Background: Lung cancer is the leading cause of cancer over the world. P53 alteration is by far the most common genetic defect in lung cancer. The mutation of p53 protein involves the loss of inhibitory function of p53 related tumor suppressor gene and resultant oncogenesis. The analysis of p53 alterations consists of immunohistochemical stain, PCR based assay, or serologic ELISA (enzyme-linked immunosorbent assay). Methods : Serum levels of p53 mutant protein were measured in 69 cases of lung cancer (adenocarcinoma n=29, epidermoid n=16, small cell n=13, large cell n=1, undifferentiated n=1, undetermined n=9) and 42 controls of respiratory disorders using ELISA. Immunohistochemical stain in tissue was performed using monoclonal antibody of p53 in lung cancer subjects. Results: Both serum p53s in nonsmall cell cancer ($0.28{\pm}0.44ng/ml$) and in small cell cancer ($0.20{\pm}0.14ng/ml$) were not different from controls ($0.34{\pm}0.20ng/ml$). Also there was no significant difference in serum p53 according to tumor stages. P53 immunohistochemical stain showed 50% positivity overall in lung cancer. There were no close correlation between serologic level and positivity of immunohistochemical stain. Conclusion: The serologic determination of p53 mutant protein is thought to have no diagnostic role in lung cancer. Immunohistochemical stain in lung cancer specimen shows 50% positivity.
Park, Ji-Hyun;Kang, Myoung-Jae;Lee, Heung-Bum;Lee, Yong-Chul;Rhee, Yang-Kuen
Tuberculosis and Respiratory Diseases
/
v.48
no.3
/
pp.324-330
/
2000
Objective : Lung cancer arises after a series of morphological changes, which take several years to progress from normal epithelium to invasive cancer. Multiple molecular changes and growth factor production have been documented in lung cancers, both small cell and non-small cell types. Insulin-like growth factors(IGFs) are important mitogenic and anabolic peptides, both in vivo and in vitro, and are thought to be significant autocrine-paracrine factors involved in normal and malignant cell proliferation. In this study, the degree of expression of IGF-1 on the immunohistochemical staining in human non-small cell lung cancer(NSCLC) cells and small cell lung cancer (SCLC) cells were investigated. Methods : Immunohistochemical staining for IGF-1 was performed in 15 cases of small cell carcinoma, 15 cases of squamous cell carcinoma, 15 cases of adenocarcinoma, and 12 cases of bronchoalveolar carcinoma. Results : The expression of IGF-1 on the immunohistochemical staining significantly increased in NSCLC cells than in SCLC cells. Conclusion : These results suggest the expression of IGF-1 in human lung cancer cells. The immunohistochemical staining of IGF-1 in lung cancer cell lines may assist in the differentiation of NSCLC and SCLC.
International Ass ciation for the Study of Lung Cancer(IASLC) recommended the following classification of small cell lung carcinoma(SCLC) : (1) Small cell carcinoma (2) Mixed small cell/large cell carcinoma (3) Combined small cell carcinoma. Combined small cell carcinomas contain a squamous cell carcinoma or adenocarcinoma component. The prognostic significance of these elements is not known, but since the frequency and extent of non-small cell elements are considerably greater in posttherapy and autopsy tissues, it is possible that the non-SCLC elements are more resistant to therapy than the SCLC cells. Metaplasia & dysplasia of the bronchial surface epithelium are frequently observed in the bronchial biopsy specimens that contain small cell carcinoma of the lung. We report a case of combined small cell carcinoma with squamous element associated with microinvasive squamous cell carcinoma of the bronchial surface epithelium in 68 year old male patient, stage was IIIa. The two lesion are not connected n serial sections.
