記述言語：英語  

DOI： 10.3390/cancers13184604

PubMed

記述言語：英語  

DOI： 10.3390/cancers13163972

PubMed

記述言語：英語  

DOI： 10.3390/cells9061518

PubMed

記述言語：日本語  

DOI： 10.3390/cancers12051147

Web of Science

PubMed

記述言語：日本語  

DOI： 10.1053/j.semtcvs.2019.09.002

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PubMed

記述言語：英語   出版者・発行元：Nagoya journal of medical science  

There is little known about predictors of the effects of induction therapy in locally advanced lung cancer, including superior sulcus tumors. We analyzed whether intra-tumoral blood feeding could predict a pathologic complete response (pCR). Patients who underwent induction therapy followed by surgery for locally advanced lung cancer were retrospectively reviewed. The intra-tumoral blood feeding was defined by the CT value (HU, Hounsfield unit), which was calculated by subtracting the non-enhanced value from the contrast-enhanced value (divided into the early and delayed phase) at the maximum diameter of the tumor on dynamic CT. The cases were classified, according to the efficacy of induction therapy, into the pCR and residual tumor (pRT) group. There were 38 cases of T3 and 12 of T4; the induction therapy consisted of chemoradiotherapy in 39 patients, chemotherapy in 6, and radiotherapy in 5. A pCR was obtained in 15 (30%) patients. The mean CT values of the early and delayed phases in the pCR group were 14.8 and 30.7 HU, while those in the pRT were 15.3 and 32.2 HU, respectively. A logistic regression analysis revealed that a smaller tumor size (< 42 mm) was a non-significant predictor of a pCR (p = 0.09); the maximum standardized uptake value on FDG-PET and the CT values on the early and delayed phases of dynamic CT were not associated with the achievement of a pCR. In conclusion, intra-tumoral blood feeding of the locally advanced lung cancer did not predict the effects of induction therapy, whereas smaller sized tumors tended to show a better response.

DOI： 10.18999/nagjms.81.2.291

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Scopus

PubMed

記述言語：英語   出版者・発行元：Annals of Thoracic Surgery  

Background: Programmed death ligand 1 (PD-L1) is reportedly expressed in various malignancies and is considered a prognostic factor. We attempted to reveal the usefulness of the PD-L1 expression as a prognostic factor in patients with thymoma. Methods: Eighty-one patients with thymoma who underwent surgical resection between 2004 and 2015 were retrospectively reviewed. The PD-L1 expression was evaluated by immunohistochemistry and stratified by the proportion of positive tumor cells. Strong membranous reactivity of the PD-L1 antibody in 1% or more of tumor cells was considered “positive.” The association between the PD-L1 expression and the clinicopathologic features was investigated. Results: The PD-L1 expression was positive in 22 patients (27%) and negative in 59 patients (73%). The PD-L1 positivity was significantly associated with type B2 and B3 thymoma (p < 0.001) and stage III and IV disease (p = 0.048). In addition, PD-L1 positive tumors showed a significantly higher maximum standardized uptake value than PD-L1 negative tumors (p = 0.026). The 5-year disease-free survival rate was 82% in PD-L1 positive patients and 88% in PD-L1 negative patients, showing no significant difference (p = 0.57). Furthermore, PD-L1 positivity was not an independent prognostic factor for the disease-free survival on a Cox proportional hazards analysis (p = 0.59). Conclusions: A strong expression of PD-L1 in thymoma was significantly associated with type B2 and B3 and higher pathologic stages. In addition, PD-L1 positivity was associated with an increased maximum standardized uptake value of the tumor. However, patients with PD-L1 positive thymomas did not show a significantly worse prognosis than patients with PD-L1 negative tumors.

