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BACKGROUND: Corticosteroids are often used to treat fatigue and anorexia, but occasionally produce delirium. Information on the predictors of delirium in corticosteroid-treated cancer patients remains limited. OBJECTIVE: To identify potential factors predicting the development of delirium in corticosteroid-treated cancer patients. DESIGN: An exploratory, multicenter, prospective, observational study. SETTING/SUBJECTS: Inclusion criteria for this study were patients who had metastatic or locally advanced cancer and a fatigue or anorexia intensity score of 4 or more on a 0-10 Numerical Rating Scale. MEASUREMENT: Univariate and multivariable analyses were performed to identify the predictors of delirium diagnosed by the Confusion Assessment Method (CAM) within three days of initiation of corticosteroids. RESULTS: Among 207 patients administered corticosteroids, 35 (17%; 95% confidence interval [CI] 12%-23%) developed at least one episode of delirium diagnosed by the CAM. Factors predictive of the development of delirium were as follows: Palliative Performance Scale ≤20, Eastern Cooperative Oncology Group Performance Status (ECOG PS) = 4, the Support Team Assessment Schedule (STAS) score of drowsiness >1, concurrent opioid use, parenteral hydration volume ≤500 mL, and the absence of lung metastasis. A multivariable analysis identified the independent factors predicting responses as ECOG PS = 4 (odds ratio [OR] 4.0; 95% CI 1.7-9.3), STAS score of drowsiness >1 (OR 3.4; 95% CI 1.4-8.2), and concurrent opioid use (OR 3.7; 95% CI 1.0-13). CONCLUSION: Delirium in corticosteroid-treated advanced cancer patients may be predicted by PS, drowsiness, and concurrent opioid use. Larger prospective studies are needed to confirm these results.

DOI： 10.1089/jpm.2016.0323

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PURPOSE: Although corticosteroids can relieve dyspnea in advanced cancer patients, factors predicting the response remain unknown. We aimed to explore potential factors predicting the response to corticosteroids for dyspnea in advanced cancer patients. METHODS: In this preliminary multicenter prospective observational study, we included patients who had metastatic or locally advanced cancer, were receiving specialized palliative care services, and had a dyspnea intensity of ≥3 on a 0-10 Numerical Rating Scale (NRS) (worst during the last 24 h). The primary endpoint was NRS of dyspnea on day 3 after the administration of corticosteroids. Univariate/multivariate analyses were conducted to identify factors predicting ≥1-point reduction in NRS. RESULTS: Of 74 patients who received corticosteroids, 50 (68%) showed ≥1-point reduction in dyspnea NRS. Factors that significantly predicted the response were an age of 70 years or older (82 vs. 53%, p = 0.008), absence of liver metastases (77 vs. 46%, p = 0.001), Palliative Prognostic Index (PPI) ≤ 6 (90 vs. 61%, p = 0.041), presence of pleuritis carcinomatosa with a small collection of pleural effusions (84 vs. 55%, p = 0.011), presence of audible wheezes (94 vs. 60%, p = 0.014), and baseline dyspnea NRS ≥7 (76% vs. 52%, p = 0.041). In a multivariate analysis, factors predicting response included PPI <6 (odds ratio (OR), 36.2; p = 0.021), baseline dyspnea NRS (worst) ≥7 (OR, 6.6; p = 0.036), and absence of liver metastases (OR, 0.19; p = 0.029) or ascites/liver enlargement (OR, 0.13; p = 0.050). CONCLUSIONS: The patient characteristics, etiologies of dyspnea, and clinical manifestations may predict responses to corticosteroids for dyspnea. Larger prospective studies are promising to confirm our findings.

DOI： 10.1007/s00520-016-3507-5

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PURPOSE: Although corticosteroids are widely used to relieve anorexia, information regarding the factors predicting responses to corticosteroids remains limited. The purpose of the study is to identify potential factors predicting responses to corticosteroids for anorexia in advanced cancer patients. METHODS: Inclusion criteria for this multicenter prospective observational study were patients who had metastatic or locally advanced cancer and had an anorexia intensity score of 4 or more on a 0-10 Numerical Rating Scale (NRS). Univariate and multivariate analyses were conducted to identify the factors predicting ≥2-point reduction in NRS on day 3. RESULTS: Among 180 patients who received corticosteroids, 99 (55 %; 95 % confidence interval [CI], 47-62 %) had a response with ≥2-point reduction. Factors that significantly predicted responses were Palliative Performance Scale (PPS) > 40 and absence of drowsiness. In addition, factors that tended to be associated with ≥2-point reduction in NRS included PS 0-3, absence of diabetes mellitus, absence of peripheral edema, presence of lung metastasis, absence of peritoneal metastasis, baseline anorexia NRS of >6, presence of pain, and presence of constipation. A multivariate analysis showed that the independent factors predicting responses were PPS of >40 (odds ratio = 2.7 [95 % CI = 1.4-5.2]), absence of drowsiness (2.6 [1.3-5.0]), and baseline NRS of >6 (2.4 [1.1-4.8]). CONCLUSIONS: Treatment responses to corticosteroids for anorexia may be predicted by PPS, drowsiness, and baseline symptom intensity. Larger prospective studies are needed to confirm these results.