Background: The surgical indications of stage IV non-small cell lung cancer(NSCLC) are extremely limited with its controversial results. We analyzed the surgical results and survival in selected patients with resectable stage IV NSCLC. Material and Method: We reviewed the medical records of 21 patients who underwent operation for stage IV NSCLC from Jan. 1992 to Sep. 1999. Result: The mean age of patients was 55.6 years(range: 35 to 78). Sixteen were men and 5 were women. Tissue types were squamous cell carcinoma in 10(45.5%), adenocarcinoma in 9(40.9%), large cell carcinoma in 1 and carcinosarcoma in 1. Distant metastatic lesions were ipsilateral other lobe of lung in 18, brain in 2 and adrenal gland in 1. Pneumonectomy was performed in 16 patients, bilobectomy in 3, and lobectomy in 2 who underwent previous operatin for brain metastasis. Mean follow-up duration was 21.2$\pm$17.7 months. During follow-up period, 13 patients died. Three-and 5-year survival of patients were 38.0% and 19.0%, the median survival time was 19.1$\pm$7.8 months. In the group with ipsilateral pulonary metastasis(PM, n=18), 3- and 5-year survival of patients with N0 and N1(n=9) disease were 64.8% and 32.4%, median survival time was 55.3$\pm$27.2 months. Three-year survival of patients with N2(n=9) disease was 11.1%, median survival time was 10.6$\pm$0.3 months. The survival of N0 and N1 disease group was significantly better than that of N2 disease group(p=0.042). Also the disease free survival of N0 and N1 was significantly better than that of N2 disease in overall group(53.3 months vs 12.1 months, p=0.036) and ipsilateral PM group(63.4 months vs 8.8 months, p=0.001). Conclusion: We suggest that surgical treatment is worthful modality in well selected patients with stage IV NHSCLC especially with ipsilateral PM and N0 or N1 disease,. Nevertheless our study indicate questions that will need to be experienced further in larger studies.
Kim, Seo-Woo;Kim, Hyun-Kyung;Jeun, Sung-Joung;Park, Hye-Sung;Jang, Jung-Hyun;Lee, Jin-Hwa;Ryu, Yon-Ju;Sim, Sung-Shin;Chun, Eun-Mi
Tuberculosis and Respiratory Diseases
/
v.68
no.4
/
pp.231-235
/
2010
Lymphadenopathy in the thoracic cavity is frequently caused by inflammatory diseases. In very rare cases, the node-bronchial fistula has been reported to be the cause of complications of pulmonary tuberculosis. A male patient with necrotizing pneumonia and mediastinal lymph node enlargements identified by chest computed tomography was also found to have a node-bronchial fistula caused by lung cancer. The patient was treated for tuberculosis with pneumonia for one week before a definitive diagnosis was made. A further investigation revealed him to have non-small cell lung cancer (NSCLC, adenocarcinoma) and multiple mediastinal lymphadenopathies accompanied with the node-bronchial fistula. We report this specific case that had been previously treated for tuberculosis but was later revealed to be NSCLC accompanied with a node-bronchial fistula.
Background : It has been generally known that the incidence of lung cancer is higher in the patients with idopathic pumonary fibrosis (IPF) than those in general population. The reported incidence was variable from 4.8 to 43.2%. There were controversies on the most frequent cell type (squamous cell carcinoma vs. adenocarcinoma) and no study was done about the real concordance of cancer and the fibrotic lesion. And the pulmonary fibrosis may influence not only the development of cancer but also the treatment and prognosis of the cancer, but there was no report on that point. Method : Total 63 patients ($66.8{\pm}7.8$ year, M : F=61 : 2) were diagnosed as IPF combined with lung cancer (IFF-CA) at Asan Medical Center. A retrospective analysis was done about the risk factors of the lung cancer, pulmonary function test, the site of cancer(especially the relationship of the cancer with the fibrotic lesion), the histologic types, and the stage of cancer. The histologic types were compared with those of 2,660 patients with lung cancer who were diagnosed at the same institute for the same period. The effect of IPF on the treatment of the cancer was evaluated with the survival time after the detection of lung cancer. Results : The lung cancer was found in 63(22.9%) out of 281 patients with IPF. But in most of them(45 patients), lung cancer was detected at the same time with IPF and only in 18 patients, the cancer was diagnosed during the follow-up($25.2{\pm}17.7$ months) of IPF. So in our study, 6.7% of patients with IPF developed lung cancer during the course of the disease. The age ($66.8{\pm}7.84$ vs. $63.4{\pm}11.1$ years), percentage of smoker (88.9 vs. 67.2%), and the male gender (96.8 vs. 67.6%) were significantly higher in IPF-CA compared with lone IPF (p<0.05). The odds ratio of smoking was 4.7 compared with non smoking IPF controls. The lung cancer was located more frequently in the upper lobe and 55.5% was in the periphery of lung. The cancer was developed in the fibrotic lesion in 23 patients (35.9%), and in the majority of the patients, the cancer was separated from the fibrosis. The cell type of the lung cancer in IPF-CA was squamous cell carcinoma 34.9%, adenocarcinoma 30.2%, small cell carcinoma 19.0%, large cell undifferenciated carcinoma 6.3%, and others 9.5%. No significant difference in the distribution of histologic type of the lung cancer was found between IPF-CA and lone lung cancer. There was no significant difference in demographic features, cell types, location and the stage of the cancer between the group with concurrent IPF-CA and the group with cancer diagnosed during the follow up of IPF. There was a tendency (but statistically not significant : p=0.081) of higher incidence of adenocarcinoma among the cancers developed in the fibrotic area(43.5%) (F-CA) than in the cancers in non-fibrotic area (22.5%) (NF-CA). The prognosis of the patients with F-CA was poor (median survival : 4 months) compared with the patients with NF-CA (7 months, p=0.013), partly because the prevalence of severe IPF (the extent of fibrosis in HRCT 50%) was higher in F-CA group. Conclusion : These data suggest that the lung cancer in the patients with IPF has similar features to the ordinary lung cancer.
Background: Many functional molecules controlling diverse cellular function are included in low-molecular weight proteins and peptides. Materials and Methods: To identify proteins controlling function in lung adenocarcinomas (AC), we performed two-dimensional gel electrophoresis employing tricine-SDS polyacrylamide in the second dimension (tricine 2-DE). This system was able to detect proteins under 1 kDa even with post-translational modifications. To confirm the utility of detected proteins as novel tumor markers for AC, we performed immunohistochemical analysis using 170 formalin-fixed and paraffin-embedded lung AC tissues. Results: Tricine 2-DE revealed that five proteins including S100A16 were overexpressed in lung AC-derived cells compared with lung squamous cell carcinoma, small cell carcinoma, and large cell neuroendocrine carcinoma-derived cells. Immunohistochemically, S100A16 showed various subcellular localization in lung cancer tissues and a membranous staining status was correlated with the T-factor (P=0.0008), pathological stage (P=0.0015), differentiation extent (P=0.0001), lymphatic invasion (P=0.0007), vascular invasion (P=0.0001), pleural invasion (P=0.0087), and gender (P=0.039), but not with the age or smoking history. More importantly, membranous staining of S100A16 was significantly correlated with a poorer overall survival of either stage I (P=0.0088) or stage II / III (P=0.0003) lung AC patients, and multivariate analysis confirmed that membranous expression of S100A16 was an independent adverse prognostic indicator (P=0.0001). Conclusions: The present results suggest that S100A16 protein is a novel prognostic marker for lung AC.
From May 1988 to December 1995, 77 patients underwent surgical re ection for primary non-small cell lung cancer at GNUH, and were evaluated clinically. There were 65 males and 12 females(M:P=5.4:1), and the peak incidence of age was 6th decade of life(44.5%). The major symptoms were cough, hemoptysis and chest pain due to anatomical effects of the mass. Histopathologically, squamous cell carcinoma was 81.8%, adenocarcinoma 14.3%, and adenosquamous carcinoma 3.9% . There was no significant difference in survival among three groups. The pneumonectomy was performed in 26 cases(33.8%), lobectomy 30 cases(38.9%), bilobectomy 9 cases(11.7%), and overall resectability was 84.4%. The postoperative official stagings were as follows ; 26 patients of stage I(34%), 14 patients of stage II(18%), 22 patients of stage IIIa(29%), 14 patients of stage IIIb(18%), and one patients of stage IV(1%). In all cases, 3 year survival rate are showed stage 183%, stage II 26%, stage IIIa 17%, and stage IIIb 0%.
