{"title":"Treatment of Non-Small-Cell Lung Cancer with Erlotinib following Gefitinib-Induced Hepatotoxicity: Review of 8 Clinical Cases.","authors":"Yukihiro Yano, Yoshinobu Namba, Masahide Mori, Yukie Nakazawa, Ayumi Nashi, Shinichi Kagami, Manabu Niinaka, Tsutomu Yoneda, Hiromi Kimura, Toshihiko Yamaguchi, Soichiro Yokota","doi":"10.1155/2012/354657","DOIUrl":"https://doi.org/10.1155/2012/354657","url":null,"abstract":"<p><p>Objective. Gefitinib often induces liver damage. A few reports have described that the subsequent administration of erlotinib was associated with less hepatotoxicity, but the safety and efficacy of this treatment are still not fully investigated. Therefore, we evaluated retrospectively the patients with erlotinib following gefitinib-induced hepatotoxicity. Methods and Patients. We retrospectively reviewed the medical records between December 2007 and March 2010. The patients were evaluated including the following information: age, gender, histology of lung cancer, performance status, smoking status, epidermal growth factor receptor (EGFR) mutation status, liver metastasis, viral hepatitis, alcoholic liver injury, clinical response, and hepatotoxicity due to EGFR tyrosine kinase inhibitors. Results. We identified 8 patients with erlotinib following gefitinib-induced hepatotoxicity. All achieved disease control by gefitinib. Hepatotoxicity was grades 2 and 3 in 3 and 5 patients, respectively. The median duration of treatment with gefitinib was 112.5 days and the median time to gefitinib-induced hepatotoxicity was 51.5 days. The median duration of treatment with erlotinib was 171.5 days. Grade 1 and 2 erlotinib-induced hepatotoxicity was observed in 2 and 1 patient, respectively. Conclusions. Erlotinib administration with careful monitoring is thought to be a good alternative strategy for patients who respond well to gefitinib treatment but experience hepatotoxicity. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2012 ","pages":"354657"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/354657","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33959370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Preoperative Total Serum Cholesterol and Patients' Survival in Resected Nonsmall Cell Lung Cancer.","authors":"Masaki Tomita, Takanori Ayabe, Tetsuya Shimizu, Kunihide Nakamura","doi":"10.1155/2012/463520","DOIUrl":"https://doi.org/10.1155/2012/463520","url":null,"abstract":"<p><p>The association between hypocholesterolemia and lung cancer risk has been confirmed in some studies. The purpose of the study was to determine whether preoperative hypocholesterolemia (below normal range) is a prognostic factor for survival after nonsmall cell lung cancer (NSCLC) resection. Two hundred and sixty-two consecutive cases of resected NSCLC with a followup period for more than 5 years were reviewed retrospectively. In our results, there were only 13/262 patients having hypocholesterolemia. A significant association was observed between preoperative hypocholesterolemia and patients' survival. However, we failed to find the prognostic significance of preoperative hypocholesterolemia by univariate analysis. No statistical differences were also found by the comparison between 5-year survivors and the others. Our data indicates a trend toward an association between preoperative hypocholesterolemia and poorer survival in NSCLC; however, it did not reach statistical significance. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2012 ","pages":"463520"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/463520","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Against Lung Cancer Cells: To Be, or Not to Be, That Is the Problem.","authors":"Naoko Okumura, Hitomi Yoshida, Yasuko Kitagishi, Yuri Nishimura, Shio Iseki, Satoru Matsuda","doi":"10.1155/2012/659365","DOIUrl":"https://doi.org/10.1155/2012/659365","url":null,"abstract":"<p><p>Tobacco smoke and radioactive radon gas impose a high risk for lung cancer. The radon-derived ionizing radiation and some components of cigarette smoke induce oxidative stress by generating reactive oxygen species (ROS). Respiratory lung cells are subject to the ROS that causes DNA breaks, which subsequently bring about DNA mutagenesis and are intimately linked with carcinogenesis. The damaged cells by oxidative stress are often destroyed through the active apoptotic pathway. However, the ROS also perform critical signaling functions in stress responses, cell survival, and cell proliferation. Some molecules enhance radiation-induced tumor cell killing via the reduction in DNA repair levels. Hence the DNA repair levels may be a novel therapeutic modality in overcoming drug resistance in lung cancer. Either survival or apoptosis, which is determined by the balance between DNA damage and DNA repair levels, may lender the major problems in cancer therapy. The purpose of this paper is to take a closer look at risk factor and at therapy modulation factor in lung cancer relevant to the ROS. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2012 ","pages":"659365"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/659365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Molecular Markers with Predictive and Prognostic Relevance in Lung Cancer.","authors":"Alphy Rose-James, Sreelekha Tt","doi":"10.1155/2012/729532","DOIUrl":"https://doi.org/10.1155/2012/729532","url":null,"abstract":"<p><p>Lung cancer accounts for the majority of cancer-related deaths worldwide of which non-small-cell lung carcinoma alone takes a toll of around 85%. Platinum-based therapy is the stronghold for lung cancer at present. The discovery of various molecular alterations that underlie lung cancer has contributed to the development of specifically targeted therapies employing specific mutation inhibitors. Targeted chemotherapy based on molecular profiling has shown great promise in lung cancer treatment. Various molecular markers with predictive and prognostic significance in lung cancer have evolved as a result of advanced research. Testing of EGFR and Kras mutations is now a common practice among community oncologists, and more recently, ALK rearrangements have been added to this group. This paper discusses various predictive and prognostic markers that are being investigated and have shown significant relevance which can be exploited for targeted treatment in lung cancer. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2012 ","pages":"729532"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/729532","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cigarette Smoking and Lung Cancer: Pediatric Roots.","authors":"Norman Hymowitz","doi":"10.1155/2012/790841","DOIUrl":"https://doi.org/10.1155/2012/790841","url":null,"abstract":"<p><p>A vast array of data suggests that early age of smoking onset enhances the risk for development of lung cancer in adulthood. Initiation of smoking at a young age may influence the development of lung cancer because of its effect on duration of smoking. Early onset of smoking also may serve as an independent risk factor. It may increase the likelihood that smoking occurs during a critical period of development that enhances susceptibility to the adverse effects of cancer causing agents in cigarette smoke, thereby facilitating the initiation of the carcinogenic process. While evidence for the latter hypothesis derives from a variety of sources, definitive proof has proven elusive. Whether or not early age of smoking serves as an independent risk factor for lung carcinogenesis, the consensus of the public health community is that prevention of smoking onset at a young age and early cessation are keys to stemming the current lung cancer pandemic. Population approaches to tobacco prevention and control, such as measures contained in the World Health Organization Framework Convention Tobacco Control Treaty, offer the best opportunity, on the scale needed, to create a smoke-free world and bring an end to the pandemic of tobacco-related disease. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2012 ","pages":"790841"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2012/790841","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34129111","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Aggressive Palliation in Extensive Stage Small Cell Lung Cancer, Practice Guidelines versus Clinical Practice: A Case Report and Review of the Literature.","authors":"Edward F Miles, Laura L Jacimore, John W Nelson","doi":"10.4061/2011/659807","DOIUrl":"https://doi.org/10.4061/2011/659807","url":null,"abstract":"<p><p>Small cell lung cancer (SCLC) constitutes approximately 16% of all primary lung cancers, with more than 35,000 new cases per year. Two-thirds of patients present with extensive stage disease (ES-SCLC) due to a tendency to metastasize early. Outcomes remain poor, with a median survival of approximately 10 months and a two-year overall survival of <10%. Current recommendations call for combination chemotherapy alone in patients without localized symptoms. Thoracic radiation therapy following a good clinical response is controversial. We report on a patient with ES-SCLC that had an excellent response to chemotherapy and underwent whole brain radiotherapy for a known brain metastasis and consolidative radiotherapy to the thorax. His latest follow-up demonstrates only a stable residual pulmonary nodule and no evidence of active metastatic disease. ES-SCLC is a relatively common presentation with a variable burden of metastatic disease. In the absence of randomized trials demonstrating the efficacy of thoracic radiation therapy, the community radiation oncologist is placed in a difficult position when addressing these patients, particularly those with otherwise good performance status and a good response to initial systemic chemotherapy. More research in this area is sorely needed to help guide treatment recommendations. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2011 ","pages":"659807"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4061/2011/659807","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33959368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prognostic Factors in Advanced Non-Small-Cell Lung Cancer Patients: Patient Characteristics and Type of Chemotherapy.","authors":"Salah Abbasi, Ahmed Badheeb","doi":"10.4061/2011/152125","DOIUrl":"https://doi.org/10.4061/2011/152125","url":null,"abstract":"<p><p>Eleven prognostic factors were retrospectively analyzed in 270 newly diagnosed patients with advanced non-small-cell lung cancer including age, sex, performance status, histology, stage, smoking status, hemoglobin level, forced expiratory volume in one second (FEV1), weight loss >5% in 3 months preceding therapy, number of involved organs, and type of first-line chemotherapy. Response rate was 35.6%, and median survival was 8.2 months (95% CI, 7.8 to 8.7) for the whole group. Age ≤60 years (P = .016), FEV1 ≥ 2L (P = .03), and the use of platinum/docetaxel (P < .0001) were significantly associated with an improved survival. Histology did not affect outcome in the absence of targeted therapies. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2011 ","pages":"152125"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4061/2011/152125","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33959367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"An Atypical Presentation with Diagnostic Challenge of a Large Cell Neuroendocrine Cancer of Lung: A Case Report and Review of the Literature.","authors":"Pavan Kumar Bhamidipati, Amanda Ribbeck, Goldees Liaghati-Nasseri, Ramesh Kumar, Babu Paidipaty B, John Bartnik","doi":"10.4061/2011/912098","DOIUrl":"https://doi.org/10.4061/2011/912098","url":null,"abstract":"<p><p>Large-cell neuroendocrine carcinomas (LCNECs) are relatively rare and aggressive neoplasms of the lung with very poor prognosis. Even though they are included in the classification of nonsmall cell carcinomas, they have a biological behaviour and physiological response to treatment more like small cell carcinomas of lung. We report an atypical case presentation of LCNEC in a 51-year-old gentleman who presented with diffuse metastases to the thoracic and lumbar spine, brain, and liver, posing a diagnostic challenge. The primary small central lung tumor was in close proximity to major vessels, rendering a biopsy of the primary cancer challenging and nearly impossible. The final diagnosis was established through immunohistochemistry staining and examination of liver biopsy from a metastatic lesion. We also included a review of the current literature pertinent to LCNEC, as well as the important role of tumor markers plus immunohistochemistry profiles in determining the origin of unknown primary tumors in such difficult patient presentations. </p>","PeriodicalId":91139,"journal":{"name":"Lung cancer international","volume":"2011 ","pages":"912098"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4061/2011/912098","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33959369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}