Journal of lung cancer最新文献

{"title":"Pulmonary Metastasectomy for Colorectal Carcinoma","authors":"K. Choi, Yang-Haeng Lee, Kyoung Taek Park, Il-Yong Han, Y. Yoon, Kwangjo Cho","doi":"10.6058/JLC.2010.9.2.91","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.91","url":null,"abstract":"Purpose: Surgical resection is an important curative treatment for pulmonary metastases from colorectal adenocarcinoma. We analyzed the outcomes and the prognostic factors related to the post operative mortality after surgical resection for pulmonary metastases from colorectal adenocarcinoma. Materials and Methods: Between January 1994 and December 2009, 28 patients underwent complete pulmonary resection of metastatic colorectal carcinoma. We performed a retrospective review of the patient’s characteristics and the factors affecting survival. Survival was analyzed by the Kaplan-Meier method and comparison between groups was performed by a log-rank analysis. Results: The median survival was 53.07 months (Kaplan-Meier method). The number of pulmonary metastases (p=0.0151) and a prethoracotomy carcinoembryonic antigen (CEA) level over 5 ng/mL (p=0.0217) were significantly related with survival. Conclusion: The prethoracotomy CEA level and the number of metastases were significantly related with the survival rate. Resection of pulmonary metastatic lung lesion from colorectal cancer may improve the survival rate in a selected group of patients. (J Lung Cancer 2010;9(2):91 󰠏 96)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"91-96"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.91","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160864","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum Carcinoembryonic Antigen as an Index of the Therapeutic Effect of EGFR-TKIs in Patients with Advanced Non-Small Cell Lung Cancer","authors":"Jin Hee Park, Sung Bin Kim, S. Nam, S. H. Jeong, C. Oak, T. Jang, M. Jung","doi":"10.6058/JLC.2010.9.2.97","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.97","url":null,"abstract":"Purpose: For treating advanced non-small cell lung cancer (NSCLC), epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are known to be very effective in nonsmokers, women, Asian and person with EGFR mutations. The efficacy of EGFR-TKI was analyzed based on the radiologic studies and the serum levels of carcinoembryonic antigen (CEA) to evaluate whether serum CEA can be used as a predicative marker of the response to EGFR-TKI therapy. Materials and Methods: Forty-one patients with NSCLC treated with gefitinib at Kosin Medical Center from January 2007 to August 2009 were the subjects of this study. We assayed the serum CEA levels before and after gefitinib therapy with concomitant assessments of the tumor response by serial chest X-ray and chest computer tomograms (CT). Results: The median age of the patients was 62.6 years (range, 32∼77 years), 29 patients were women, 36 had adenocarcinoma (87.8%) and the baseline serum CEA was equal or above 5 ng/mL in 31 patients (75.6%). These 31 patients were more responsive to the gefitinib therapy (p=0.021). The overall response rate of the patients was 51.2%, the median survival time was 21.9 months and the time to progression was 8.3 months. Among the 21 responding patients, the serum CEA was decreased after 2 months in 17 (80.9%), and among the 14 progressed patients, the serum CEA was increased in 12 (85.7%) (p=0.000). Conclusion: The changes of serum CEA at 2 months after gefitinib therapy were closely related to the radiologic changes. The serum CEA could be used as a complimentary tool for monitoring the tumor response to EGFR-TKI in the advanced NSCLC patients. (J Lung Cancer 2010;9(2):97 �� 102)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"97-102"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.97","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71161032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory Effect of Epidermal Growth Factor on the Proliferation of Lung Cancer Cell Lines","authors":"Seunghee Lee, Hong-Gyun Wu","doi":"10.6058/JLC.2010.9.2.64","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.64","url":null,"abstract":"Purpose: Epidermal growth factor (EGF) is known to cause cellular proliferation, differentiation and survival. However, there are a few articles that have reported on the cell killing effect of EGF. We evaluated the effects of EGF on the survival of some lung cancer cell lines and we tried to determine the mechanism of action. Materials and Methods: We examined various lung cancer cell lines. The cultured cells were exposed to radiation alone (0, 2, 5, and 10 Gy), EGF alone (0 ∼1,000 nM) or a combination of radiation and