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Lung Cancer Patients (lung + cancer_patient)
Kinds of Lung Cancer Patients Selected AbstractsFalse Beliefs a Threat to Lung Cancer PatientsCA: A CANCER JOURNAL FOR CLINICIANS, Issue 1 2004Article first published online: 31 DEC 200 No abstract is available for this article. [source] Breath gas aldehydes as biomarkers of lung cancerINTERNATIONAL JOURNAL OF CANCER, Issue 11 2010Patricia Fuchs Abstract There is experimental evidence that volatile substances in human breath can reflect presence of neoplasma. Volatile aldehydes were determined in exhaled breath of 12 lung cancer patients, 12 smokers and 12 healthy volunteers. Alveolar breath samples were collected under control of expired CO2. Reactive aldehydes were transformed into stable oximes by means of on-fiber-derivatization (SPME-OFD). Aldehyde concentrations in the ppt and ppb level were determined by means of gas chromatography-mass spectrometry (GC-MS). Exhaled concentrations were corrected for inspired values. Exhaled C1,C10 aldehydes could be detected in all healthy volunteers, smokers and lung cancer patients. Concentrations ranged from 7 pmol/l (161 pptV) for butanal to 71 nmol/l (1,582 ppbV) for formaldehyde. Highest inspired concentrations were found for formaldehyde and acetaldehyde (0,55 nmol/l and 0,13 nmol/l, respectively). Acetaldehyde, propanal, butanal, heptanal and decanal concentrations showed no significant differences for cancer patients, smokers and healthy volunteers. Exhaled pentanal, hexanal, octanal and nonanal concentrations were significantly higher in lung cancer patients than in smokers and healthy controls (ppentanal = 0.001; phexanal = 0.006; poctanal = 0.014; pnonanal = 0.025). Sensitivity and specificity of this method were comparable to the diagnostic certitude of conventional serum markers and CT imaging. Lung cancer patients could be identified by means of exhaled pentanal, hexanal, octanal and nonanal concentrations. Exhaled aldehydes reflect aspects of oxidative stress and tumor-specific tissue composition and metabolism. Noninvasive recognition of lung malignancies may be realized if analytical skills, biochemical knowledge and medical expertise are combined into a joint effort. [source] Lack of Evidence of Association of p21WAF1/CIP1 Polymorphism with Lung Cancer Susceptibility and Prognosis in TaiwanCANCER SCIENCE, Issue 1 2000Chuen-Ming Shih An association between the Arg allele of the p21WAF1/CIP1 codon 31 polymorphism and lung cancer has been reported. However, the genotype distribution of the p21 codon 31 polymorphism, as well as the association of this polymorphism with lung cancer risk and prognosis, remain undefined in the Taiwanese population. Therefore, we investigated the genotype distribution of the p21 codon 31 polymorphism in 155 lung cancer patients and 189 non-cancer controls. The genotype frequencies in the Taiwanese non-cancer controls were 0.51 (Ser) and 0.49 (Arg). ,2 analysis indicated significant differences in Taiwanese genotype distribution of p21 from those reported for Swedes (P=0.001), Caucasians (P=0.001), Indians (P=0.001), and African-Americans (P=0.001). However, our data did not demonstrate an association of the Arg allele of the p21 polymorphism with lung cancer risk in Taiwan. Lung cancer patients with Ser/Arg and Arg/Arg genotypes were at a nonsignificant 1.15-fold increased risk of lung cancer when compared to individuals with the Ser/Ser genotype (95%CI, 0.70,1.86). In addition, although p21 is a downstream target of p53, we found no significant correlation of the p21 polymorphism with the p53 polymorphism and p53 gene mutation in lung cancer patients. We further investigated the association of the p21 polymorphism with prognosis in 154 lung cancer patients. Patients with the Ser/Ser genotype tended to have a poorer prognosis than those with the Ser/Arg and Arg/Arg genotypes (P=0.097, by the log rank test). Our data suggest that the p21 codon 31 polymorphism may not play a significant role in cancer susceptibility and the prognosis of lung cancer patients in Taiwan. [source] Chemotherapy for an elderly lung cancer patient with chronic lymphocytic leukeamia (CCL)AUSTRALASIAN JOURNAL ON AGEING, Issue 3 2002Hiroaki Satoh No abstract is available for this article. [source] A possible role for dihydrodiol dehydrogenase in the formation of benzo[a]pyrene-DNA adducts in lung cancer cells and tumor tissuesENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 1 2007Ya-Wen Cheng Abstract Epidemiological studies indicate that there is a gender difference in the susceptibility to tobacco and environmental carcinogens, and this gender difference is suspected to result in a higher risk for lung cancer among women. However, the molecular mechanisms underlying this sexual dimorphism remain unclear. In the present study, we have evaluated the roles of CYP1A1 and dihydrodiol dehydrogenase (DDH) in the formation of benzo[a]pyrene (BaP) DNA adducts in various lung cancer cell lines. Among six lung cancer cell lines tested, higher adduct levels were observed in CL-3 and CL1-1 cells, which had relatively high expression of both CYP1A1 and DDH isoform 1 (DHH1). To determine whether a reduction in DDH expression changed the adduct levels, an siRNA was used to knock down DDH1 expression in CL-3 cells. The BaP adduct levels in siDDH-CL-3 cells increased 1.4,2.2-fold relative to that of the parental CL-3 cells. We also examined BaP-like DNA adducts, and CYP1A1 and DDH1 expression by immunohistochemistry in 120 lung tumors. Detection of DNA adducts correlated with CYP1A1-positive tumors (P = 0.023), but not with DDH1-positive tumors. In addition, 28 of 33 tumors (85%) that were CYP1A1-positive and DDH1-negative contained detectable levels of DNA adducts, a proportion that was higher than for tumors from the other three categories of CYP1A1 and DDH1 expression (P = 0.012). Finally, a greater proportion of adduct-positive tumors from females were CYP1A1-positive/DDH1-negative (45.3%) than were tumors from males (27.3%). These results suggest that the reduction of DDH expression in