, we show that there are driver gene mutations in AAH, and they may exacerbate as a sequence in a histological continuum, supporting the Darwinian evolution model of cancer genome. The intertumoral and intratumoral heterogeneity of synchronous LUAD implies that multi-biomarker strategies might be necessary for appropriate treatment.

Although TP53 mutations have been widely studied in lung cancer, the majority of studies have focused on exons 5-8 of the gene. In addition, TP53 mutations in Korean patients with lung cancers have not been investigated. We searched for mutations in the entire coding exons, including splice sites of the gene, in Korean patients with non-small cell lung cancer (NSCLC). Mutations of the gene were determined by direct sequencing in 176 NSCLCs. Sixty-nine mutations (62 different mutations) were identified in 65 tumors. Of the 62 mutations, 12 were novel mutations. TP53 mutations were more frequent in males, ever-smokers and squamous cell carcinomas than in females, never-smokers and adenocarcinomas, respectively (all comparisons, P<0.001). Missense mutations were most common (52.2%), but frameshift, nonsense, and splice-site mutations were frequently observed at frequencies of 18.8%, 15.9% and 10.1%, respectively. Of the 69 mutations, 9 (13.0%) were found in the oligomerization domain. In addition, the proportion of mutations in the oligomerization domain was significantly higher in adenocarcinomas than in squamous cell carcinomas (23.5% vs. 2.9%, P=0.01). Our study provides clinical and molecular characteristics of TP53 mutations in Korean patients with NSCLCs.
Carcinoma, Non-Small-Cell Lung/*epidemiology/*genetics ; Female ; Genetic Predisposition to Disease/*epidemiology/*genetics ; Humans ; Incidence ; Korea/epidemiology ; Lung Neoplasms/*epidemiology/*genetics ; Male ; Middle Aged ; Polymorphism, Single Nucleotide/genetics ; Risk Assessment/methods ; Risk Factors ; Tumor Suppressor Protein p53/*genetics

Background/Aims: We performed a large-scale, retrospective, nationwide, cohort study to investigate the risk factors for lung cancer among never-smoking Korean females. Methods: The study data were collected from a general health examination and questionnaire survey of eligible populations conducted between January 1, 2003 and December 31, 2004; the data were acquired from the tailored big data distribution service of the National Health Insurance Service. After a 1-year clearance period, 5,860,922 of 6,318,878 never-smoking female participants with no previous history of lung cancer were investigated. After a median follow-up of 11.4 years, 43,473 (0.74%) participants were defined as “newly diagnosed lung cancer”. Results: After adjusting for all variables at baseline, the variables older age, lower body mass index (BMI), less exercise, frequent alcohol drinking, meat-based diet, rural residence, and previous history of cancer were associated with a higher incidence of lung cancer. Low BMI (< 18.5 kg/m2: hazard ratio [HR], 1.33; 95% confidence interval [CI], 1.27 to 1.40) was a significant independent risk factor; as BMI decreased, HR increased. Negative associations between BMI and lung-cancer development were also observed after controlling for age (p for trend < 0.001). Drinking alcohol one to two times a week (HR, 1.25; 95% CI, 1.21 to 1.28) and eating a meat-based diet (HR, 1.08; 95% CI, 1.01 to 1.15) were associated with lung-cancer incidence. Conclusions Modifiable baseline characteristics, such as BMI, exercise, alcohol consumption, and diet, are risk factors for lung-cancer development among never- smoking females. Thus, lifestyle modifications may help prevent lung cancer.

Recently, genetic variants in the WNT signaling pathway have been reported to affect the survival outcome of Caucasian patients with early stage non-small cell lung cancer (NSCLC). We therefore attempted to determine whether these same WNT signaling pathway gene variants had similar impacts on the survival outcome of NSCLC patients in a Korean population. A total of 761 patients with stages I-IIIA NSCLC were enrolled in this study. Eight variants of WNT pathway genes were genotyped and their association with overall survival and disease-free survival were analyzed. None of the eight variants were significantly associated with overall survival or disease-free survival. There were no differences in survival outcome after stratifying the subjects according to age, gender, smoking status, and histological type. These results suggest that genetic variants in the WNT signaling pathway may not affect the survival outcome of NSCLC in a Korean population.
Aged ; Asian Continental Ancestry Group/*genetics ; Carcinoma, Non-Small-Cell Lung/*genetics/mortality/pathology ; Demography ; Disease-Free Survival ; Female ; Genotype ; Humans ; Kaplan-Meier Estimate ; Lung Neoplasms/*genetics/mortality/pathology ; Male ; Middle Aged ; *Polymorphism, Single Nucleotide ; Republic of Korea ; Smoking ; Wnt Signaling Pathway/*genetics