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CONTEXT: Although corticosteroids are widely used to relieve cancer-related fatigue (CRF), information regarding the factors predicting responses to corticosteroids remains limited. OBJECTIVES: The aim of this study was to identify potential factors predicting responses to corticosteroids for CRF in advanced cancer patients. METHODS: Inclusion criteria for this multicenter, prospective, observational study were patients who had metastatic or locally advanced cancer and had a fatigue intensity score of 4 or more on a 0-10 Numerical Rating Scale (NRS). Univariate and multivariate analyses were conducted to identify the factors predicting two-point reduction or more in NRS on day 3. RESULTS: Among 179 patients who received corticosteroids, 86 (48%; 95% CI 41%-56%) had a response with two-point reduction or more. Factors that significantly predicted responses were performance status score of 3 or more, Palliative Performance Scale score more than 40, absence of ascites, absence of drowsiness, absence of depression, serum albumin level greater than 3 mg/dL, serum sodium level greater than 135 mEq/L, and baseline NRS score greater than 5. A multivariate analysis showed that the independent factors predicting responses were baseline NRS score greater than 5 (odds ratio [OR] 6.6, 95% CI 2.8-15.4), Palliative Performance Scale score more than 40 (OR 4.4, 95% CI 2.1-9.3), absence of drowsiness (OR 3.4, 95% CI 1.7-6.9), absence of ascites (OR 2.3, 95% CI 1.1-4.7), and absence of pleural effusion (OR 2.2, 95% CI 1.0-5.0). CONCLUSION: Treatment responses to corticosteroids for CRF may be predicted by baseline symptom intensity, performance status, drowsiness, and severity of fluid retention symptoms. Larger prospective studies are needed to confirm these results.

DOI： 10.1016/j.jpainsymman.2016.01.015

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Malignant pleural mesothelioma (MPM) is an aggressive disease that is resistant to conventional therapies. Cell lines are useful models for studying the biological characteristics of tumors; therefore, the establishment of MPM cell lines is valuable for exploring novel therapeutic strategies for MPM. In the present study, 4 MPM cell lines (YUMC8, YUMC44, YUMC63, and YUMC64) were established, which consisted of 2 epithelioid and 2 sarcomatoid mesothelioma histological subtypes, from Japanese patients with MPM. The DNA methylation status, mutations, copy number gains, protein expression of representative genes, and the sensitivity to several drugs were examined in these 4 cell lines. Methylation of P16 was demonstrated in 3/4 cell lines, in which the protein expression of p16 was lost. Methylation of RASSF1A was observed in 3/4 cell lines. Copy number gains of EGFR, HER2 or MET were not detected in the 4 cell lines. Mutations in various genes, including EGFR, KRAS, HER2, BRAF, and PIK3CA, which are frequently detected in non-small cell lung cancer, were not detected in the 4 cell lines. microRNA-34b/c is a direct transcriptional target of p53 and is often silenced in MPM by promoter methylation. In the present study, miR-34b/c was heavily methylated in 2/4 established MPM cell lines. For cell adhesion molecules, E-cadherin expression was detected in the 2 epithelioid MPM cell lines, whereas N-cadherin expression was detected in all 4 established cell lines by western blotting. Vimentin was strongly expressed in the 2 sarcomatoid MPM cell lines. None of the established MPM cell lines demonstrated significant responses to the drugs tested, including NVP-AUY922, 17-DMAG, Trichostatin A, and Vorinostat. Although novel molecular findings were not observed in the current characterization of these MPM cell lines, these lines will be useful for future extensive analyses of the biological behavior of MPM and the development of novel therapeutic strategies.

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Acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is characterized by severe worsening dyspnea of unknown etiology and high mortality without effective treatment. Recently, direct hemoperfusion with polymyxin B (PMX)-immobilized fiber cartridge (PMX-DHP) has been reported to improve pulmonary oxygenation and survival in patients with AE-IPF although its mechanism of action remains unknown. To gain insights into the pathobiology of AE-IPF through the beneficial effects of PMX-DHP, we analyzed the profile of cytokines adsorbed onto PMX-fibers used in 9 AE-IPF patients. In addition, the sera of these AE-IPF patients collected immediately before and after PMX-DHP, 9 stable IPF patients and 8 healthy individuals were also analyzed. The serum levels of cytokines including IL-9, IL-12, IL-17, PDGF and VEGF were significantly decreased immediately after PMX-DHP (P<0.02), and VEGF and IL-12 were most prominently reduced. In addition to PDGF and VEGF, IL-1β, IL-1ra, IL-8, IL-23, FGF basic, GM-CSF, IP-10, RANTES and TGF-β were eluted from used PMX-fibers. Interestingly, improved pulmonary oxygenation after PMX-DHP was correlated well with the quantities of eluted VEGF. These results suggest that adsorption of proinflammatory, profibrotic and proangiogenic cytokines onto PMX-fibers is one of the mechanisms of action of PMX-DHP in AE-IPF. Notably, removal of VEGF by PMX-DHP may contribute to the rapid improvement in oxygenation by suppressing vascular permeability in the lung.