lung tumors may contribute to an increase in DNA adduct levels, which may be partly responsible for the higher susceptibility of female lung cancer patients to DNA damage. Environ. Mol. Mutagen., 2007. © 2006 Wiley-Liss, Inc. [source] Association of epidermal growth factor receptor mutations in lung cancer with chemosensitivity to gefitinib in isolated cancer cells from Japanese patientsEUROPEAN JOURNAL OF CANCER CARE, Issue 3 2007K. NAKATANI md, assistant professor Somatic mutations in the tyrosine kinase domain of the epidermal growth factor receptor (EGFR) gene are reported to be associated with clinical responsiveness of lung cancer to gefitinib, an EGFR tyrosine kinase inhibitor. To elucidate the association between somatic mutations and the pharmacological actions of gefitinib, the chemosensitivity of isolated cancer cells from the lungs of Japanese patients to gefitinib was examined by the collagen gel-droplet embedded culture drug sensitivity test in vitro. In 30 specimens isolated from non-small-cell lung cancer patients, mutations were observed in eight tumour specimens (27%) and chemosensitivity to gefitinib was observed in seven specimens (23%). However, somatic mutations were not predominantly associated with chemosensitivity to gefitinib in vitro. Both mutation and chemosensitivity frequencies in this study were higher than those reported in studies from the United States, indicating a possible ethnic difference. Moreover, both frequencies were much higher in females than in males. Since a gender difference in chemosensitivity to gefitinib was observed in isolated cancer cells in vitro, this suggests that gefitinib works in part through the suppression of EGFR signalling, but that other factors, including sex-related factors, may participate in gefitinib action. [source] Quality of life in lung cancer patients: impact of baseline clinical profile and respiratory statusEUROPEAN JOURNAL OF CANCER CARE, Issue 3 2007A. MOHAN md, assistant professor As cure is attainable in very few cases of lung cancer, the imperative issue is to make quality of life (QOL) as good as possible as part of the palliative care package. The aim of this paper was to evaluate the baseline QOL of lung cancer patients and observe its association with various clinical parameters and overall respiratory status. A total of 101 patients were administered the European Organization for Research and Treatment of Cancer core quality of life (EORTC QLQ-C30, version 3) questionnaire. Clinical profile and measures of respiratory status, including spirometry, measures of dyspnoea, and 6-min walk test, were recorded. Higher Karnofsky Performance Status (KPS) significantly correlated with better global health status (P < 0.001) and healthy level of functioning (P < 0.001). The cumulative symptom burden was significantly associated with global QOL (P = 0.01) and physical, role and cognitive function scales (P < 0.05). All dyspnoea measures negatively correlated with global QOL and functioning scales. Spirometric indices showed a positive correlation with all functional scales (P < 0.05) except social. In conclusion, lung cancer patients have unsatisfactory QOL, with the global health status and physical functions being most affected. Number of symptoms, KPS, dyspnoea and spirometry significantly affect QOL. [source] Breath gas aldehydes as biomarkers of lung cancerINTERNATIONAL JOURNAL OF CANCER, Issue 11 2010Patricia Fuchs Abstract There is experimental evidence that volatile substances in human breath can reflect presence of neoplasma. Volatile aldehydes were determined in exhaled breath of 12 lung cancer patients, 12 smokers and 12 healthy volunteers. Alveolar breath samples were collected under control of expired CO2. Reactive aldehydes were transformed into stable oximes by means of on-fiber-derivatization (SPME-OFD). Aldehyde concentrations in the ppt and ppb level were determined by means of gas chromatography-mass spectrometry (GC-MS). Exhaled concentrations were corrected for inspired values. Exhaled C1,C10 aldehydes could be detected in all healthy volunteers, smokers and lung cancer patients. Concentrations ranged from 7 pmol/l (161 pptV) for butanal to 71 nmol/l (1,582 ppbV) for formaldehyde. Highest inspired concentrations were found for formaldehyde and acetaldehyde (0,55 nmol/l and 0,13 nmol/l, respectively). Acetaldehyde, propanal, butanal, heptanal and decanal concentrations showed no significant differences for cancer patients, smokers and healthy volunteers. Exhaled pentanal, hexanal, octanal and nonanal concentrations were significantly higher in lung cancer patients than in smokers and healthy controls (ppentanal = 0.001; phexanal = 0.006; poctanal = 0.014; pnonanal = 0.025). Sensitivity and specificity of this method were comparable to the diagnostic certitude of conventional serum markers and CT imaging. Lung cancer patients could be identified by means of exhaled pentanal, hexanal, octanal and nonanal concentrations. Exhaled aldehydes reflect aspects of oxidative stress and tumor-specific tissue composition and metabolism. Noninvasive recognition of lung malignancies may be realized if analytical skills, biochemical knowledge and medical expertise are combined into a joint effort. [source] Methylation profile in tumor and sputum samples of lung cancer patients detected by spiral computed tomography: A nested case,control studyINTERNATIONAL JOURNAL OF CANCER, Issue 5 2006Rosalia Cirincione Abstract We evaluated the aberrant promoter methylation profile of a panel of 3 genes in DNA from tumor and sputum samples, in view of a complementary approach to spiral computed tomography (CT) for early diagnosis of lung cancer. The aberrant promoter methylation of RAR,2, p16INK4A and RASSF1A genes was evaluated by methylation-specific PCR in tumor samples of 29 CT-detected lung cancer patients, of which 18 had tumor-sputum pairs available for the analysis, and in the sputum samples from 112 cancer-free heavy smokers enrolled in a spiral CT trial. In tumor samples from 29 spiral CT-detected patients, promoter hypermethylation was identified in 19/29 (65.5%) cases for RAR,2, 12/29 (41.4%) for p16INK4A and 15/29 (51.7%) for RASSF1A. Twenty-three of twenty-nine (79.3%) samples of the tumors exhibited methylation in at least 1 gene. In the sputum samples of 18 patients, methylation was detected in 8/18 (44.4%) for RAR,2 and 1/18 (5%) for both RASSF1A and p16INK4A. At least 1 gene was methylated in 9/18 (50%) sputum samples. Promoter hypermethylation in sputum from 112 cancer-free smokers was observed in 58/112 (51.7%) for RAR,2 and 20/112 (17.8%) for p16, whereas methylation of the RASSF1A gene was found in only 1/112 (0.9%) sputum sample. Our study indicates that a high frequency of hypermethylation for RAR,2, p16INK4A and RASSF1A promoters is present in spiral CT-detected tumors, whereas promoter hypermethylation of this panel of genes in uninduced sputum has a limited diagnostic value in early lung cancer detection. © 2005 Wiley-Liss, Inc. [source] ,93G,A polymorphism of hMLH1 and risk of primary lung cancerINTERNATIONAL JOURNAL OF CANCER, Issue 4 2004Sun Ha Park Abstract Polymorphisms in DNA repair genes may be associated with differences in the repair capacity of DNA damage and may thereby influence an individual's susceptibility to smoking-related cancer. We investigated the association between the ,93G,A polymorphism in the hMLH1 gene and the risk of lung cancer in a Korean population. The hMLH1 ,93G,A polymorphism was typed in 372 lung cancer patients and 371 healthy controls that were frequency-matched for age and sex. There was no significant association between the hMLH1 ,93G,A genotype and the risk for adenocarcinoma or small cell carcinoma. However, the AA genotype was associated with a significantly increased risk for squamous cell carcinoma compared with both the GG genotype (adjusted OR = 2.02; 95% CI = 1.15,3.55; p = 0.014) and the combined GG and GA genotype (adjusted OR = 1.83; 95% CI = 1.24,2.71; p = 0.003). When the subjects were stratified by smoking exposure, the AA genotype was associated with a significantly increased risk for squamous cell carcinoma in lighter smokers (, 39 pack-years; adjusted OR = 1.95; 95% CI = 1.03,3.66; p = 0.039) compared with the combined GG and GA genotype, whereas there was no significant association in heavier smokers (> 39 pack-years; adjusted OR = 1.47; 95% CI = 0.82,2.61). These results suggest that the hMLH1 ,93G,A polymorphism could be used as a marker of genetic susceptibility to squamous cell carcinoma of the lung. © 2004 Wiley-Liss, Inc. [source] Myeloperoxidase (MPO) genotype and lung cancer histologic types: The MPO ,463 A allele is associated with reduced risk for small cell lung cancer in smokersINTERNATIONAL JOURNAL OF CANCER, Issue 5 2002Heike Dally Abstract MPO participates in the metabolic activation of tobacco carcinogens such as PAHs. A frequent MPO ,463 G,A polymorphism in the promoter region reduces MPO transcription and has been correlated with >4-fold lower benzo[a]pyrene,DNA adduct levels in the skin of coal tar,treated patients. Four of 7 case-control studies found significantly reduced lung cancer risk associated with the A allele. Due to their different etiologies, we examined whether the MPO genotype affects histologic lung cancer types differentially. A case-control study was conducted in 625 ever-smoking lung cancer patients, including 228 adenocarcinomas, 224 SCCs, 135 SCLCs and 340 ever-smoking hospital controls. MPO genotyping was performed by capillary PCR followed by fluorescence-based melting curve analysis. Combining the MPO ,463 (G/A+A/A) genotypes, a protective effect approaching significance (OR = 0.75, 95% CI 0.55,1.01) was observed when comparing all lung cancer cases to controls. Among histologic types of lung cancer, a weak protective effect was found for both adenocarcinoma (OR = 0.81, CI 0.55,1.19) and SCC (OR = 0.82, CI 0.56,1.21); a stronger and significant effect was found for SCLC (OR = 0.58, CI 0.36,0.95; p = 0.029). Our results also suggest that the MPO genotype varies among inflammatory nonmalignant lung diseases. In conclusion, our results emphasize the need for a separate analysis of lung cancer histologic types and an adjustment for inflammatory nonmalignant lung diseases in future MPO-related studies. We confirm that the MPO ,463 A variant affords a protective effect against lung cancer risk in smokers, which was strongest for SCLC patients. © 2002 Wiley-Liss, Inc. [source] Serum KL-6 levels in lung cancer patients with or without interstitial lung diseaseJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 5 2010Kunihiko Miyazaki Abstract Background: It is not known whether lung cancer patients with interstitial lung disease (ILD) might have higher serum levels of KL-6, a high molecular weight glycoprotein classified as a polymorphic epithelial mucin. In addition, prognosis of these patients with elevated serum KL-6 levels might be poorer than that with normal KL-6 levels, but it has not been well clarified. Methods: Serum KL-6 levels in 273 lung cancer patients with or without ILD, and prognostic significance of elevated serum KL-6 levels in these patients were studied using uni- and multivariate analyses. Results: Serum KL-6 levels were elevated (>500,U/ml) in 73.5% of lung cancer patients with ILD and in 33.7% of those without ILD. Serum KL-6 levels in lung cancer patients with ILD were significantly higher than those without ILD. In lung cancer patients with ILD, elevated serum KL-6 has no prognostic significance, but in those without ILD, however, it was one of the unfavorable prognostic factors. Conclusions: Elevated serum KL-6 levels can be observed in lung cancer patients both with and without ILD. Having ILD has strong prognostic impact in patients with lung cancer. In those without ILD, however, elevated KL-6 levels may be related to poor prognosis. J. Clin. Lab. Anal. 24:295,299, 2010. © 2010 Wiley-Liss, Inc. [source] Monitoring the care of lung cancer patients: linking audit and care pathwaysJOURNAL OF EVALUATION IN CLINICAL PRACTICE, Issue 1 2001E. Kaltenthaler BSc Abstract Clinical audit plays an important role in monitoring the provision of care for patients