EGF (10 nM). Survival was measured using a clonogenic assay and the expressions of epidermal growth factor receptor (EGFR), Ki-67 and cleavedPARP were detected by western blot analysis. K-ras mutations were detected using polymerase chain reaction and sequencing. Results: Treatment of EGF induced cell death in the lung cancer cell lines. The addition of EGF (10 nM) to radiation (0, 2, 5, and 10 Gy) resulted in an increased cell killing effect of radiation. The EGFR expression decreased with the addition of EGF. EGF increased the expression of cleaved-PARP, but it did not increase the expression of Ki-67. The effects of EGF were not correlated with EGFR mutation or K-ras mutation. Conclusion: In our study, EGF inhibited the proliferation of lung cancer cell lines and it induced apoptosis. EGF enhanced the radiosensitivity of lung cancer cells when EGF was combined with radiation. It is suggested that EGF seem to be one of the cytotoxic agents for lung cancer cell lines. (J Lung Cancer 2010;9(2):64 �� 71)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"64-71"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tumor Lysis Syndrome Induced by Radiotherapy in Non-Small Cell Lung Cancer.","authors":"D. Noh, K. Hwang, J. Shin, Dong Kim, Kyung-Hwa Cho, K. Choi, S. Park, E. Jeong, H. Kim","doi":"10.6058/JLC.2010.9.2.106","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.106","url":null,"abstract":"Tumor lysis syndrome (TLS) is an oncologic emergency that is characterized by numerous metabolic abnormalities, including hyperuricemic nephropathy, hyperphosphatemia, hypocalcemia, hyperkalemia and increased serum creatinine. This syndrome is common for tumors with rapid cell turnover and growth rates, and for bulky tumors with high sensitivity to anti-neoplastic treatments. Hence, TLS is a well-recognized clinical problem in hematologic malignancies. TLS is rarely observed to be induced in solid tumors by chemotherapy. Herein we present the second case of TLS that developed during radiotherapy in a patient with non-small cell lung cancer. (J Lung Cancer","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"106-109"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.106","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High-Dose Involved Field Radiotherapy and Concurrent Chemotherapy for Limited-Disease Small Cell Lung Cancer","authors":"N. Jang, J. Kim, J. Lee, C. Song","doi":"10.6058/JLC.2010.9.2.85","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.85","url":null,"abstract":"Purpose: We evaluated the effect of high dose involved field radiotherapy and concurrent chemotherapy for treating patients with limited disease, small cell lung cancer. Materials and Methods: We reviewed the medical records of 37 patients who had a limited stage of small cell lung cancer. All the patients were treated with induction chemotherapy followed by definitive radiotherapy and concurrent chemotherapy. The radiation dose was 60 Gy for 31 patients and 50 ∼58 Gy for 6 patients with once-daily 2 Gy fractions. Elective nodal irradiation was not performed. The chemotherapy regimen was either combinations of etoposide and cisplatin or irinotecan and cisplatin. Prophylactic cranial irradiation of 25 Gy at 2.5 Gy per fraction was administered to the patients who had a complete or near complete response. The median follow-up period was 17 months (range, 5 ∼57). Results: The 2-year overall survival and locoregional control rates were both 55%. A complete response was achieved in 17 patients (46%), a partial response was achieved in 19 patients (51%) and 1 patient (3%) had progressive disease. Seven patients experienced tumor recurrence in the radiation field and four of those recurrences were isolated local recurrences. There was only one isolated regional recurrence outside the radiation field. Grade 3 treatment- related esophageal toxicity occurred in 2 patients. Two patients died of treatment-related pulmonary complications. Conclusion: Involved field radiotherapy of 60 Gy can achieve favorable survival and a low rate of isolated nodal failure outside the radiation field. However, a considerable number of patients still experienced in-field failure. Further studies to establish the optimal radiation doses and fractionation are needed in the future. (J Lung Cancer 2010;9(2):85 �� 90)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"85-90"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.85","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutational and Expressional Analysis of ATG5 Gene in Non-Small Cell Lung Cancers","authors":"M. S. Kim, N. Yoo, S. Lee","doi":"10.6058/JLC.2010.9.2.72","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.72","url":null,"abstract":"Purpose: Several lines of evidence have indicated that perturbations of autophagy are involved in the development of many human diseases, including cancer. The autophagy-related genes (ATG) encode proteins that play important roles in autophagic processes. The aim of this study was to see whether alterations of the ATG5 protein expression and somatic mutations of the ATG5 gene are present in human non-small cell lung cancers (NSCLCs). Materials and Methods: We analyzed the ATG5 somatic mutations in 45 NSCLCs by performing single-strand conformation polymorphism (SSCP). We examined the ATG5 protein expression in 45 NSCLCs by performing immunohistochemistry. Results: The SSCP analysis revealed no evidence of somatic mutation in the DNA sequences encoding the ATG5 gene in the 45 NSCLCs. On the immunohistochemistry, ATG5 protein was expressed in the normal bronchial epithelial cells, while it was lost in 9 (20%) of the NSCLCs. Conclusion: Our data indicates that ATG5 is altered in NSCLC at the expressional level, but not at the mutational level. The data also suggests that the loss of expression of ATG5 might play a role in the pathogenesis of NSCLC by altering autophagic and apoptotic cell death. (J Lung Cancer 2010;9(2):72 �� 76)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"72-76"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.72","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160636","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combination Therapy of Bortezomib (PS-341) and SAHA (Vorinostat) in Non-Small Cell Lung Cancer Cell Lines","authors":"M. Park, Dalrae Kim, Jong-Sun Park, Y. Cho, S. Lee, H. Yoon, Jae Ho Lee, C. Lee","doi":"10.6058/JLC.2010.9.2.77","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.77","url":null,"abstract":"Purpose: The recent introduction of targeted therapy for non-small cell lung cancer (NSCLC) has changed the paradigm of lung cancer chemotherapy. However, only a small portion of NSCLC patients received the benefit of these new drugs. A proteasome inhibitor (bortezomib) and a histone deacetylase inhibitor (SAHA) were approved for clinical use for treating some hematologic malignancies. In this study, we investigated the combination treatment of bortezomib and SAHA in NSCLC cell lines. Materials and Methods: The combined effects of bortezomib and SAHA on lung cancer cell lines were measured by Calcusyn software. Induction of apoptosis was examined by performing an Annexin V assay. Generation of reactive oxygen species (ROS) and protection by N-acetylcysteine were measured by flow cytometry after staining with DCFH-DA. The effect of the combination of drugs on apoptosis and autophagy was investigated by Western blot assay. Results: Strong synergism was found for the combination of bortezomib and SAHA. The synergistic interaction was mediated by strong apoptosis. Increased ROS generation was partly responsible for the induction of apoptosis, and this was suppressed by the ROS scavenger N-acetylcysteine. Combined treatment induced the strong activation of caspase-3 and the breakdown of the antiapoptotic molecule Bcl-2. Furthermore, increased breakdown of beclin-1, which is known to be an autophagic molecule, was also found. Conclusion: Combination therapy with bortezomib and SAHA showed a strong synergistic antitumor effect on human lung cancer cell lines. Enhanced induction of apoptosis was a responsible mechanism, and this was partly mediated by ROS generation. Further studies are warranted for determining the role of apoptosis and autophagy for this combination therapy. (J Lung Cancer","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"77-84"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.77","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphological Features of the Most Advanced Intra-Tumor Component in Multistep Progression","authors":"Y. Yatabe","doi":"10.6058/JLC.2010.9.2.53","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.53","url":null,"abstract":"Advances in basic life science during the past decade have exponentially increased our understanding of the molecular bases of lung cancers and this improved insight has had great effects on diagnosis, prognosis, classification, and treatment of cancer. Similar to colorectal carcinoma, stepwise development of lung cancer has been proposed. For squamous neoplasm, dysplasia is considered to progress to invasive cancer through carcinoma in-situ in association with accumulations of genetic and epigenetic alterations. In lung adenocarcinoma, a preinvasive lesion, termed atypical adenomatous hyperplasia, progresses to an adenocarcinoma in situ, namely a bronchioloalveolar carcinoma, followed