DOI： 10.1016/j.athoracsur.2018.08.037

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Scopus

PubMed

記述言語：日本語  

Web of Science

記述言語：英語   出版者・発行元：International Journal of Clinical Oncology  

Background: Differences in individual body sizes have not been well considered when analyzing the survival of patients with non-small cell lung cancer (NSCLC). We hypothesized that physique-adjusted tumor size is superior to actual tumor size in predicting the prognosis. Methods: Eight hundred and forty-two patients who underwent R0 resection of NSCLC between 2005 and 2012 were retrospectively reviewed, and overall survival (OS) was evaluated. The physique-adjusted tumor size was defined as: x-adjusted tumor size = tumor size × mean value of x/individual value of x [x = height, weight, body surface area (BSA), or body mass index (BMI)]. Tumor size category was defined as ≤2, 2–3, 3–5, 5–7, and >7 cm. The separation index (SEP), which is the weighted mean of the absolute value of estimated regression coefficients over the subgroups with respect to a reference group, was used to measure the separation of subgroups. Results: The mean values of height, weight, BSA, and BMI were 160.7 cm, 57.6 kg, 1.59 m2, and 22.2 kg/m2, respectively. The 5-year survival rates ranged from 88−59% in the non-adjusted tumor size model (SEP 1.937), from 90−57% in the height-adjusted model (SEP 2.236), from 91−52% in the weight-adjusted model (SEP 2.146), from 90−56% in the BSA-adjusted model (SEP 2.077), and from 91−51% in the BMI-adjusted model (SEP 2.169). Conclusions: The physique-adjusted tumor size can separate the survival better than the actual tumor size.

DOI： 10.1007/s10147-017-1219-6

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Scopus

PubMed

記述言語：日本語  

Web of Science

記述言語：日本語  

DOI： 10.1093/ejcts/ezx124

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PubMed

記述言語：日本語  

Web of Science

記述言語：日本語  

Web of Science

記述言語：英語   出版者・発行元：General Thoracic and Cardiovascular Surgery  

Objectives: The aim of this study was to investigate the feasibility and safety of our surgical experiences conducted in collaboration with cardiovascular surgeons at our institution. Methods: From May 2002 to December 2015, among 3595 general thoracic surgeries, 75 (2.1%) operations were carried out collaboratively with cardiovascular surgeons at Nagoya University Hospital. We investigated the surgical procedures, manipulated organs, morbidity and mortality, completeness of surgical resection, and prognosis of these 75 cases. Results: The study cohort consisted of 56 males and 19 females, ranging in age from 18 to 79 years (median 60 years). Fifty-eight patients had a malignant disease, and 17 had a benign disease. Out of 75 collaborative surgeries, 53 (71%) were scheduled cases (cardiovascular surgeons’ support was considered to be necessary preoperatively), and 22 (29%) were emergent cases (cardiovascular surgeons’ support was considered to be necessary intraoperatively). No 30- or 90-day mortality was observed. Respiratory failure, defined as the requirement of mechanical ventilation or non-invasive positive pressure ventilation for ≥5 days, was the most common morbidity (n = 14, 18%). Forty-three patients (78%) out of 55 with thoracic neoplasms achieved microscopic complete resection. The resection status of the remaining 12 (22%) was microscopic residual tumor. Conclusion: Collaborative surgeries with cardiovascular surgeons at our institution were feasible. High-quality surgeries with a good balance between safety and completeness of resection are important not only for treatment, but also in terms of education for general thoracic surgeons.

DOI： 10.1007/s11748-017-0800-2

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PubMed

記述言語：英語   出版者・発行元：Oncogene  

Malignant mesothelioma (MM) is an aggressive tumor commonly caused by asbestos exposure after a long latency. Focal adhesion kinase (FAK) inhibitors inhibit the cell growth of Merlin-deficient MM cells; however, their clinical efficacy has not been clearly determined. The aim of this study was to evaluate the growth inhibitory effect of the FAK inhibitor VS-4718 on MM cell lines and identify biomarkers for its efficacy. Although most Merlin-deficient cell lines were sensitive to VS-4718 compared with control MeT-5A cells, a subset of these cell lines exhibited resistance to this drug. Microarray and qRT-PCR analyses using RNA isolated from Merlin-deficient MM cell lines revealed a significant correlation between E-cadherin mRNA levels and VS-4718 resistance. Merlin- and E-cadherin-negative Y-MESO-22 cells underwent apoptosis upon treatment with a low concentration of VS-4718, whereas Merlin-negative, E-cadherin-positive Y-MESO-9 cells did not undergo VS-4718-induced apoptosis. Furthermore, E-cadherin knockdown in Merlin-negative MM cells significantly sensitized cells to VS-4718 and induced apoptotic cell death upon VS-4718 treatment. Together, our results suggest that E-cadherin serves as a predictive biomarker for molecular target therapy with FAK inhibitors for patients with mesothelioma and that its expression endows MM cells with resistance to FAK inhibitors.

DOI： 10.1038/onc.2017.147

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PubMed

担当区分：筆頭著者  

DOI： 10.1007/s11748-015-0525-z