Biomedical subjects

Kenji Sugio

Publications and source records attributed to Kenji Sugio.

At least 37 records · Page 2Linked to original sources

PubMed2005

Expression of endoplasmic reticulum molecular chaperone Grp78 in human lung cancer and its clinical significance.

All eukaryotic cells respond to the accumulation of unfolded proteins in the endoplasmic reticulum (ER) by signaling an adaptive pathway termed the unfolded protein response (UPR). Glucose-regulated protein (Grp) 78 is a molecular chaperone involved in the UPR. The aim of this study was to detect Grp78 expression in lung cancer using immunohistochemical (IHC) staining, and also to evaluate the relationship between the Grp78 expression level and the prognosis of patients with lung cancer. We used immunohistochemistry to analyze the protein expression of Grp78 in paraffin-embedded tumor samples from 132 well-characterized lung cancer patients and compared the expression level of Grp78, clinical variables and survival outcome. A positive expression of Grp78 was detected in the cytoplasm of tumor cells in 88 of the 132 patients (66.7%) with lung cancer. No significant difference was observed between the Grp78 expression and the gender, age at operation, histological type, pathologic stage, pathologic T status, and pathologic N status. Lung cancer patients with a positive Grp78 expression tended to show a better prognosis than those with a negative Grp78 expression. In addition, a multivariate analysis of the clinicopathologic characteristics of lung cancer indicated a positive expression of Grp78 to be a significant factor for predicting a favorable prognosis (p < 0.001, risk ratio = 2.35). A positive expression of Grp78 may thus be a useful marker for predicting a favorable prognosis in patients undergoing a resection of lung cancer. The ER stress pathway mediated by Grp78 may therefore be responsible for controlling the growth of lung cancer cells.

Adult↗

PubMed2005

A lack of prognostic significance regarding DeltaNp63 immunoreactivity in lung cancer.

DeltaNp63 is an isoform of the p53 homologue p63, which lacks an amino-terminal transactivation domain and antagonizes the induction of the gene expression by Deltap63. The aim of this study was to detect the DeltaNp63 expression in lung cancer using immunohistochemical (IHC) staining, and to evaluate the relationship between theDeltaNp63 expression level and the prognosis based on resected lung cancer tissues specimens from the of patients. We used immunohistochemistry to analyze the protein expression of DeltaNp63 in paraffin-embedded tumor samples from 161 well-characterized squamous cell carcinoma patients and compared the expression level of DeltaNp63, clinical variables and the survival outcome. Seventy-seven patients (47.8%) showed positive staining for DeltaNp63 in the nuclei of tumor cells. No significant difference was observed between the DeltaNp63 expression and the gender, age at operation, pathologic stage, pathologic T status, and pathologic N status. Based on the actuarial survival method, Kaplan-Meier method, and the log-rank test, the DeltaNp63 expression was not associated with survival for lung cancer. Differences in survival remained insignificant even after lung cancer patients were stratified according to stage or differentiation. The prognostic effects of DeltaNp63 expression do not appear to act as an important prognostic indicator in lung cancer. Our findings do not support that immunocytochemical markers demonstrate a relevant prognostic role in lung cancer.

Aged↗

PubMed2005

Identification of tumor associated antigens recognized by IgG from tumor-infiltrating B cells of lung cancer: correlation between Ab titer of the patient's sera and the clinical course.

We previously demonstrated that TIB recognize tumor antigens and produce antibodies against them. In the present study, we identified three tumor antigens recognized by TIB in lung cancer and evaluated whether changes in the antibody titer against these antigens correlated with the patient's clinical course. A lung cancer cell line, G603L, was established from a primary lung tumor of a patient, G603. Seven months later, adrenal metastasis was detected and surgically resected. The latter tumor was mildly infiltrated with B cells and xenotransplanted into SCID mice to obtain human IgG. A cDNA library was constructed from G603L and SEREX was carried out using TIB-derived IgG. The sero-reactive clones were sequenced and one of these antigens was revealed to be MAGE-B2 whereas the others were novel antigens. In the immuno-monitoring of the patient's sera, high antibody titer against MAGE-B2 was observed before operation and the titer decreased after resection of the primary tumor. It was elevated again at the time of adrenal metastasis, but then decreased after resection. The change in antibody titer against the second antigen was similar to MAGE-B2, and the antibody titer against the third antigen was low before the primary operation but increased at the time of recurrence. Our results suggest that TIB recognized tumor antigens and the antibody titers against these antigens were changed along with the patient's clinical course. Therefore, these antibodies could be used as tumor markers for the patient.