DOI： 10.1016/j.cyto.2012.08.032

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CONTEXT: Although an evidence-based clinical guideline for parenteral hydration therapy was established in Japan, the efficacy of the guideline has not been assessed. OBJECTIVES: Our purpose was to explore the effect of parenteral hydration therapy based on this clinical guideline on quality of life (QoL), discomfort, symptoms, and fluid retention signs in patients with advanced cancer. METHODS: This multicenter, prospective, observational study included 161 patients with advanced abdominal cancer who received guideline-based hydration therapy. We evaluated the longitudinal changes of the global QoL (Item 30 of European Organization for Research and Treatment of Cancer Quality-of-Life Questionnaire-C30); the Discomfort Scale; the intensity of seven physical symptoms; and the severity of fluid retention signs. We also evaluated patient satisfaction and the feeling of benefit from hydration one week after the study commenced, and bronchial secretions, hyperactive delirium, communication capacity, and agitation 48 hours before a patient's death. RESULTS: The global QoL, the Discomfort Scale, and the intensities of all physical symptoms, except for vomiting and drowsiness, were stable throughout the study period. More than 80% of patients maintained all fluid retention signs. Patient global satisfaction was 76.4 (0-100) and feeling of benefit was 5.43 (range 0-7). CONCLUSION: Guideline-based parenteral hydration therapy contributed to maintaining global QoL and provided satisfaction and a feeling of benefit without increasing discomfort and worsening symptoms and fluid retention signs in patients with advanced cancer.

DOI： 10.1016/j.jpainsymman.2011.06.028

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Malignant pleural mesothelioma (MPM) usually develops pleural fluid. We investigated the value of DNA methylation in the pleural fluid for differentiating MPM from lung cancer (LC). Pleural fluid was collected from 39 patients with MPM, 46 with LC, 25 with benign asbestos pleurisy (BAP) and 30 with other causes. The methylation of O(6)-methylguanine-DNA methyltransferase (MGMT), p16(INK4a) , ras association domain family 1A (RASSF1A), death-associated protein kinase (DAPK), and retinoic acid receptor β (RARβ) was examined using quantitative real-time PCR. DNA methylation of RASSF1A, p16(INK4a), RARβ, MGMT and DAPK was detected in 12 (30.8%), 3 (7.7%), 11 (28.2%), 0 (0.0%) and five patients (12.8%) with MPM, and in 22 (47.8%), 14 (30.4%), 24 (52.2%), 1 (2.2%) and six patients (13.0%) with LC, respectively. The mean methylation ratios of RASSF1A, p16(INK4a) and RARβ were 0.37 (range 0.0-2.84), 0.11 (0.0-2.67) and 0.44 (0.0-3.32) in MPM, and 0.87 (0.0-3.14), 1.16 (0.0-5.35) and 1.69 (0.0-6.49) in LC, respectively. The methylation ratios for the three genes were significantly higher in LC than in MPM (RASSF1A, P = 0.039; p16(INK4a), P = 0.005; and RARβ, P = 0.002). Patients with methylation in at least one gene were 3.51 (95% confidence interval, 1.09-11.34) times more likely to have LC. Hypermethylation seemed no greater with MPM than with BAP. Extended exposure to asbestos (≧30 years) was correlated with an increased methylation frequency (P = 0.020). Hypermethylation of tumor suppressor genes in pleural fluid DNA has the potential to be a valuable marker for differentiating MPM from LC.

DOI： 10.1111/j.1349-7006.2011.02180.x

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Cisplatin is used to treat lung cancer; however, it is also a known carcinogen. Cyclooxygenase-2 (COX-2) inhibitors have been shown to prevent carcinogen-induced experimental tumors. We investigated the effect of a COX-2 inhibitor, celecoxib, on cisplatin-induced lung tumors. One hundred twenty 4-week-old A/J mice were divided into 6 groups: group 1, no treatment; group 2, low-dose celecoxib (150 mg/kg); group 3, high-dose celecoxib (1,500 mg/kg); group 4, cisplatin alone; group 5, cisplatin plus low-dose celecoxib;and group 6, cisplatin plus high-dose celecoxib. Mice in groups 4-6 were administered cisplatin (1.62 mg/kg, i.p.) once a week for 10 weeks between 7 and 16 weeks of age. All mice were sacrificed at week 30. Tumor incidence was 15.8% in group 1, 25% in group 2, 26.3% in group 3, 60% in group 4, 50% in group 5, and 50% in group 6. Tumor multiplicity was 0.2, 0.3, 0.3, 1.3, 1.0, and 0.6 in groups 1-6, respectively. Tumor multiplicity in the cisplatin-treated mice was reduced by celecoxib treatment in a dose-dependent manner (p < 0.05, group 4 vs. group 6). Celecoxib significantly reduced COX-2 expression in cisplatin-induced tumors (p < 0.01, group 4 vs. group 6).