whatever their condition. Care pathways define the steps and expected course of events in the care of patients with a specific clinical problem over a set time scale. This paper describes a study undertaken in a multisite cancer unit to develop a tool for monitoring the progress of lung cancer patients through a care pathway and auditing key standards within the pathway. Important issues associated with the development of this tool are highlighted. The process of developing this tool involved the following steps: a review of the literature dealing with the management of lung cancer patients; interviews with key personnel in primary, secondary, tertiary and palliative care; development of a paper-based series of forms representing key steps in the patient's care pathway; 3-month trial of the paper-based tool; analysis of completion rates and interviews with form users to evaluate effectiveness; and recommendations for creating an electronic record using the experience and lessons learned from the paper version. The paper forms developed through this multistage process were found to be acceptable to users and have the potential to provide accurate information at key points for audit throughout the patient's time within the health-care system for their lung cancer condition. The flexibility of this methodology allows it to be adapted readily to a variety of clinical situations and conditions. [source] Intratumoural chemotherapy of lung cancer for diagnosis and treatment of draining lymph node metastasisJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 3 2010Firuz Celikoglu Abstract Objectives Reviewed here is the potential effectiveness of cytotoxic drugs delivered by intratumoural injection into endobronchial tumours through a bronchoscope for the treatment of non-small cell lung cancer and the diagnosis of occult or obvious cancer cell metastasis to mediastinal lymph nodes. Key findings Intratumoural lymphatic treatment may be achieved by injection of cisplatin or other cytotoxic drugs into the malignant tissue located in the lumen of the airways or in the peribronchial structures using a needle catheter through a flexible bronchoscope. This procedure is termed endobronchial intratumoural chemotherapy and its use before systemic chemotherapy and/or radiotherapy or surgery may provide a prophylactic or therapeutic treatment for eradication of micrometastases or occult metastases that migrate to the regional lymph nodes draining the tumour area. Conclusions To better elucidate the mode of action of direct injection of cytotoxic drugs into tumours, we review the physiology of lymphatic drainage and sentinel lymph node function. In this light, the potential efficacy of intratumoural chemotherapy for prophylaxis and locoregional therapy of cancer metastasis via the sentinel and regional lymph nodes is indicated. Randomized multicenter clinical studies are needed to evaluate this new and safe procedure designed to improve the condition of non-small cell lung cancer patients and prolong their survival. [source] Five years survival in metastatic non-small cell lung cancer patients treated with chemotherapy alone or chemotherapy and melatonin: a randomized trialJOURNAL OF PINEAL RESEARCH, Issue 1 2003P. Lissoni Abstract: Numerous experimental data have documented the oncostatic properties of melatonin. In addition to its potential direct antitumor activity, melatonin has proved to modulate the effects of cancer chemotherapy, by enhancing its therapeutic efficacy and reducing its toxicity. The increase in chemotherapeutic efficacy by melatonin may depend on two main mechanisms, namely prevention of chemotherapy-induced lymphocyte damage and its antioxidant effect, which has been proved to amplify cytotoxic actions of the chemotherapeutic agents against cancer cells. However, the clinical results available at present with melatonin and chemotherapy in the treatment of human neoplasms are generally limited to the evaluation of 1-year survival in patients with very advanced disease. Thus, the present study was performed to assess the 5-year survival results in metastatic non-small cell lung cancer patients obtained with a chemotherapeutic regimen consisting of cisplatin and etoposide, with or without the concomitant administration of melatonin (20 mg/day orally in the evening). The study included 100 consecutive patients who were randomized to receive chemotherapy alone or chemotherapy and melatonin. Both the overall tumor regression rate and the 5-year survival results were significantly higher in patients concomitantly treated with melatonin. In particular, no patient treated with chemotherapy alone was alive after 2 years, whereas a 5-year survival was achieved in three of 49 (6%) patients treated with chemotherapy and melatonin. Moreover, chemotherapy was better tolerated in patients treated with melatonin. This study confirms, in a considerable number of patients and for a long follow-up period, the possibility to improve the efficacy of chemotherapy in terms of both survival and quality of life by a concomitant administration of melatonin. This suggests a new biochemotherapeutic strategy in the treatment of human neoplasms. [source] Elevated activities of MMP-2 in the non-tumorous lung tissues of curatively resected stage I NSCLC patients are associated with tumor recurrence and a poor survival,JOURNAL OF SURGICAL ONCOLOGY, Issue 4 2007Sang-Hui Kim Abstract Background and Objectives We wanted to assess whether the level of enzyme activity for a particular matrix metalloproteinase (MMP), and not the amount of expressed protein, in lung tissue could be used as a reliable prognostic biomarker for tumor recurrence leading to poorer survival in a certain subgroup of patients who have undergone curative resection for stage I human NSCLC. Methods We determined what type of MMP was significant for tumor recurrence by using a mouse model of pulmonary metastasis with inoculating the footpad with H460 human cancer cells. We then looked for any association between tumor recurrence and the level of enzyme activities for the selected MMP in the tumor