Background: Recent studies have demonstrated that the epidermal growth factor receptor (EGFR) genotype is the most important predictive marker to EGFR-tyrosine kinase inhibitors (TKIs) and first-line gefitinib treatment will be approved in the near future for use in non-small cell lung cancer (NSCLC) patients with the EGFR mutation. Direct sequencing is known to be the standard for detecting EGFR mutations; however, it has limited sensitivity. Peptide nucleic acids (PNA)-mediated PCR clamping method is a newly introduced method for analyzing EGFR mutations with increased sensitivity and stability. Methods: A total of 71 NSCLC patients were analyzed for EGFR mutations using the PNA-mediated PCR clamping technique. Sixty-nine patients were analyzed for clinicopathologic correlation with EGFR genotype; 2 patients with indeterminate results were excluded. In order to determine EGFR-TKI drug response, 57 patients (42 gefitinib, 15 erlotinib) were included in the analysis. Results: The EGFR mutation rate was 47.8%. Being female, a non-smoker, and having adenocarcinoma were favorable clinicopathologic factors, as expected. However, more than a few smokers (33.3%), male (28.1%), and patients with non-adenocarcinoma (28.6%) had the EGFR mutation. Having a combination of favorable clinicopathologic factors did not increase the EGFR mutation rate significantly. Drug response to EGFR-TKIs showed significant differences depending on the EGFR genotype; ORR was 14.3% for wild type vs 69.0% for mutant type; DCR is 28.6% for wild type vs 96.6% for mutant type. The median EGFR-TKI treatment duration is 7.6 months for mutant type group and 1.4 months for wild type group. Conclusion: EGFR genotype determined using the PNA-mediated PCR clamping method is significantly correlated with the clinical EGFR-TKI responses and PNA-mediated PCR.
Lee, Ghie Dong;Shin, Min Ki;Lee, Kang Wan;Cho, Yu Ji;Kim, Ho Chul;Hwang, Young Sil
Tuberculosis and Respiratory Diseases
/
v.54
no.5
/
pp.563-569
/
2003
Background : Pleural effusions with high amylase levels are reported frequently in patients with pancreatic diseases, a rupture of the esophagus and a malignancy. However, there is no data available on the clinical features of an amylase-rich pleural effusion in Korea. This report describes the causes of the high amylase levels in a pleural effusion and analyzes its association with malignancy. Methods : The records of patients with an amylase-rich pleural effusion who were assessed at the Gyeongsang National University Hospital from January 1998 to August 2002 were examined retrospectively, and the distribution of amylase levels in those patients, the causative diseases, and the histological type in the case of a malignancy were analyzed. Among the 532 patients whose pleural effusion was evident on a chest X-ray, there were 36 cases with an amylase-rich pleural effusion. The amylase levels were determined by an enzyme method (Hitach 747 autoanalyzer). Results : Of the 36 patients with an amylase-rich pleural effusion, there were 18 patients(50%) associated with a malignancy, 8 patients(22%) with a parapneumonic effusion, 7 patients(19%) with pancreatic disease, and 3 patients with other causes. The amylase level in a pleural effusion due to pancreatic disease was much higher than that due to other causes(p<0.01). Among the malignant pleural effusions with high amylase levels, the origin of the malignancy was a primary lung cancer in 13 cases and metastatic lung cancer in 5 cases. The histological types of malignant causes were adenocarcinoma in 10 cases(56%), squamous cell carcinoma in 2 cases(11%) and unknown type of carcinoma in 6 cases. The amylase level in the adenocarcinoma cases was much higher than that in the other cell type carcinomas(p<0.01). There was no significant association between the amylase level and the glucose level among the malignant cases with amylase-rich pleural effusion(p=0.21). Conclusion : The most frequent cause of an amylase-rich pleural effusion was a malignancy. Primary lung cancer and adenocarcinoma were the most common malignancies and histological types associated with a malignant pleural effusion with high amylase levels. The amylase level in a pleural effusion secondary to pancreatic disease was much higher than from any other causes.
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