Aged↗

PubMed2004

Tumor specific expression of survivin-2B in lung cancer as a novel target of immunotherapy.

BACKGROUND: Survivin-2B is reported to be specifically expressed in numerous malignant tissues. Furthermore, survivin-2B includes the epitope peptide (survivin-2B(80-88)) which is capable of binding to HLA-A24. In this study, we evaluated whether survivin-2B could be a novel vaccine target against lung cancer. METHOD: (1) The differences in the survivin-2B expression between 15 sets of lung cancer tissues and normal lung tissues were investigated using RT-PCR. (2) The expression of survivin-2B was further examined in 42 lung cancer tissues, and the relationship between the expression and clinicopathologic factors was analyzed. (3) To compare the frequency of precursor CTL between survivin-2B positive and negative lung cancer patients, surivivin-2B(80-88) peptide-specific CTL were induced from regional lymph node lymphocytes (LNL) of four HLA-A24 (+) lung cancer patients, in whom two showed a positive survivin-2B expression of lung cancer while another two were negative, after stimulation with surivivin-2B(80-88). RESULTS: Survivin-2B was specifically expressed in lung cancer tissues, and was expressed in 17 of 42 lung cancer tissues (42.9%). Histologically, it was significantly more frequently expressed in squamous cell carcinoma than in adenocarcinoma (p=0.014). The frequency of precursor CTL in LNL was approximately one in 2.0 x 10(7) in patients with survivin-2B expression (-) lung cancer, however, it was one in 5.0 x 10(6) to 6.0 x 10(6) in those with survivin-2B expression (+) lung cancer. CONCLUSIONS: Survivin-2B was specifically expressed in lung cancer tissue, and found to specifically elicit a cellular immune response in lung cancer patients and therefore it may be a novel candidate for peptide vaccination.

Antigens, Neoplasm↗

PubMed2004

[Tumor marker in primary lung cancer].

Serum tumor markers are non-invasive diagnostic tools for malignant tumor and commonly used for screening of cancer and as an indicator of treatment-effect. In small cell lung cancer, NSE and proGRP are effective markers. In non-small cell lung cancer (NSCLC), CEA, SCC, CYFRA21-1, SLX and CA19-9 are commonly used for screening, and at least one marker among CEA, SCC or CYFRA21-1 is positive in 77% of patients with NSCLC. According to the histological type, the positive rate of CEA and CYFRA21-1 is high in adenocarcinoma patients, and the positive rate of CYFRA21-1 and SCC is high in squamous cell carcinoma patients. This review summarizes the clinical usefulness of tumor markers in primary lung cancer.

Antigens, Neoplasm↗

PubMed2004

Expression of deltaNp73 predicts poor prognosis in lung cancer.

PURPOSE: DeltaNp73 is an isoform of the p53 homologue p73, which lacks an NH(2)-terminal transactivation domain and antagonizes the induction of gene expression by p53/p73. The aim of this study was to detect DeltaNp73 expression in lung cancer and to evaluate the relationship between the DeltaNp73 expression level and the prognosis of patients with resected lung cancer. EXPERIMENTAL DESIGN: We used immunohistochemistry to analyze the protein expression of DeltaNp73 in paraffin-embedded tumor samples from 132 well-characterized lung cancer patients and compared the expression level of DeltaNp73, clinical variables, and survival outcome. RESULTS: Positive expression of DeltaNp73 was detected mainly in the cytoplasm of tumor cells in 77 of 132 patients (58.3%) with lung cancer. The incidence of positive expression of DeltaNp73 was 52.2, 50.0, and 70.2% in patients with stage I, II, and III, respectively (P = 0.04). Positive expression of DeltaNp73 was associated with gender but not associated with age, histologic type, pathological stage, pathological T status, and pathological N status. Lung cancer patients with positive DeltaNp73 expression had a poorer prognosis than those with negative DeltaNp73 expression. In addition, multivariate analysis of the clinicopathological characteristics of lung cancer indicated that positive expression of DeltaNp73 was a significant independent factor for predicting poor prognosis (P < 0.0001, risk ratio = 3.39). CONCLUSIONS: Expression of DeltaNp73 may be a useful marker for predicting poor prognosis of patients who underwent resection of lung cancer.