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Gefitinib is an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI). N-Nitrosamine-4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a potent carcinogen found in tobacco smoke, induces lung tumors in A/J mice. NNK induces cellular transformation resulting in the over-expression of EGFR. Accordingly, EGFR may be a target for cancer prevention. In this study, we investigated the effect of gefitinib on NNK-induced tumorigenesis and the carcinogenicity of gefitinib in A/J mice. A total of 180 four-week-old female A/J mice were randomly divided into six groups: group 1 (controls), treated with deionized water; group 2, treated with 5 mg/kg p.o. gefitinib; group 3, treated with 50 mg/kg p.o. gefitinib (to test the carcinogenicity of gefitinib); group 4 (controls for NNK treatment), treated with deionized water; group 5, treated with 5 mg/kg p.o. gefitinib; and group 6, treated with 50 mg/kg p.o. gefitinib and injected with NNK once at 8 weeks of age to test the chemopreventive activity of gefitinib. Gefitinib was given once a day, 5 days a week by gavage, beginning at 4 weeks of age and continuing for 26 weeks. All mice were sacrificed at 30 weeks of age. The multiplicities of the NNK-induced lung tumors were significantly suppressed in a dose-dependent manner. Gefitinib had no effect on body weight at a low dose. The administration of gefitinib alone for 26 weeks did not induce tumorigenesis; instead, it significantly suppressed the incidence of spontaneous tumors in the mice, in contrast with other anti-cancer agents. Gefitinib did not induce lung fibrosis when compared with control mice by Azan-Mallory staining. Our results suggest that gefitinib has a weak but significant chemopreventive effect with no carcinogenicity or pulmonary toxicity in A/J mice.

DOI： 10.1016/j.lungcan.2008.11.021

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Accumulating evidence implicates epigenetic changes such as hypermethylation in carcinogenesis. We investigated whether DNA methylation of 5 tumor suppressor genes in pleural fluid samples could aid in diagnosis of malignant effusion. In samples from 47 patients with malignant pleural effusions and 34 with nonmalignant effusions, we used a methylation-specific polymerase chain reaction to detect aberrant hypermethylation of the promoters of the DNA repair gene O(6)-methylguanine-DNA methyltransferase (MGMT), p16(INK4a), ras association domain family 1A (RASSF1A), apoptosis-related genes, death-associated protein kinase (DAPK), and retinoic acid receptor beta (RARbeta). Promoter hypermethylation was associated with malignant effusion for MGMT (Odds ratio (OR) = infinity), p16(INK4a) (OR = infinity), RASSF1A (OR = 13.8; CI, 1.71-112), and RARbeta (OR = 3.17; CI, 1.10-9.11), but not for DAPK. Instead, DAPK methylation was associated with the length of smoking (p < 0.05). Patients with hypermethylation of MGMT, p16(INK4a), RASSF1A or RARbeta were 5.68 times more likely to have malignant effusions than patients without methylation (p = 0.008). Methylations per patient were more numerous for lung cancer than nonmalignant pulmonary disease (0.915 vs. 0.206, p < 0.001). Sensitivity, specificity, and positive predictive value of methylation in one or more genes for diagnosis of malignant effusion were 59.6%, 79.4%, and 80.0% respectively. In conclusion, aberrant promoter methylation of tumor suppressor genes in pleural fluid DNA could be a valuable diagnostic marker for malignant pleural effusion.

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Insulin-like growth factor binding protein-3 (IGFBP-3) is postulated to be a mediator of growth suppression signals. Here, we examined the methylation status of IGFBP-3 to correlate to clinicopathological factors in human cancers. The methylation status of IGFBP-3 was determined by bisulfite DNA sequencing and was correlated with expression semi-quantified by real-time RT-PCR to develop a methylation-specific PCR (MSP) assay for IGFBP-3. Using the MSP assay, we examined the methylation status of IGFBP-3 in gastric cancer (GC), colorectal cancer (CRC), breast cancer (BC) and malignant mesothelioma (MM). IGFBP-3 methylation was detected in 6 of 13 (46%) and 16 of 24 (67%) GC cell lines and tumors, respectively; 4 of 8 (50%) and 15 of 26 (58%) CRC cell lines and tumors, respectively; 3 of 11 (27%) and 7 of 39 (18%) BC cell lines and tumors, respectively and 1 of 5 (20%) and 18 of 56 (32%) MM cell lines and tumors, respectively. Interestingly, the methylation status of MM specimens from Japanese patients (75%, 12 out of 16 patients) was significantly higher than those from the USA (15%, 6 out of 40 patients) (p < 0.0001), suggesting the presence of ethnic differences in the IGFBP-3 methylation status. We also found that IGFBP-3 methylation was preferentially present in GCs arising in the lower-third of the stomach (p = 0.079). In summary, our results showed that IGFBP-3 methylation played an important role in the silencing of its expression, suggesting that IGFBP-3 may act as a tumor suppressor gene in several human cancers examined.

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Despite its tremendous antitumor effect in a subset of patients with non-small cell lung cancer (NSCLC), the exact mechanism of gefitinib-induced cell death has not been fully determined. In this study, forms of cell death in various NSCLC cell lines after gefitinib exposure was analyzed to elucidate the cell death mechanism of gefitinib. Though higher concentration of gefitinib (10 microM) induced extensive apoptosis in two cell lines (EGFR-mutated PC-9 cells and EGFR wild- type EBC-2/R cells), clinically relevant concentrations of gefitinib (1 microM) induced prominent premature senescence instead of apoptosis in these cells. This induction of senescence was preceded by immediate increase of p16INK4A, p21WAF1/Cip1 and p27Kip1 levels and subsequent G1 cell cycle arrest. These phenomena were not observed in gefitinib-resistant (RERF-LC-MS) cells. Additionally, ex vivo exposure to gefitinib induced senescence in short-term cultured tumor cells that were obtained from malignant pleural effusion of a patient with NSCLC, whose tumor was later revealed to be clinically sensitive to gefitinib. Our results indicate that senescence might be a major anti-tumor mechanism of gefitinib in these NSCLC cells regardless of the EGFR gene mutation status.