Vascular endothelial growth factor (VEGF) contributes to tumor angiogenesis. The role of VEGF single nucleotide polymorphisms (SNPs) in lung cancer susceptibility and its prognosis remains inconclusive and controversial. This study was performed to investigate whether VEGF polymorphisms affect survival outcomes of patients with early stage non-small cell lung cancer (NSCLC) after surgery. Three potentially functional VEGF SNPs (rs833061T>C, rs2010963G>C, and rs3025039C>T) were genotyped. A total of 782 NSCLC patients who were treated with surgical resection were enrolled. The association of the SNPs with overall survival (OS) and disease free survival (DFS) was analyzed. In overall population, none of the three polymorphisms were significantly associated with OS or DFS. However, when the patients were stratified by tumor histology, squamous cell carcinoma (SCC) and adenocarcinoma (AC) had significantly different OS (Adjusted hazard ratio [aHR] = 0.76, 95% CI = 0.56–1.03 in SCC; aHR = 1.33, 95% CI = 0.98–1.82 in AC; P for heterogeneity = 0.01) and DFS (aHR = 0.75, 95% CI = 0.58–0.97 in SCC; aHR = 1.26, 95% CI = 1.00–1.60 in AC; P for heterogeneity = 0.004) according to the rs833061T>C genotypes. Our results suggest that the prognostic role of VEGF rs833061T>C may differ depending on tumor histology.
Adenocarcinoma ; Carcinoma, Non-Small-Cell Lung* ; Carcinoma, Squamous Cell ; Disease-Free Survival ; Genotype ; Humans ; Lung Neoplasms ; Polymorphism, Single Nucleotide ; Population Characteristics ; Prognosis* ; Vascular Endothelial Growth Factor A*

PURPOSE: Lung cancers presenting as subsolid nodule commonly have peripheral location, making the cancer-pleura relationship noteworthy. We aimed to evaluate the effect of pleural attachment and/or indentation on visceral pleural invasion (VPI) and recurrence-free survival. MATERIALS AND METHODS: Patients who underwent curative resection of lung cancer as subsolid nodules from April 2007 to January 2016 were retrospectively evaluated. They were divided into four groups according to their relationship with the pleura. Clinical, radiographical, and pathological findings were analyzed. RESULTS: Among 404 patients with malignant subsolid nodule, 120 (29.7%) had neither pleural attachment nor indentation, 26 (6.4%) had attachment only, 117 (29.0%) had indentation only, and 141 (34.9%) had both. VPI was observed in nodules of 36 patients (8.9%), but absent in nonsolid nodules and in those without pleural attachment and/or indentation. Compared to subsolid nodules with concurrent pleural attachment and indentation, those with attachment only (odds ratio, 0.12; 95% confidence interval [CI], 0.02 to 0.98) and indentation only (odds ratio, 0.10; 95% CI, 0.03 to 0.31) revealed lower odds of VPI. On subgroup analysis, the size of the solid portion was associated with VPI among those with pleural attachment and indentation (p=0.021). Such high-risk features for VPI were associated with earlier lung cancer recurrence (adjusted hazard ratio, 3.31; 95% CI, 1.58 to 6.91). CONCLUSION: Concurrent pleural attachment and indentation are risk factors for VPI, and the odds increase with larger solid portion in subsolid nodules. Considering the risk of recurrence, early surgical resection could be encouraged in these patients.
Carcinoma, Non-Small-Cell Lung ; Humans ; Lung Neoplasms ; Lung ; Neoplasm Invasiveness ; Pleura ; Prognosis ; Recurrence ; Retrospective Studies ; Risk Factors