Adult↗

PubMed2004

Regulation of p27 by S-phase kinase-associated protein 2 is associated with aggressiveness in non-small-cell lung cancer.

PURPOSE: The F-box protein S-phase kinase-associated protein 2 (Skp2) is one of the positive regulators of the cell cycle that promote ubiquitin-mediated proteolysis of the cyclin-dependent kinase inhibitor p27. In this study, we investigated the significance of Skp2 expression in human non-small-cell lung cancer (NSCLC). PATIENTS AND METHODS: Clinicopathologic features and immunohistochemical expression of Skp2 and p27 proteins were studied in 138 patients with NSCLC. Survival analyses were performed using the Kaplan-Meier method and the Cox regression model. To analyze the role of Skp2 in vitro, NSCLC cells were transfected with an Skp2-expressing vector or small interfering RNA. RESULTS: Skp2 was overexpressed in males, smokers, patients with squamous cell carcinomas, and patients with poorly differentiated cancers (P = .034, < .0001, < .0001, and .002, respectively). The multivariant analysis revealed that Skp2 expression is an independent prognostic factor for survival in NSCLC. An inverse relationship of Skp2 with p27 expression was observed (P = .012), and patients with both a higher expression of Skp2 and a lower expression of p27 showed a significantly unfavorable prognosis (P = .0002). In vitro ectopic expression of Skp2 in NSCLC cells reduced the protein level of p27. Conversely, induction of Skp2 siRNA increased the protein level of p27, leading to growth inhibition in NSCLC cells. CONCLUSION: Skp2 overexpression is closely associated with the suppression of p27 and the aggressiveness in NSCLC. It also could be a therapeutic target in NSCLC.

Adult↗

PubMed2004

Simultaneous cellular and humoral immune response against mutated p53 in a patient with lung cancer.

We recently identified several Ags recognized by tumor-infiltrating B lymphocyte-derived Ab using SCID mice and a xenografted non-small cell lung cancer system. One of these identified Ags was mutated p53 with a point mutation resulting in the alteration of codon 158 from Arg to Leu. The aim of this study was to ascertain whether cellular immunity against mutated p53 exists in the same patient together with humoral immunity. Two different nona peptides (mutated p53(150) and p53(155) peptides), including a mutated amino acid derived from p53, were synthesized according to the binding motif of HLA class I of the established cancer cell line A904L from the patient. Mediastinal lymph node lymphocytes of the patient were stimulated weekly with the peptides. The mutated p53(155) peptide-stimulated lymphocytes showed specific cytotoxicity against both autologous EBV-transformed B cells pulsed with mutated p53(155) peptide and A904L. The mutated p53(155) peptide-specific CTL clone in an HLA-Cw*0702 restriction was established and analyzed for its TCR usage. Clonotypic PCR using CDR3-specific primers was applied to the tumor tissue containing the tumor-infiltrating lymphocytes. The specific amplification of PCR was found in the tumor tissue. These results demonstrated that not only B lymphocytes producing specific Ab against the p53 protein, but also CTL against mutated p53, expressed in autologous lung cancer cells exist in the tumor tissue. This approach may allow us to better understand the mechanisms of T and B cell immunity against the same tumor Ag in cancer patients.

Amino Acid Sequence↗

PubMed2004

Hypermethylation of FHIT as a prognostic marker in nonsmall cell lung carcinoma.

BACKGROUND: Methylation of CpG islands in the promoter and upstream coding regions has been identified as a mechanism for transcriptional inactivation of tumor suppressor genes. The purpose of the current study was to determine the correlation between the aberrant promoter methylation of multiple genes and survival in patients with nonsmall cell lung carcinoma (NSCLC). METHODS: The methylation status of nine genes was determined in 124 surgically resected NSCLC cases using methylation-specific polymerase chain reaction. RESULTS: The methylation frequencies of the genes tested in NSCLC specimens were 52% for E-cadherin (CDH1), 41% for RAS association domain family protein (RASSF1A), 38% for fragile histidine triad (FHIT) and adenomatous polyposis coli (APC), 27% for retinoic acid receptor beta (RARbeta) and H-cadherin (CDH13), 20% for p16INK4A, 0.8% for O6-methylguanine-DNA-methyltransferase (MGMT), and 0% for glutathione S-transferase P1 (GSTP1). The survival of the patients with FHIT methylation-positive tumors was found to be significantly shorter than that for those patients with methylation-negative tumors (P=0.03), even in those patients with International Union Against Cancer TNM Stage I or Stage II disease (P=0.007). In contrast, there were no significant survival differences noted between the methylation-positive and methylation-negative tumors for the other genes tested. In addition, based on multivariate analyses, FHIT methylation-positive status was found to be independently associated with poor survival (P=0.046) and disease stage (P<0.0001). CONCLUSIONS: The results of the current study suggest that methylation of FHIT is a useful biomarker of biologically aggressive disease in patients with NSCLC.