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The aim of this study was to investigate the prognostic value of hypermethylation of tumor suppressor genes in patients with non-small cell lung cancer (NSCLC). In samples from 34 lung patients with malignant pleural effusions, we used a methylation-specific polymerase chain reaction to detect aberrant hypermethylation of the promoters of the DNA repair gene O6-methylguanine-DNA methyltransferase (MGMT), p16INK4a, ras association domain family 1A (RASSF1A), apoptosis-related genes, death-associated protein kinase (DAPK), and retinoic acid receptor beta(RARbeta). There is no association between methylation status of five tumor suppressor genes including MGMT, p16INK4a, RASSF1A, DAPK and RARbeta in pleural fluid DNA and clinicopathological parameters including clinical outcome. Aberrant promoter methylation of tumor suppressor genes in pleural fluid DNA could not be a valuable prognostic marker of NSCLC patients with malignant pleural effusion.

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The importance of epidermal growth factor receptor (EGFR) gene mutation has been recognized in nonsmall cell lung cancer (NSCLC), requiring the standardization of mutation screening system including the kind of samples. Here, we examined the EGFR mutation status in 61 pleural fluid samples from NSCLC cases using direct sequencing, nonenriched PCR, mutant-enriched PCR and peptide nucleic acid-locked nucleic acid (PNA-LNA) PCR clamp assay. The mutant-enriched PCR assay detected 16 mutant cases. Among them, the nonenriched PCR assay failed to detect 3 mutant cases. Regarding the discrepancy between mutant-enriched PCR and PNA-LNA PCR clamp assays, 3 cases of exon19-deletions were detected only by mutant-enriched PCR assay and no difference at the L858R mutation. There was no difference in results between direct sequencing and nonenriched PCR assay. We also correlated the EGFR mutation with clinical outcome of gefitinib-treated 29 cases. EGFR mutations were present in 10 cases, revealing 7 partial response and 3 no change (NC). In EGFR wild-type cases, 10 revealed NC and 9 progressive disease. The responders were significantly more frequent among the EGFR mutant cases than among the wild-type (p < 0.0001). Overall survival (p = 0.0092) and progression-free survival (p = 0.018) were significantly longer among the EGFR mutant cases than among the wild-type. In summary, we evaluated the utility of EGFR mutation screening in pleural fluid using 4 assays that showed some discrepancies arising from the designs of the assays. As clinical importance, the EGFR mutation status in pleural fluid can be a biomarker for the favorable outcome of gefitinib-treated NSCLC cases.

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PURPOSE: Mutations in the epidermal growth factor receptor (EGFR) gene have been reported to be present in non-small cell lung cancer (NSCLC) and related to the responsiveness of tumors to EGFR tyrosine kinase inhibitors, suggesting its usefulness as a biomarker. Because clinical samples contain tumor and normal cells or genes, a highly sensitive assay for detecting mutation is critical for clinical applications. EXPERIMENTAL DESIGN: The mutant-enriched PCR is a rapid and sensitive assay with selective restriction enzyme digestion. We developed the mutant-enriched PCR assay targeting exons 19 and 21 of EGFR and applied the developed assay to detect mutations in 108 cases of surgically resected specimens of NSCLCs, 18 samples of computed tomography (CT)-guided needle lung biopsies, and 20 samples of pleural fluid. In addition, results were then compared with those from direct sequencing and a nonenriched PCR assay. RESULTS: The mutant-enriched PCR that was proved to enrich one mutant of 2 x 10(3) normal genes detected mutations in 37 cases of 108 resected tumors, seven samples of CT-guided lung biopsies, and seven samples of pleural fluid. Among mutant cases, four resected tumors, two CT-guided lung biopsies, and two pleural fluid were identified as additional mutant cases by the mutant-enriched PCR, which were considered normal based on nonenriched assays. CONCLUSIONS: Our results indicate that EGFR mutations are readily detectable by mutant-enriched PCR in various clinical samples. Thus, mutant-enriched PCR may provide a valuable method of potentially detecting a small fraction of mutant genes in heterogeneous specimens, indicating its possible use in clinical application for NSCLC.

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OBJECTIVES: Anemia is observed in various malignancies including lung cancer and is recently considered to be a poor prognostic indicator. We investigated whether there is a correlation between anemia, other clinicopathologic factors, and survival. METHODS: We retrospectively examined the clinical records of 611 patients with lung cancer. RESULTS: Of those, 298 (48.8%) patients had anemia at the time of their first visit to our hospital. There was a significant correlation between anemia and age (p=0.0006) or ECOG performance status (p=0.0002), however, there was no correlation of anemia with gender, histological type, clinical stage, or serum level of lactate dehydrogenase. Survival was significantly shorter in 298 patients with anemia (median survival time (MST): 7.5 months) compared with 313 patients without anemia (MST: 11.8 months, p<0.0001). Multivariate analysis of prognostic factors using the Cox proportional hazards model revealed that anemia appeared to be an independent prognostic indicator. CONCLUSION: Anemia observed at the first presentation is an independent poor prognostic indicator in patients with lung cancer.