and also in the pathologically non-tumorous tissues from 34 stage I lung cancer patients. Results We obtained H460/PM6 cells having a highly metastatic potential after six repeated cycles of pulmonary metastasis by using the mouse footpad inoculated with the metastasized cancer cells in the previous cycle. We started with human lung cancer cells, H460, and we found that among the tested MMPs we tested for, the level of MMP-2 mRNA was elevated. No significant difference was seen in the level of enzyme activity of the MMP-2 cells from the curatively resected tumor tissues of the stage I NSCLC patients who were later found with or without recurrence. However, the level of MMP-2 enzyme activity was found to be significantly different between the non-tumorous lung tissues from patients later found with and without recurrence, and it was associated with the 5-year survival rate. Conclusions This observation suggests that the higher level of MMP-2 enzyme activity in the non-tumorous tissues from the patients could be used as a prognostic biomarker to predict post-operative tumor recurrence and survival for patients with stage I NSCLC. The elevated enzyme activity of MMP-2 in the non-tumorous tissue resected from stage I NSCLC could be used as a prognostic indicator for post-operative tumor recurrence and the patients' poor survival. Further, this could be an important aid for physicians' making decision on whether to subject particular patients to post-operative adjunct chemotherapy. J. Surg. Oncol. 2007;95:337,346. © 2007 Wiley-Liss, Inc. [source] Plasma proteomics of lung cancer by a linkage of multi-dimensional liquid chromatography and two-dimensional difference gel electrophoresisPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 13 2006Tetsuya Okano Abstract To investigate aberrant plasma proteins in lung cancer, we compared the proteomic profiles of serum from five lung cancer patients and from four healthy volunteers. Immuno-affinity chromatography was used to deplete highly abundant plasma proteins, and the resulting plasma samples were separated into eight fractions by anion-exchange chromatography. Quantitative protein profiles of the fractionated samples were generated by two-dimensional difference gel electrophoresis, in which the experimental samples and the internal control samples were labeled with different dyes and co-separated by two-dimensional polyacrylamide gel electrophoresis. This approach succeeded in resolving 3890 protein spots. For 364 of the protein spots, the expression level in lung cancer was more than twofold different from that in the healthy volunteers. These differences were statistically significant (Student's t -test, p -value less than 0.05). Mass spectrometric protein identification revealed that the 364 protein spots corresponded to 58 gene products, including the classical plasma proteins and the tissue-leakage proteins catalase, clusterin, ficolin, gelsolin, lumican, tetranectin, triosephosphate isomerase and vitronectin. The combination of multi-dimensional liquid chromatography and two-dimensional difference gel electrophoresis provides a valuable tool for serum proteomics in lung cancer. [source] Discrimination between worry and anxiety among cancer patients: development of a brief cancer-related worry inventoryPSYCHO-ONCOLOGY, Issue 12 2008Kei Hirai Abstract Objectives: A psychometric scale for assessing cancer-related worry among cancer patients, called the Brief Cancer-Related Worry Inventory (BCWI), was developed. Methods: A cross-sectional questionnaire survey for item development was conducted of 112 Japanese patients diagnosed with breast cancer, and test,retest validation analysis was conducted using the data from another prospective study of 20 lung cancer patients. The questionnaire contained 15 newly developed items for cancer-related worry, the Hospital Anxiety and Depression Scale, The Impact of Event Scale Revised, and the Medical Outcomes Study Short Form-8. Results: Exploratory factor analysis of the 15 items yielded a 3-factor structure including (1) future prospects, (2) physical and symptomatic problems and (3) social and interpersonal problems. A second-order confirmatory factor analysis identified a second-order factor called cancer-related worry and confirmed the factor structure with an acceptable fit (chi-square (df=87)=160.16, P=0.001; GFI=0.83; CFI=0.92; RMSEA=0.09). The internal consistency and test,retest reliability were confirmed with the lung cancer sample. Multidimensional scaling found that cancer-related worry is separate from anxiety, depression, and posttraumatic stress disorder (PTSD) symptoms. Conclusion: Our study succeeded in developing and confirming the validity and reliability of a BCWI. The study also confirmed the discriminable aspects of cancer-related worry from anxiety, depression, and PTSD symptoms. Copyright © 2008 John Wiley & Sons, Ltd. [source] Course of psychological distress and its predictors in advanced non-small cell lung cancer patientsPSYCHO-ONCOLOGY, Issue 6 2006Tatsuo Akechi Abstract This study investigated longitudinal changes and predictive factors for psychological distress among 85 newly diagnosed advanced non-small cell lung cancer (NSCLC) patients. Whereas tension-anxiety after diagnosis (T1) was significantly reduced at two months (T2) and six months (T3) after diagnosis and depression-dejection at T1 was significantly reduced at T2, other forms of psychological distress, including anger,hostility, vigor, fatigue, and confusion, did not show significant changes. Total mood disturbance did not show significant change. Only a higher total mood disturbance at T1 was a significant predictor of total mood disturbance at T3. These findings demonstrate that most types of psychological distress experienced by advanced NSCLC patients is likely to persist during the subsequent clinical course. The findings also suggest that initial psychological distress itself after cancer diagnosis is the most important predictor for subsequent psychological distress and that early intervention beginning immediately after the disclosure of a diagnosis