Acid Anhydride Hydrolases↗

PubMed2004

Carinal resection after induction bronchial arterial infusion for locally advanced non-small cell lung cancer.

We herein describe 3 cases of a carinal resection after induction bronchial arterial infusion (BAI) for locally advanced non-small cell lung cancer (NSCLC). Case 1 was a 44-year-old man with T1N2M0 adenocarcinoma. After undergoing Nd-YAG laser treatment (5079 J) and BAI [cis-diamminedichloro platinum (CDDP) 100 mg/body], a right sleeve upper lobectomy with a carinal resection and reconstruction (Montage type) was performed. Case 2 was a 67-year-old man with T4N1M0 squamous cell carcinoma. After BAI (CDDP 120 mg/body), an operation (same as case 1) was performed. Case 3 was a 72-year-old man with T4N2M0 squamous cell carcinoma. After BAI (CDDP 120 mg/body), a right sleeve peumonectomy was performed. There was neither BAI-related intraoperative nor postoperative complications. BAI with CDDP was thus found to be a useful and effective therapeutic modality for locally advanced NSCLC invading the carina.

Adult↗

PubMed2004

The significance of serum active matrix metalloproteinase-9 in patients with non-small cell lung cancer.

Matrix metalloproteinase-9 (MMP-9) plays an essential role for metastasis. The purpose of this study is to investigate the significance of active MMP-9 quantified in serum of patients with non-small cell lung cancer. Immunohistochemical staining of the primary tumors was also performed to analyze how much the secretion of MMP-9 from cancer cells influences the concentration of MMP-9 in serum. The preoperative sera of 39 patients with NSCLC, who underwent an operation at our institution from 1996 to 1999, were taken before the operation. Forty-three samples of sera were drawn postoperatively. Of these 43 samples, 16 sera were taken from patients who suffered with recurrence, 27 sera were taken from patients who did not suffer with recurrence. The serum level of active MMP-9 of preoperative state was 24.3 +/- 21.2 ng/ml, which was higher than that of control was 14.6 +/- 18.8 ng/ml, but no significance was recognized statistically between them (P = 0.0666). The immunoreactivity of MMP-9 was not correlated statistically with serum level of total MMP-9 and active MMP-9. The activity ratio of non-recurrent group was also a lower level than that of recurrent group (P = 0.0082). In conclusion, our results suggest that the concentration of serum active MMP-9 has a possibility of being an available marker to detect a recurrent disease. Our findings strongly suggest that measuring the activity ratio of serum MMP-9 appears to be a potentially useful tumor maker.

Adult↗

PubMed2003

Aberrant methylation of the cyclin D2 promoter in primary small cell, nonsmall cell lung and breast cancers.

DNA methylation alteration of several genes contributes to human tumorigenesis. Cyclin D2, a member of the D-type cyclins, is implicated in cell cycle regulation and malignant transformation. In our study, we examined the methylation status of the cyclin D2 promoter in small cell lung cancer (SCLC), nonsmall cell lung cancer (NSCLC), breast tumors and tumor cell lines. We observed that aberrant methylation of cyclin D2 was present in 32 of 56 (57%) SCLC cell lines, 7 of 32 (22%) SCLC tumor tissues; 25 of 61 (47%) NSCLC cell lines, 19 of 48 (40%) NSCLC tumor tissues; 18 of 30 (60%) breast tumor cell lines and 19 of 63 (30%) breast tumor tissues. Methylation was more frequent in the tumor cell lines compared to the primary breast and SCLC tumors (p = 0.007 and p = 0.001, respectively). Methylation was rare in the control tissue samples; 0 of 12 peripheral blood lymphocytes; 0 of 12 buccal epithelial cells; 0 of 18 nonmalignant lung tissues and 3 of 28 (11%) nonmalignant breast tissues. Promoter methylation correlated with loss of transcript by reverse transcription PCR (RT-PCR) in 9 of 11 (6 lung, 5 breast) tumor cell lines tested. Two cell lines that were not methylated also lacked expression, suggesting that other mechanisms of inactivation may be involved. Expression was restored by treatment with the demethylating agent, 5 aza 2' deoxycytidine, in all 9 methylated cell lines. Our results confirm earlier reports in breast cancer and indicate that aberrant methylation of cyclin D2 may contribute to the pathogenesis of the 2 major types of lung cancers.