by an invasive adenocarcinoma. Currently, molecular alterations, which are involved in each transition, have been also revealed. In this review, I would like to discuss correlation of morphological features with the progression of lung adenocarcinoma with special reference to the most advanced component within the tumor. (J Lung Cancer 2010;9(2):53 �� 56)","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"53-56"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.53","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Female Lung Cancer: Re-Analysis of National Survey of Lung Cancer in Korea, 2005","authors":"T. Jang, Young-chul Kim, Yong-Soo Kwon, I. Oh, K. S. Kim, S. Kim, J. Ryu, H. Yum, K. Lee, S. Yong, C. Lee, Sang Yeub Lee, Sung-Yong Lee, E. Jeong, K. In, M. Jung","doi":"10.6058/JLC.2010.9.2.57","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.2.57","url":null,"abstract":"Purpose: Female lung cancers have different clinical features and therapeutic results as compared to those of male lung cancers. The aim of this study was to analyze the differences of Korean men and women with lung cancer. Materials and Methods: We re-analyzed the results of a national survey of lung cancer conducted by the Korean Association for the Study of Lung Cancer in 2005. Results: Of the 8,788 patients, 2,124 (24.2%) were female. The mean age at the diagnosis was 62.5 years for the females and 64.8 years for the males and the difference was significant (p ＜0.001). An age ＜50 years was more frequent for the women than for the men (16.2% vs. 7.9%, respectively; p=0.001). The stages between genders were different for the patients with non-small cell carcinoma (NSCLC) (p ＜0.001), but not for the patients with small cell carcinoma. The overall survival time was longer for woman than that for the man (p ＜0.001). However, the male patients had longer survival for the smokers with adenocarcinoma and the smokers with squamous cell carcinoma. The never smoker female patients had a better survival time than did the smoking female patients, but the male patient’ survival was not influenced by the smoking status. The stage-specific survival rates were better for the women at all stages of NSCLC (p ＜0.001). The women who received chemotherapy had a longer survival time did the men who received chemotherapy (p ＜0.001). Conclusion: Women with lung cancer were relatively overrepresented among the younger patients and they smoked less intensively, raising the question of gender- specific differences in the carcinogenesis of lung cancer. Over-representation of adenocarcinoma was observed in the women regardless of their smoking status. Women with lung cancer had a better prognosis than men; however, the smoking females showed the worst prognosis. Gender and the smoking status are clearly important factors in the therapeutic approach to lung cancer.","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"57-63"},"PeriodicalIF":0.0,"publicationDate":"2010-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.2.57","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary Acinic Cell Carcinoma of the Lung: A Case Report","authors":"Junhun Cho, Tae-Eun Kim, Joungho Han, Kwhanmien Kim, T. S. Kim","doi":"10.6058/JLC.2010.9.1.20","DOIUrl":"https://doi.org/10.6058/JLC.2010.9.1.20","url":null,"abstract":"Primary acinic cell carcinoma (ACC) of the lung is very rare and this tumor is thought to arise from pluripotent cells of the submucosal glands of the tracheobronchial tree. We report here on a case of primary ACC of the lung in a 68-year-old man who had a solitary pulmonary nodule in the left lower lobe. The patient was symptomless and the lesion was found on a chest X-ray taken during a regular health checkup. The video assisted thoracoscopic surgery wedge resection revealed an ovoid yellow tan solid mass that was 1.8 cm at the largest diameter. Microscopically, the neoplastic cells grew in solid sheets of round cells with eccentric nuclei and abundant basophilic granular cytoplasm. There were no mitotic figures or areas of pleomorphic or anaplastic cells. Immunohistochemical staining for cytokeratin (AE1/AE3) was positive, but the staining for chromogranin A and CD56 was negative. Ultrastructural examination revealed polyhedral cells with many zymogen granules of varying electron density. The patient is well 4 months postoperatively.","PeriodicalId":90901,"journal":{"name":"Journal of lung cancer","volume":"9 1","pages":"20-23"},"PeriodicalIF":0.0,"publicationDate":"2010-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.6058/JLC.2010.9.1.20","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71160696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}