of cancer is one way to prevent and/or reduce subsequent psychological distress in advanced NSCLC patients. Copyright © 2005 John Wiley & Sons, Ltd. [source] Smoking behavior of 226 patients with diagnosis of stage IIIA/IIIB non-small cell lung cancerPSYCHO-ONCOLOGY, Issue 6 2002Lisa Sanderson Cox There is limited research of smoking cessation following diagnosis of lung cancer. This prospective study assessed cigarette smoking behavior among 226 patients (142 males, 84 females) prior to, at the time of, and after the diagnosis of unresectable stage IIIA/IIIB non-small cell lung cancer and entry into a phase III trial examining combined thoracic radiation therapy and chemotherapy. Their mean ±S.D. age was 62.7±9.4 years and 95.6% were Caucasian. Of 215 patients with a history of cigarette smoking, 69% (148/215) stopped smoking prior to entry in the trial, 9% (20/215) stopped smoking at some point during the course of the trial, 11% (24/215) continued smoking throughout the trial, 7% (16/215) were smoking at baseline but did not report subsequent smoking status, and smoking status at study entry was missing for the remaining patients. The majority of lung cancer patients were able to stop smoking. A notable subset of patients continued smoking despite diagnosis of lung cancer, enrollment in a clinical trial, treatment-related toxicity, and encouragement from clinicians to stop smoking. Smoking cessation interventions are needed for lung cancer patients who continue to smoke. Copyright © 2002 John Wiley & Sons, Ltd. [source] Role of pleural viscosity in the differential diagnosis of exudative pleural effusionRESPIROLOGY, Issue 2 2007Ozkan YETKIN Objective and background: Determining the aetiology of an effusion involves assessing if it is an exudate or a transudate. However, a reliable test for determining the aetiology of a pleural effusion is lacking. Pleural viscosity has a high sensitivity and specificity and a high positive and negative predictive value for discriminating exudative and transudative pleural effusions. The aim of this study was to use pleural fluid viscosity to discriminate between various aetiologies of exudative effusions, namely malignant, parapneumonic and tuberculous. Methods: Seventy consecutive patients (24 women, 46 men, mean age = 67 years) with exudative pleural effusion due to pneumoniae in 24 patients, tuberculous pleurisy in 21 and lung cancer in 25 were studied prospectively. Measurements of pleural fluid and plasma viscosity were performed using Brookfield DV-II viscometer. Results: Pleural viscosity and pleural LDH were highest in the tuberculous pleurisy patients and lowest in the lung cancer patients. Pleural viscosity ,1.57 was found to be indicative of tuberculous pleurisy with a sensitivity of 100% and specificity of 95%. Pleural viscosity <1.39 was found to be indicative of lung cancer with a sensitivity of 100% and specificity of 94%. Pleural viscosity was significantly correlated with pleural albumin (r = 0.34, P = 0.004), protein (r = 0.40, P = 0.001), LDH (r = 0.70, P < 0.001) and plasma viscosity (r = 0.44, P < 0.001), having the most significant value with pleural LDH. Conclusion: The pleural fluid viscosity of patients with parapneumonic, tuberculous and malignant effusions are significantly different from each other. Among these groups, tuberculous effusions had the highest viscosity, and malignant effusions from lung cancer the lowest. [source] Differential effects of propofol and isoflurane on the activation of T-helper cells in lung cancer patientsANAESTHESIA, Issue 5 2010X. F. Ren Summary It is suggested that activation and differentiation of T-helper cells are required for peri-operative anti-tumor and anti-infection immunity. The present study aimed to evaluate whether propofol stimulates the activation and differentiation of these cells in patients undergoing pulmonary lobectomy for non-small-cell lung cancer. Thirty patients were randomly allocated to receive propofol or isoflurane throughout surgery. The CD4+CD28+ percentage (p < 0.0001) and the ratio of interferon-,:interleukin-4 (p = 0.001) all increased with propofol but showed no change with isoflurane. In contrast, cortisol increased with isoflurane (p < 0.0001) but not with propofol over time (p = 0.06). We conclude that propofol promotes activation and differentiation of peripheral T-helper cells. [source] Prognostic model to predict outcomes in nonsmall cell lung cancer patients treated with gefitinib as a salvage treatmentCANCER, Issue 7 2009Min Jae Park MD Abstract BACKGROUND: A prognostic model based on clinical parameters for nonsmall cell lung cancer (NSCLC) patients treated with gefitinib (250 mg/day) as a salvage therapy was devised. METHODS: Clinical data regarding a total of 316 metastatic or recurrent NSCLC patients who were treated with gefitinib were analyzed. RESULTS: Poor prognostic factors for overall survival (OS) by multivariate analysis were an Eastern Cooperative Oncology Group (ECOG) performance status of 2 to 3 (hazards ratio [HR] of 2.07; 95% confidence interval [CI], 1.57-2.73 [P < .001]), the presence of intra-abdominal metastasis (HR of 1.76; 95% CI, 1.33-2.34 [P < .001]), elevated serum alkaline phosphatase (HR of 1.50; 95% CI, 1.13-2.00 [P = .005]), time interval from diagnosis to gefitinib therapy of ,12 months (HR of 1.48; 95% CI, 1.12-1.95 [P = .005]), low serum albumin (HR of 1.45; 95% CI, 1.09-1.92 [P = .009]), progression-free interval for previous chemotherapy of ,12 weeks (HR of 1.40; 95% CI, 1.0-1.84 [P = .015]), white blood cell >10,000/,L (HR of 1.38; 95% CI, 1.02-1.85 [P = .032]), and ever-smoker (HR of 1.33; 95% CI, 1.02-1.75 [P = .033]). Of the 272 patients applicable to this prognostic model, 41 patients (15%) were categorized as a good prognosis group (0-1 risk factors), 100 patients (37%) as an intermediate prognosis group (2-3 risk factors), 81 patients (30%) as a poor prognosis group (4-5 risk factors), and 50 patients (16%) as a very poor prognosis group (,6 risk factors). The median OS from the time of gefitinib treatment for the good, intermediate, poor, and very poor