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Gefitinib is an oral selective inhibitor of the epidermal growth factor receptor tyrosine kinase which is effective for patients with advanced non-small cell lung cancer. A 75-year-old man with advanced adenocarcinoma of the lung was treated with gefitinib. He had a history of allergy to several antibiotics and Welder's lung. Two days after initiation, he developed acute interstitial lung disease (ILD) and died of respiratory failure due to progression of ILD. Critical assessment pointed to gefitinib as the likely cause of this complication. This is the first report of rapid gefitinib-induced ILD. This case should alert physicians to the potential for dangerous pulmonary side-effects of gefitinib therapy, especially in patients with drug allergy.

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A pilot study was conducted to assess the efficacy and feasibility of daily low-dose cisplatin with concurrent thoracic irradiation for clinically unresectable non-small-cell lung cancer (NSCLC). Patients with inoperable NSCLC who had poor risk factors such as advanced age, poor performance status, poor lung function, or concomitant active malignancy were entered into the study. Low-dose cisplatin (6 mg/m2) was administered daily before concurrent thoracic irradiation (2 Gy/day; total dose of 60 Gy) was given. Twenty-five patients were registered. The majority of the patients had either stage IIIA (24.0%) or stage IIIB (60.0%) disease. Fifteen patients (60.0%) completed the planned treatment. Both chemotherapy and radiotherapy were stopped in 3 patients (12.0%) due to poor response, and 7 patients (28.0%) partly received radiotherapy alone as a result of their toxicity response. The proportion of total administered dose to planned dose was 90.9% for chemotherapy and 99.3% for radiotherapy, which were comparable to those in previous studies for LA-NSCLC patients without poor risk factors. Grade 3 leukopenia and neutropenia developed in 14 patients (56.0%) and 10 patients (40.0%), respectively, but grade 4 toxicity was not encountered. Grade 3 pneumonitis and esophagitis were observed in 4 patients (16.0%) and 2 patients (8.0%), respectively. The overall response rate was 60.0%. The median survival time was 22 months, and the 2-year survival rate was 50.3%. Daily low-dose cisplatin and concurrent thoracic irradiation were well tolerated even by poor-risk patients with NSCLC, and showed a therapeutic efficacy similar to that for good-risk patients.

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BACKGROUND: Patients with recurrent soft tissue sarcoma (STS) are seldom curable, with 5-year survival rates of less than 10% in all large series. The role of high-dose chemotherapy (HDC) with hematopoietic stem cell support in this disease has not been established. CASE REPORT: We report on two patients with recurrent STS who were treated with tandem HDC supported by autologous peripheral blood stem cell transplantation (PBSCT). One patient with malignant fibrous histiocytoma recurred with multiple lung metastases. This patient achieved a partial response after two cycles of induction chemotherapy consisting of ifosfamide and epirubicin. During four cycles of induction chemotherapy, peripheral blood stem cells (PBSCs) were harvested. Tandem high-dose ICE regimen (ifosfamide 3 g/m2 on days-7 to -3, carboplatin 400 mg/m2 on days-7, -5 and 3, etoposide 500 mg/m2 on days-7, -5 and 3) supported by autologous PBSCT gave rise to further regression of the tumors. Another patient with malignant hemangiopericytoma was treated by tandem high-dose ICE regimen supported by autologous PBSCT after the 3rd removal of abdominal tumors. Relapse-free intervals until the 1st, 2nd and 3rd relapses were 40, 19 and 22 months, respectively. Tandem high-dose ICE regimen might delay the relapse. CONCLUSION: These observations suggest that a tandem high-dose ICE regimen with autologous PBSCT is feasible with some clinical efficacy in the control of refractory STS.

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(一社)日本皮膚悪性腫瘍学会  

近年、免疫チェックポイント阻害剤やBRAF+MEK阻害剤などの進行期悪性黒色腫に対する新規治療が生存期間の延長に寄与している。さらに進行した場合でも緩和治療を行いながら、積極的な治療介入も可能である。しかし緩和ケア病棟など緩和ケアを専門に提供する病院では原病の新規治療が困難な場合がある。がん診療専門病院と在宅医が連携することにより悪性黒色腫の新規治療をしながら在宅療養することも1つの選択肢となる。当科で経験した新規治療中で、訪問診療専門クリニックと連携した4例について検討した。男性3名、女性1名、年齢は36～84歳、全例病期IV、在宅医紹介時の治療は、BRAF+MEK阻害剤1例、ニボルマブ2例、イピリブマブ1例、在宅診療期間は24～84日であった。1例は当院、3例は自宅での看取りとなった。在宅診療の介入パターンはさまざまであるが、患者の希望に沿う進行期の治療が提供できた。(著者抄録)

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2020&ichushi_jid=J02197&link_issn=&doc_id=20200714360001&doc_link_id=10.5227%2Fskincancer.35.1&url=https%3A%2F%2Fdoi.org%2F10.5227%2Fskincancer.35.1&type=J-STAGE&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00007_2.gif

Language：Japanese   Publisher：緩和医療研究会  

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Language：English   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(株)羊土社  

＜Point＞・がん患者の痛みや吐き気をコントロールすることががん治療の基本である・オピオイドをはじめとした鎮痛薬の使い方を身につける・初回治療で吐かせないことが重要。リスクに応じてしっかり制吐療法を行う(著者抄録)

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(一社)日本皮膚悪性腫瘍学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(一社)日本緩和医療薬学会  