Adult↗

PubMed2003

Aberrant methylation of TMS1 in small cell, non small cell lung cancer and breast cancer.

TMS1 (target of methylation-induced silencing) is a CpG island-associated gene that functions in the regulation of apoptosis and encodes a caspase recruitment domain, a recently described motif found in apoptotic signaling molecules. Recent evidence suggests that silencing of genes in the apoptotic pathway contribute to human carcinogenesis. We examined the DNA methylation status of the TMS1 promoter in lung and breast tumor tissues, tumor cell lines and nonmalignant tissues by methylation-specific polymerase chain reaction (MSP) and its mRNA expression by reverse transcription PCR. Aberrant methylation of TMS1 was present in 70% (40 of 57) of small cell lung cancer (SCLC) cell lines and 41% (13 of 32) of SCLC tumor tissues, 48% (29 of 61) of non small cell lung cancer (NSCLC) cell lines and 40% (28 of 70) of NSCLC tumor tissues and 46% (12 of 26) of breast cancer cell lines and 32% (20 of 63) of breast tumor tissues. Methylation was absent in the peripheral blood lymphocytes and buccal epithelium from healthy volunteers, as well as in nonmalignant lung tissues and was rare in nonmalignant breast tissues 7% (2 of 30). DNA methylation was confirmed by sequence analysis and the methylation status correlated inversely with TMS1 RNA expression in 18 cell lines tested. RNA expression was restored by treatment with the demethylating agent 5-aza-2'-deoxycytidine, in 4 of 4 methylated cell lines that lacked the TMS1 transcript. Our results suggest that methylation of TMS1 may play a role in the pathogenesis of small cell and non small lung and breast cancers.

Adult↗

PubMed2003

Smoke exposure, histologic type and geography-related differences in the methylation profiles of non-small cell lung cancer.

Aberrant methylation of several known or putative tumor suppressor genes occurs frequently during the pathogenesis of lung cancers. There are major smoke exposure, histology, geography and gender-related changes in non-small cell lung cancer (NSCLC). We investigated smoking-related, histologic, geographic and gender differences in the methylation profiles of resected NSCLCs. We examined 514 cases of NSCLC and 84 corresponding nonmalignant lung tissues from 4 countries (USA, Australia, Japan and Taiwan) for the methylation status of 7 genes known to be frequently methylated in lung cancers [p16, RASSF1A (RAS association domain family 1), APC, RARbeta, CDH13, MGMT and GSTP1]. Multivariate analyses were used for data analysis. Adenocarcinoma was the major histologic type in women and never smokers; analyses that involved smoke exposure and gender were limited to this histology. Our major findings are a) methylation status of any single gene was largely independent of methylation status of other genes; b) the rates of methylation of p16 and APC and the mean Methylation Index (MI), a reflection of the overall methylation status, were significantly higher in ever smokers than in never smokers; c) the mean MI of tumors arising in former smokers was significantly lower than the mean of current smokers; d) the methylation rates of APC, CDH13 and RARbeta were significantly higher in adenocarcinomas than in squamous cell carcinomas; e) methylation rates of MGMT and GSTP1 were significantly higher in the USA and Australian cases than in those from Japan and Taiwan; and (f) no significant gender-related differences in methylation patterns were noted. Our findings demonstrate important smoke exposure, histologic type and geography-related differences in the methylation profiles of NSCLC tumors.

Adenomatous Polyposis Coli Protein↗

PubMed2003

Risk factors for multicentric occurrence of carcinoma in the upper aerodigestive tract-analysis with a serial histologic evaluation of the whole resected-esophagus including carcinoma.