prognosis groups were 18.0 months, 11.2 months, 4.0 months, and 1.3 months, respectively (P < .001). CONCLUSIONS: This prognostic model based on easily available clinical variables would be useful to identify patients who might derive more benefit from gefitinib treatment and to make decisions in clinical practice. Cancer 2009. © 2009 American Cancer Society. [source] Modulation of lung molecular biomarkers by ,-carotene in the Physicians' Health Study,CANCER, Issue 5 2009Chun Liu MD Abstract BACKGROUND: ,-Carotene supplementation showed neither benefit nor harm among apparently healthy physicians (all men) in the Physicians' Health Study (PHS) trial. The objective of the current investigation was to evaluate how long-term ,-carotene supplementation affects molecular markers of lung carcinogenesis in the PHS. METHODS: The protein levels of total p53, cyclin D1, proliferating cellular nuclear antigen (PCNA), retinoic acid receptor , (RAR,), and cytochrome p450 enzyme 1A1 (CYP1A1) were measured using the immunohistochemical method in 40 available archival lung tissue samples from patients who were diagnosed with lung cancer in the PHS. The protein levels of these markers were compared by category of ,-carotene treatment assignment and other characteristics using unconditional logistic regression models. RESULTS: The positivity for total p53, RAR,, cyclin D1, and PCNA was nonsignificantly lower among lung cancer patients who were assigned to receive ,-carotene than those who were assigned to receive ,-carotene placebo. There was a borderline significant difference in CYP1A1 positivity with an OR of 0.2 (95% confidence interval, 0.2-1.1; P = .06) in a comparison of men who received ,-carotene and men who received ,-carotene placebo. CONCLUSIONS: The 50-mg ,-carotene supplementation on alternate days had no significant influence on molecular markers of lung carcinogenesis that were evaluated in the PHS. This finding provides mechanistic support for the main PHS trial results of ,-carotene, which demonstrated no benefit or harm to the risk of developing lung cancer. Cancer 2009. © 2009 American Cancer Society. [source] The value of medical interventions for lung cancer in the elderly,CANCER, Issue 11 2007Results from SEER-CMHSF Abstract BACKGROUND. Lung cancer is the leading source of cancer mortality and spending. However, the value of spending on the treatment of lung cancer has not been conclusively demonstrated. The authors evaluated the value of medical care between 1983 and 1997 for nonsmall cell lung cancer in the elderly US population. METHODS. The authors used Surveillance, Epidemiology, and End Results (SEER) data to calculate life expectancy after diagnosis over the period 1983 to 1997. Direct costs for nonsmall cell lung cancer detection and treatment were determined by using Part A and Part B reimbursements from the Continuous Medicare History Sample File (CMHSF) data. The CMHSF and SEER data were linked to calculate lifetime treatment costs over the time period of interest. RESULTS. Life expectancy improved minimally, with an average increase of approximately 0.60 months. Total lifetime lung cancer spending rose by approximately $20,157 per patient in real, ie, adjusted for inflation, 2000 dollars from the early 1980s to the mid-1990s, for a cost-effectiveness ratio of $403,142 per life year (LY). The cost-effectiveness ratio was $143,614 for localized cancer, $145,861 for regional cancer, and $1,190,322 for metastatic cancer. CONCLUSIONS. The cost-effectiveness ratio for nonsmall cell lung cancer was higher than traditional thresholds used to define cost-effective care. The most favorable results were for persons diagnosed with early stage cancer. These results suggested caution when encouraging more intensive care for lung cancer patients without first considering the tradeoffs with the costs of this therapy and its potential effects on mortality and/or quality of life. Cancer 2007. © 2007 American Cancer Society. [source] Hormone replacement therapy and lung cancer risk in ChineseCANCER, Issue 8 2007Kuan-Yu Chen MD Abstract BACKGROUND. The association between hormone replacement therapy (HRT) and a reduced lung cancer risk has been reported in previous studies. There is a high female to male ratio in Chinese lung cancer patients, and female patients have different clinicopathological characteristics compared with Western patient populations. The authors investigated whether HRT may reduce lung cancer risk in Taiwan. METHODS. The authors used a case-control study design to investigate 826 women with lung cancer and 531 healthy controls. Personal interviews based on a structured questionnaire were performed to collect information on HRT use of at least 3 months, age, ethnicity, active and passive smoking, exposure to air pollution, cooking or incense fumes, body mass index (BMI), menopause, and family history of cancers. RESULTS. HRT use was associated with reduced lung cancer risk with a multivariate, adjusted odds ratio of 0.70 (95% CI, 0.53,0.94; P = .019). HRT use was associated with reduced odds ratio of lung cancer in all subset analyses stratified by histology, active and passive cigarette smoking, BMI, history of incense burning, cooking, and motorcycle riding, as well as family history of certain cancers. CONCLUSIONS. This study confirmed that HRT is associated with a reduced lung cancer risk. The results appeared to be applicable to Chinese female population groups. Cancer 2007. © 2007 American Cancer Society. [source] Hsp60 and Hsp10 down-regulation predicts bronchial epithelial carcinogenesis in smokers with chronic obstructive pulmonary diseaseCANCER, Issue 10 2006Francesco Cappello MD Abstract BACKGROUND. The relation between smoking, chronic obstructive pulmonary disease (COPD), and lung cancer (LC) is an open field of investigation. A higher frequency of adenocarcinoma has been reported in patients with COPD. Heat shock proteins (Hsps) are implicated in tumoral cell growth and differentiation. The aim of the present study was to investigate the expression of Hsp60 and Hsp10 in bronchial biopsies from smokers