フェンタニル舌下錠は、がん疼痛の中で突出痛に用いられるレスキュー薬である。しかし、従来の速放性製剤と異なり、1日の使用回数や開始時の適正用量の検索など煩雑さを感じる薬剤である。そのため、多くの施設での積極的な使用には至っていない。岡山大学病院でフェンタニル舌下錠が処方された入院患者31名を対象に、患者の背景、至適投与量、至適投与量までに要した使用回数および日数、定期オピオイド鎮痛薬の1日投与量を後方視的に調査した。至適投与量は61%が100μgであり、至適投与量決定までに要した平均投与回数は3.8回、平均投与日数は2.3日であった。定期オピオイド鎮痛薬とフェンタニル舌下錠の至適量に相関はみられなかったが、6割の患者は最低用量で疼痛のコントロールが可能であり、外来での導入も可能であることが示唆された。そこで、患者記録シートを作成し、外来で安全に導入することを目的に取り組みを行った。(著者抄録)

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Language：English   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2013&ichushi_jid=J00298&link_issn=&doc_id=20130415260039&doc_link_id=%2Fcf0brond%2F2013%2Fs03502%2F021%2F0226-0226%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcf0brond%2F2013%2Fs03502%2F021%2F0226-0226%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本緩和医療学会  

緩和ケア病棟へ入院中の進行がん患者48名の血清マグネシウム値を測定し,マグネシウム製剤の内服の有無や全身状態とその臨床的意義を検討した.血清マグネシウムの平均値は2.09mg/dlであり,マグネシウム製剤投与例の平均値は2.17mg/dlと,マグネシウム製剤非投与例の平均値1.80mg/dlに比べて有意に高値であった(p=0.006).基準値(1.8～2.8mg/dl)を外れた高マグネシウム血症を2例,低マグネシウム血症を8例に認めたが,臨床的にマグネシウム異常に関連した症状は認められなかった.また,マグネシウム製剤の投与期間,投与量と血清マグネシウム値との関連も認められなかった.今回の検討では血清マグネシウム値の著明な異常は認められず,臨床的にもマグネシウム異常に関連した症状はみられなかった.しかし,緩和ケア病棟の患者はマグネシウム異常をきたしやすい状態であり,かつマグネシウム異常に伴う症状はがんの進行時にみられる症状と類似している.そのため,特に終末期でそのような症状を呈した場合,血清マグネシウム値の異常についても留意する必要があると考えられた.(著者抄録)

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：English   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

症例は61歳,男性.胃がんの診断で胃全摘術を施行されたのち,リンパ節転移と骨転移で再発し,両側尿管閉塞による慢性腎不全を併発したため緩和ケア病棟へ紹介されて転院となった.遷延する尿路感染症に対して抗生剤点滴を行い改善がみられたが,その後,食事摂取量が減少し,血尿が出現し,さらに口腔内にも出血が認められるようになった.PT,APTTは測定不能と延長していたが,血小板,フィブリノーゲン,FDPは正常でDICは否定された.血清のPIVKA-IIが著明高値,ビタミンKは低値であり,ビタミンKの投与にてPT,APTT,出血症状の改善を認めた.本症例では,食欲低下と抗生剤投与によりビタミンK欠乏が起こり,その結果,出血症状が出現したと考えられる.進行がん患者を対象とする緩和ケア領域では,経口摂取の低下や抗生剤使用などのためビタミンKの欠乏が生じやすく,出血症状がビタミンK欠乏症と終末期DICとの鑑別が必要な場合もあり,注意が必要と考えられた.(著者抄録)

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(株)自然科学社  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(公社)日本医学放射線学会  

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Language：Japanese   Publisher：(一社)日本職業・災害医学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(公社)日本医学放射線学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(NPO)日本緩和医療学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：English   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：English   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(株)最新医学社  

小細胞肺癌に対する標準的治療法は,限局型に対するシスプラチン,エトポシドとhyperfractionation法による胸部照射の同時併用療法,進展型に対するシスプラチンとエトポシドかイリノテカンの2剤併用療法,著効例に対する予防的全脳照射である.amrubicinなど新規抗がん剤の開発が期待されている.(著者抄録)

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2007&ichushi_jid=J00516&link_issn=&doc_id=20070319160009&doc_link_id=%2Fap7saisa%2F2007%2F0062s1%2F011%2F0634-0641%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fap7saisa%2F2007%2F0062s1%2F011%2F0634-0641%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2006&ichushi_jid=J01244&link_issn=&doc_id=20061120260305&doc_link_id=%2Fec7jaluc%2F2006%2F004605%2F303%2F0526-0526%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2006%2F004605%2F303%2F0526-0526%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2006&ichushi_jid=J00298&link_issn=&doc_id=20060719370011&doc_link_id=%2Fcf0brond%2F2006%2F002804%2F013%2F0315-0315%26dl%3D2&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcf0brond%2F2006%2F002804%2F013%2F0315-0315%26dl%3D2&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_5.gif

Language：Japanese   Publisher：(NPO)日本呼吸器内視鏡学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2006&ichushi_jid=J00298&link_issn=&doc_id=20060719370025&doc_link_id=%2Fcf0brond%2F2006%2F002804%2F027%2F0317-0317%26dl%3D2&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcf0brond%2F2006%2F002804%2F027%2F0317-0317%26dl%3D2&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_5.gif