BACKGROUND AND OBJECTIVES: We have reported that both lifestyle and family history might be related to multiplicity of carcinoma in the upper aerodigestive tract (UADT). The aim of this study was to elucidate the relationship between the number of carcinomas and risk factors. METHODS: A serial histologic evaluation of the entire non-irradiated esophagus was performed in 114 males with esophageal cancer who were divided into three groups (group I: 88 cases with solitary cancer, group II: 11 with double cancers, group III: 15 with three or more cancers). As controls, 228 males with benign diseases were selected. RESULTS: Among group III patients, both the incidence of heavy smoking and that of heavy drinking were 67% and 60%, which were significantly higher than those of group I (28% and 30%) and control subjects (14% and 10%, respectively). Heavy drinkers who were also heavy smokers were observed in 2, 10, 27, and 47% in control subjects, groups I, II, and III, respectively. Regarding family history, 27% of group III had a close relative with UADT or lung cancer, while the incidence was 7% in the control. CONCLUSIONS: These findings strongly support the hypothesis that heavy smoking and heavy drinking, as well as a family history of both UADT and lung cancer, might be risk factors for multicentric occurrence of UADT cancer.

Aged↗

PubMed2003

Alterations of tumor suppressor genes (Rb, p16, p27 and p53) and an increased FDG uptake in lung cancer.

OBJECTIVE: The FDG uptake in lung cancer is considered to reflect the degree of malignancy, while alterations of some tumor suppressor genes are considered to be related to the malignant biological behavior of tumors. The aim of this study is to examine the relationship between FDG-PET and alterations in the tumor suppression genes of lung cancer. METHODS: We examined 28 patients with primary lung cancer who underwent FDG-PET before surgery consisting of 17 patients with adenocarcinoma, 10 with squamous cell carcinoma and 1 with large cell carcinoma. The FDG-PET findings were evaluated based on the standardized uptake value (SUV). Alterations in the tumor suppressor genes, Rb, p16, p27 and p53, were evaluated immunohistochemically. RESULTS: The FDG uptake in lung cancer with alteration in each tumor suppressor gene tended to be higher than in those genes without alterations, although the differences were not significant. In 15 tumors with alterations in either tumor suppressor genes, the FDG uptake was 6.83 +/- 3.21. On the other hand, the mean FDG uptake was 1.95 in 2 tumors without alterations in any genes. The difference in the FDG uptake between the 2 groups was statistically significant (p < 0.001). CONCLUSIONS: In conclusion, the presence of abnormalities in the tumor suppressor genes, which results in an accelerated cell proliferation, is thus considered to increase the FDG uptake in lung cancer.

Adult↗

PubMed2003

Survival and prognostic factors of surgically resected T4 non-small cell lung cancer.

BACKGROUND: Category T4 nonsmall cell lung cancer (NSCLC) encompasses heterogenous subgroups. We retrospectively analyzed the survival of patients with surgically resected T4 NSCLC to evaluate the evidence for prognostic implications according to the subgroups of T4 category, nodal status, and resection completeness. METHODS: Seventy-six patients with T4N0-2M0 NSCLC were divided into three subgroups within the T4 category: 24 patients with the tumor invading the mediastinal organs (mediastinal group), 16 with a malignant pleural effusion or dissemination (pleural group), and 36 with satellite tumor nodules within the ipsilateral primary tumor lobe (satellite group). Complete resection was possible in 47 patients (61.8%). The pathologic N statuses were N0 in 28, N1 in 13, and N2 in 35 patients. RESULTS: The overall survival of the 76 patients was 19.1% at 5 years. The overall 5-year survivals according to the three subgroups of the T4 category were as follows: mediastinal group, 18.2%; pleural group, 0%; and satellite group, 26.7% (mediastinal/satellite versus pleural, p = 0.037). Factors significantly influencing the overall 5-year survival were the pathologic N status (N2 versus N0-1, p = 0.022) and the completeness of resection (complete versus incomplete, p = 0.0001). A multivariate survival analysis demonstrated that the pathologic N status and the completeness of resection were significant independent predictors of a poorer prognosis even after adjusting for the subgroup of the T4 category. CONCLUSIONS: Resectable T4N0-1 NSCLC that is not due to pleural disease deserves consideration of aggressive surgical resection with expected 5-year survival of about 20%.

Adult↗

PubMed2003

Hypertrophic osteoarthropathy associated with esophageal cancer.

Hypertrophic osteoarthropathy is extremely rare in patients with esophageal cancer. We herein describe a 65-year-old Japanese man whose esophageal cancer was diagnosed while examining his symptoms of hypertrophic osteoarthropathy. Esophagectomy and postoperative chemoradiation improved the typical radiologic findings of hypertrophic osteoarthropathy as well as the clinical symptoms. Furthermore, the patient has demonstrated a disease-free survival of more than 3 years.

Aged↗