with COPD and in 10 lung cancer patients and to evaluate the association between Hsps expression and carcinogenetic steps of LC. METHODS. An immunohistochemical study was performed for Hsp60 and Hsp10 in bronchial biopsies from 35 COPD (postbronchodilator forced expiratory volume in 1 second [FEV1]: 53 ± 19% [mean ± SD]) patients with a history of smoking (53 ± 34 pack/years) and in 10 patients with adenocarcinoma or adenosquamous carcinoma (ASC). Immunopositivity was quantified in the bronchial epithelium and in specimens with ASC. RESULTS. In smokers with COPD, 10 out of 35 patients had a normal bronchial epithelium (NBE), 12 showed basal cell hyperplasia (BCH), 5 squamous metaplasia (SM), and 8 dysplasia (Dy). It was found that 58 ± 23% and 54 ± 23% of NBE and 48 ± 29% and 52 ± 26% of BCH expressed Hsp60 and Hsp10, respectively; in contrast, only 3 ± 3% and 3.6 ± 2% of SM, 1.9 ± 4% and 1.1 ± 2% of Dy expressed Hsp60 and Hsp10, respectively. ASC specimens were negative for Hsps proteins. Interestingly, NBE also present at the edges of ASC specimens was negative for Hsps proteins. CONCLUSIONS. The loss of Hsp60 and Hsp10 immunopositivity is related to the development and progression of bronchial cancer in smokers with COPD. Cancer 2006. © 2006 American Cancer Society. [source] Novel spliced form of a lens protein as a novel lung cancer antigen, Lengsin splicing variant 4CANCER SCIENCE, Issue 8 2009Munehide Nakatsugawa A glutamine synthetase I family protein, Lengsin, was previously identified as a novel lens-specific transcript in the vertebrate eye. In this report, we show for the first time that Lengsin is a novel tumor-associated antigen expressed ectopically in lung cancer. Interestingly, a novel spliced form of human Lengsin termed ,splicing variant 4', gaining exon 3 that codes extra 63 amino acids, is the dominant transcript form in lung cancer cells. Lengsin mRNA could be detected in 7 of 12 (58%) lung cancer cell lines and 7 of 7 (100%) surgically resected lung cancer tissues. On the other hand, Lengsin transcripts could not be detected in normal major tissues or in other cancer cell lines, including melanoma, colorectal carcinoma, breast carcinoma and hepatocellular carcinoma. In addition, knockdown of Lengsin mRNA with RNAi caused cell death and a decrease of cell viability, suggesting that Lengsin has some essential role in cell survival. Since the lens is an immune-privileged site, we regard Lengsin as a highly immunogenic cancer antigen. Anti-Lengsin autoantibodies were detectable in sera of lung cancer patients, although these patients did not show any lens-related disturbances. Hence, Lengsin splicing variant 4 might be an immunogenic lung cancer-specific antigen that is suitable as a diagnostic marker and for molecular targeting therapy, including immunotherapy. (Cancer Sci 2009) [source] GM3 synthase gene is a novel biomarker for histological classification and drug sensitivity against epidermal growth factor receptor tyrosine kinase inhibitors in non-small cell lung cancerCANCER SCIENCE, Issue 10 2007Mariko Noguchi Expression of gangliosides and alterations in their composition have been observed during cell proliferation and differentiation and in certain cell cycle phases, brain development and cancer malignancy. To investigate the characteristics of GM3 synthase, SAT-I mRNA and ganglioside GM3 expression levels in lung cancer, we examined the expression levels of SAT-I mRNA as well as GM3 in 40 tumor tissues surgically removed from non-small cell lung cancer patients. Adenocarcinoma tissues expressed SAT-I mRNA levels that were significantly higher than those of squamous and other carcinomas (P < 0.0001). Moreover, the SAT-I mRNA levels were high in the bronchioalveolar carcinoma subtype and low in the solid and mucin subtypes of adenocarcinomas (P = 0.049, 0.049 and 0.013, respectively). To clarify the relationship between SAT-I mRNA and epidermal growth factor receptor (EGFR)-tyrosine kinase (TK) inhibitor sensitivity, we carried out drug sensitivity tests for the EGFR-TK inhibitors gefitinib and AG1478 using eight adenocarcinoma cell lines expressing no EGFR mutations. The IC50 values for gefitinib and AG1478 decreased dramatically with increasing SAT-I mRNA levels (R2 = 0.81 and 0.59, respectively), representing a wide range of drug sensitivities among adenocarcinoma cell lines. To explore a possible mechanism of how GM3 could enhance the sensitivity to EGFR-TK inhibitors, the SAT-I gene was introduced stably into a GM3-negative clone of murine 3LL lung cancer cells to produce GM3-reconstituted clones. We found an increase in EGFR protein levels and gefitinib sensitivity in GM3-reconstituted cells, suggesting the involvement of GM3 in the turnover of EGFR protein. Therefore, it is highly expected that, by measuring the expression levels of SAT-I mRNA in lung biopsy samples from non-small cell lung cancer patients, enhanced pathological identification and individualized chemotherapeutic strategies can be established for the appropriate use of EGFR-TK inhibitors. (Cancer Sci 2007; 98: 1625,1632) [source] Recent trends in the treatment of advanced lung cancerCANCER SCIENCE, Issue 6 2006Nagahiro Saijo Lung cancer is one of the major causes of death in many countries because of high rates of smoking, especially in Asian countries. Lung cancer is divided into two major categories based on their biological characteristics and the selection of treatment methods: non-small cell lung cancer (NSCLC; 85%) and small cell lung cancer (15%). Early detection and complete resection are very important in NSCLC, but the cure rate is not very high, except in stage 1A disease. It is extremely important to understand the biology of lung cancer and to introduce more effective treatments in order to improve the survival of NSCLC patients. Numerous clinical trials involving lung cancer patients have led to ,state-of-the-art' treatments for each stage of the disease. Progress in chemotherapy and molecular target based therapy have altered the standard therapy for NSCLC. (Cancer sci 2006; 97) [source] | ||||||||||||||||||||||||||||