Language：Japanese   Publisher：(株)篠原出版新社  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2005&ichushi_jid=J01244&link_issn=&doc_id=20051114300013&doc_link_id=%2Fec7jaluc%2F2005%2F004505%2F00e%2F0445-0445%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2005%2F004505%2F00e%2F0445-0445%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(株)へるす出版  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2005&ichushi_jid=J01244&link_issn=&doc_id=20051114300813&doc_link_id=%2Fec7jaluc%2F2005%2F004505%2F32e%2F0674-0674%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2005%2F004505%2F32e%2F0674-0674%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2005&ichushi_jid=J01244&link_issn=&doc_id=20051114300037&doc_link_id=%2Fec7jaluc%2F2005%2F004505%2F026%2F0465-0465%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2005%2F004505%2F026%2F0465-0465%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(一社)国立医療学会  

国立病院機構溝山陽病院一般病棟で死亡した肺癌患者63症例を対象に,ターミナル期の症状経過について検討を行った.1)26例は積極的治療を行えず,全体の90%以上が治療開始後2年以内に死亡していた.2)呼吸困難が他の癌種と比較して高頻度で,死亡30日前に約60%,死亡当日に90%異常が酸素吸入を受けていた.3)呼吸状態が悪い場合,呼吸抑制を案じてモルヒネ等のオピオイドを使用することがはばかられるため,疼痛コントロールが不十分となることが示唆された.4)呼吸困難の症状緩和技術の向上が,重要な課題であると考えられた

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2005&ichushi_jid=J00073&link_issn=&doc_id=20051215470003&doc_link_id=%2Fcl7iryoa%2F2005%2F005910%2F003%2F0539-0542%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fcl7iryoa%2F2005%2F005910%2F003%2F0539-0542%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(有)科学評論社  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本結核・非結核性抗酸菌症学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2004&ichushi_jid=J01244&link_issn=&doc_id=20041006270130&doc_link_id=%2Fec7jaluc%2F2004%2F004405%2F130%2F0368-0368%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2004%2F004405%2F130%2F0368-0368%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2003&ichushi_jid=J01244&link_issn=&doc_id=20031023340114&doc_link_id=%2Fec7jaluc%2F2003%2F004305%2F114%2F0485-0485%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2003%2F004305%2F114%2F0485-0485%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2003&ichushi_jid=J01244&link_issn=&doc_id=20031023340417&doc_link_id=%2Fec7jaluc%2F2003%2F004305%2F417%2F0561-0561%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2003%2F004305%2F417%2F0561-0561%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2003&ichushi_jid=J01244&link_issn=&doc_id=20031023340173&doc_link_id=%2Fec7jaluc%2F2003%2F004305%2F173%2F0500-0500%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2003%2F004305%2F173%2F0500-0500%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2003&ichushi_jid=J01244&link_issn=&doc_id=20031023340117&doc_link_id=%2Fec7jaluc%2F2003%2F004305%2F117%2F0486-0486%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2003%2F004305%2F117%2F0486-0486%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：English   Publisher：(一社)日本癌学会  

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Language：English   Publisher：(一社)日本癌学会  

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Language：English   Publisher：(一社)日本癌学会  

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Language：English   Publisher：(一社)日本癌学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：English   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2002&ichushi_jid=J01244&link_issn=&doc_id=20021114010070&doc_link_id=%2Fec7jaluc%2F2002%2F004205%2F071%2F0357-0357%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2002%2F004205%2F071%2F0357-0357%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2002&ichushi_jid=J01244&link_issn=&doc_id=20021114010597&doc_link_id=%2Fec7jaluc%2F2002%2F004205%2F598%2F0495-0495%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2002%2F004205%2F598%2F0495-0495%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Other Link： https://search.jamas.or.jp/default/link?pub_year=2002&ichushi_jid=J01244&link_issn=&doc_id=20021114010593&doc_link_id=%2Fec7jaluc%2F2002%2F004205%2F594%2F0494-0494%26dl%3D0&url=https%3A%2F%2Fwww.medicalonline.jp%2Fjamas.php%3FGoodsID%3D%2Fec7jaluc%2F2002%2F004205%2F594%2F0494-0494%26dl%3D0&type=MedicalOnline&icon=https%3A%2F%2Fjk04.jamas.or.jp%2Ficon%2F00004_2.gif

Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本癌治療学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：English   Publisher：(NPO)日本肺癌学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Language：Japanese   Publisher：(一社)日本呼吸器学会  

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Event date： 2019.6.21 - 2019.6.22

Language：Japanese   Presentation type：Oral presentation (general)  

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Event date： 2018.7.19 - 2018.7.21

Language：Japanese   Presentation type：Poster presentation  

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Event date： 2018.6.15 - 2018.6.16

Language：Japanese   Presentation type：Poster presentation  

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Event date： 2018.6.15 - 2018.6.16

Language：Japanese   Presentation type：Symposium, workshop panel (nominated)  

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Event date： 2018.6.15 - 2018.6.16

Language：Japanese   Presentation type：Poster presentation  

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Event date： 2016.7.28 - 2016.7.30

Language：Japanese   Presentation type：Oral presentation (general)  

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Event date： 2016.6.17 - 2016.6.18

Language：Japanese   Presentation type：Poster presentation  

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